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1
Teng, Shou-Cheng, Li-Ting Li, Shyi-Gen Chen, Tien-Mu Chen, Cheng-Hao Liao, and Hsu-Wei Fang. "DOSE-DEPENDENT EFFECTS OF ADIPOSE TISSUE-DERIVED STROMAL VASCULAR FRACTION CELLS ON ANGIOGENESIS AND FIBROSIS IN HUMAN FAT GRAFTS." Biomedical Engineering: Applications, Basis and Communications 26, no. 03 (March 17, 2014): 1450045. http://dx.doi.org/10.4015/s1016237214500458.
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Adipose tissue is not only an ideal material for soft tissue filling and augmentation, but also a plentiful source of regenerative cells in adipose-derived stromal vascular fraction. Enriched fat tissue with adipose-derived stromal vascular fraction cells (ADSVFCs) can improve the fat graft survival, as shown in previous studies. The objective of this study is to estimate the effects of various dosages of ADSVFCs on fat grafts. We hypothesized that the improvement of ADSVFCs on fat transplantation quality would be dose dependent. Fat tissues were obtained by liposuction surgery. ADSVFCs were mixed into fat tissue, and the ADSVFC-enriched fat tissues were implanted subcutaneously into nude mice. The histological findings showed that the neoangiogenesis and integrity of grafted fat cells significantly increased with increasing dosages of ADSVFCs. Higher dosages of ADSVFCs also significantly reduced the side effects of the fat grafts, including reducing inflammation, cell infiltration, fibrosis and cyst formation. In conclusion, ADSVFC supplemented fat implants can improve angiogenesis and anti-inflammation. However, these effects of ADSVFCs on fat graft quality are dose dependent.
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Khor, Victor K., Ming Han Tong, Yueming Qian, and Wen-Chao Song. "Gender-Specific Expression and Mechanism of Regulation of Estrogen Sulfotransferase in Adipose Tissues of the Mouse." Endocrinology 149, no. 11 (July 31, 2008): 5440–48. http://dx.doi.org/10.1210/en.2008-0271.
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Although primarily regarded as a sex steroid, estrogen plays an important role in many other physiological processes including adipose development and disposition. Estrogen sulfotransferase (EST) regulates estrogen activity by catalyzing the sulfoconjugation and inactivation of estrogens. In the present study, we report the gender-specific expression of EST in adipose tissues of the mouse and describe contrasting mechanisms of EST regulation in the fat and liver. EST is expressed in the white adipose tissues of the male but not female mouse. Within the various fat depots of male mice, it is most abundantly expressed in the epididymal fat pad, with variable levels in other white fats and no expression in the brown fat. Fractionation of epididymal fat cells showed EST to be predominantly associated with stromal vascular cells (preadipocyte). EST expression in male mouse adipose tissues is dependent on testosterone as castration ablated, and administration of exogenous testosterone restored, EST expression. Furthermore, testosterone treatment induced abnormal EST expression in the parametrial fat of female mice. EST induction by testosterone in female mice is tissue specific because testosterone treatment had no effect on liver EST expression. Conversely, the liver X receptor agonist TO-901317 induced EST expression in female mouse liver but not in their adipose tissues. Finally, we demonstrate that male EST knockout mice developed increased epididymal fat accumulation with enlarged adipocyte size. We conclude that EST is expressed in adipose tissues in a sexually dimorphic manner, is regulated by testosterone, and plays a physiological role in regulating adipose tissue accumulation in male mice.
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Cohen, Paul, and Bruce M. Spiegelman. "Cell biology of fat storage." Molecular Biology of the Cell 27, no. 16 (August 15, 2016): 2523–27. http://dx.doi.org/10.1091/mbc.e15-10-0749.
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The worldwide epidemic of obesity and type 2 diabetes has greatly increased interest in the biology and physiology of adipose tissues. Adipose (fat) cells are specialized for the storage of energy in the form of triglycerides, but research in the last few decades has shown that fat cells also play a critical role in sensing and responding to changes in systemic energy balance. White fat cells secrete important hormone-like molecules such as leptin, adiponectin, and adipsin to influence processes such as food intake, insulin sensitivity, and insulin secretion. Brown fat, on the other hand, dissipates chemical energy in the form of heat, thereby defending against hypothermia, obesity, and diabetes. It is now appreciated that there are two distinct types of thermogenic fat cells, termed brown and beige adipocytes. In addition to these distinct properties of fat cells, adipocytes exist within adipose tissue, where they are in dynamic communication with immune cells and closely influenced by innervation and blood supply. This review is intended to serve as an introduction to adipose cell biology and to familiarize the reader with how these cell types play a role in metabolic disease and, perhaps, as targets for therapeutic development.
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Li, Weijie, Julia Tonelli, Preeti Kishore, Randall Owen, Elliot Goodman, Philipp E. Scherer, and Meredith Hawkins. "Insulin-sensitizing effects of thiazolidinediones are not linked to adiponectin receptor expression in human fat or muscle." American Journal of Physiology-Endocrinology and Metabolism 292, no. 5 (May 2007): E1301—E1307. http://dx.doi.org/10.1152/ajpendo.00312.2006.
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Circulating adiponectin levels are increased by the thiazolidinedione (TZD) class of PPARγ agonists in concert with their insulin-sensitizing effects. Two receptors for adiponectin (AdipoR1 and AdipoR2) are widely expressed in many tissues, but their physiological significance to human insulin resistance remains to be fully elucidated. We examined the expression patterns of AdipoR1 and AdipoR2 in fat and skeletal muscle of human subjects, their relationship to insulin action, and whether they are regulated by TZDs. Expression patterns of both AdipoRs were similar in subcutaneous and omental fat depots, with higher expression in adipocytes than in stromal cells and macrophages. To determine the effects of TZDs on AdipoR expression, subcutaneous fat and quadriceps muscle were biopsied in 14 insulin-resistant subjects with type 2 diabetes mellitus after 45 mg pioglitazone or placebo for 21 days. This duration of pioglitazone improved insulin's suppression of glucose production by 41% and enhanced stimulation of glucose uptake by 27% in concert with increased gene expression and plasma levels of adiponectin. Pioglitazone did not affect AdipoR expression in muscle, whole fat, or cellular adipose fractions, and receptor expression did not correlate with baseline or TZD-enhanced insulin action. In summary, both adiponectin receptors are expressed in cellular fractions of human fat, particularly adipocytes. TZD administration for sufficient duration to improve insulin action and increase adiponectin levels did not affect expression of AdipoR1 or AdipoR2. Although TZDs probably exert many of their effects via adiponectin, changes in these receptors do not appear to be necessary for their insulin-sensitizing effects.
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Sotome, Rina, Akira Hirasawa, Motoi Kikusato, Taku Amo, Kyohei Furukawa, Anna Kuriyagawa, Kouichi Watanabe, et al. "In vivo emergence of beige-like fat in chickens as physiological adaptation to cold environments." Amino Acids 53, no. 3 (February 17, 2021): 381–93. http://dx.doi.org/10.1007/s00726-021-02953-5.
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AbstractWhile it has been hypothesized that brown adipocytes responsible for mammalian thermogenesis are absent in birds, the existence of beige fat has yet to be studied directly. The present study tests the hypothesis that beige fat emerges in birds as a mechanism of physiological adaptation to cold environments. Subcutaneous neck adipose tissue from cold-acclimated or triiodothyronine (T3)-treated chickens exhibited increases in the expression of avian uncoupling protein (avUCP, an ortholog of mammalian UCP2 and UCP3) gene and some known mammalian beige adipocyte-specific markers. Morphological characteristics of white adipose tissues of treated chickens showed increased numbers of both small and larger clusters of multilocular fat cells within the tissues. Increases in protein levels of avUCP and mitochondrial marker protein, voltage-dependent anion channel, and immunohistochemical analysis for subcutaneous neck fat revealed the presence of potentially thermogenic mitochondria-rich cells. This is the first evidence that the capacity for thermogenesis may be acquired by differentiating adipose tissue into beige-like fat for maintaining temperature homeostasis in the subcutaneous fat ‘neck warmer’ in chickens exposed to a cold environment.
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Chang, Lin, Minerva T. Garcia-Barrio, and Y. Eugene Chen. "Perivascular Adipose Tissue Regulates Vascular Function by Targeting Vascular Smooth Muscle Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (May 2020): 1094–109. http://dx.doi.org/10.1161/atvbaha.120.312464.
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Adipose tissues are present at multiple locations in the body. Most blood vessels are surrounded with adipose tissue which is referred to as perivascular adipose tissue (PVAT). Similarly to adipose tissues at other locations, PVAT harbors many types of cells which produce and secrete adipokines and other undetermined factors which locally modulate PVAT metabolism and vascular function. Uncoupling protein-1, which is considered as a brown fat marker, is also expressed in PVAT of rodents and humans. Thus, compared with other adipose tissues in the visceral area, PVAT displays brown-like characteristics. PVAT shows a distinct function in the cardiovascular system compared with adipose tissues in other depots which are not adjacent to the vascular tree. Growing and extensive studies have demonstrated that presence of normal PVAT is required to maintain the vasculature in a functional status. However, excessive accumulation of dysfunctional PVAT leads to vascular disorders, partially through alteration of its secretome which, in turn, affects vascular smooth muscle cells and endothelial cells. In this review, we highlight the cross talk between PVAT and vascular smooth muscle cells and its roles in vascular remodeling and blood pressure regulation.
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Salehi-Nik, Nasim, Maryam Rezai Rad, Lida Kheiri, Pantea Nazeman, Nasser Nadjmi, and Arash Khojasteh. "Buccal Fat Pad as a Potential Source of Stem Cells for Bone Regeneration: A Literature Review." Stem Cells International 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/8354640.
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Adipose tissues hold great promise in bone tissue engineering since they are available in large quantities as a waste material. The buccal fat pad (BFP) is a specialized adipose tissue that is easy to harvest and contains a rich blood supply, and its harvesting causes low complications for patients. This review focuses on the characteristics and osteogenic capability of stem cells derived from BFP as a valuable cell source for bone tissue engineering. An electronic search was performed on all in vitro and in vivo studies that used stem cells from BFP for the purpose of bone tissue engineering from 2010 until 2016. This review was organized according to the PRISMA statement. Adipose-derived stem cells derived from BFP (BFPSCs) were compared with adipose tissues from other parts of the body (AdSCs). Moreover, the osteogenic capability of dedifferentiated fat cells (DFAT) derived from BFP (BFP-DFAT) has been reported in comparison with BFPSCs. BFP is an easily accessible source of stem cells that can be obtained via the oral cavity without injury to the external body surface. Comparing BFPSCs with AdSCs indicated similar cell yield, morphology, and multilineage differentiation. However, BFPSCs proliferate faster and are more prone to producing colonies than AdSCs.
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Wasinski, Frederick, Reury F. P. Bacurau, Milton R. Moraes, Anderson S. Haro, Pedro M. M. Moraes-Vieira, Gabriel R. Estrela, Edgar J. Paredes-Gamero, et al. "Exercise and Caloric Restriction Alter the Immune System of Mice Submitted to a High-Fat Diet." Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/395672.
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As the size of adipocytes increases during obesity, the establishment of resident immune cells in adipose tissue becomes an important source of proinflammatory mediators. Exercise and caloric restriction are two important, nonpharmacological tools against body mass increase. To date, their effects on the immune cells of adipose tissue in obese organisms, specifically when a high-fat diet is consumed, have been poorly investigated. Thus, after consuming a high-fat diet, mice were submitted to chronic swimming training or a 30% caloric restriction in order to investigate the effects of both interventions on resident immune cells in adipose tissue. These strategies were able to reduce body mass and resulted in changes in the number of resident immune cells in the adipose tissue and levels of cytokines/chemokines in serum. While exercise increased the number of NK cells in adipose tissue and serum levels of IL-6 and RANTES, caloric restriction increased the CD4+/CD8+ cell ratio and MCP-1 levels. Together, these data demonstrated that exercise and caloric restriction modulate resident immune cells in adipose tissues differently in spite of an equivalent body weight reduction. Additionally, the results also reinforce the idea that a combination of both strategies is better than either individually for combating obesity.
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Robidoux, Jacques, Peivand Pirouzi, Julie Lafond, and Roland Savard. "Site-specific effects of sympathectomy on the adrenergic control of lipolysis in hamster fat cells." Canadian Journal of Physiology and Pharmacology 73, no. 4 (April 1, 1995): 450–58. http://dx.doi.org/10.1139/y95-057.
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Regional variations in the response of adipose tissue to lipolytic stimuli have been suggested to be involved in the development of visceral adiposity-related morbidity and mortality. Moreover, studies in humans and in laboratory rodents such as hamsters have shown that the response of adipocytes to catecholamines depends on their anatomical origin. The aim of the present study was to investigate the relative involvement of the adrenal medulla and of the sympathetic nervous system on regional differences in the adrenergic control of lipolysis in isolated adipocytes from inguinal and epididymal adipose tissues. For this purpose, we carried out adrenal demedullation or chemical sympathectomy in hamsters. The results confirmed that epididymal adipocytes were significantly more responsive to a β-adrenergic stimulation than inguinal adipocytes (p ≤ 0.05). This site specificity could originate at a step distal to receptors since tissues exhibited a similar number of binding sites for [125I]cyanopindolol. No significant regional differences were observed in the α2-adrenergic antilipolytic response, with the exception of the clonidine EC50. A 14-day sympathectomy significantly increased the β-adrenergic lipolytic response only in inguinal adipocytes (p < 0.05), and increased the α2_adrenergic response only in epididymal adipocytes (p < 0.05). On the other hand, adrenal demedullation had no effect on both adrenergic pathways. These results suggest that the sympathetic tone of adipose tissues could be involved in the α2- and β-adrenergic site-specific response in hamster fat cells. The 33% increase of the β-response in inguinal fat cells and the 38% increase of the α2-response in epididymal fat cells also suggest that the sympathetic pathway favors the lipolytic activation of the epididymal adipose tissue.Key words: white adipose tissue, adrenal demedullation, α2-adrenergic receptors, β-adrenergic receptors.
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Bashir, Muhammad M., Muhammad Sohail, Fridoon J. Ahmad, and Mahmood S. Choudhery. "Preenrichment with Adipose Tissue-Derived Stem Cells Improves Fat Graft Retention in Patients with Contour Deformities of the Face." Stem Cells International 2019 (November 20, 2019): 1–9. http://dx.doi.org/10.1155/2019/5146594.
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Quick absorption of adipose tissue grafts makes the outcomes less satisfactory for clinical applications. In the current study, adipose tissue grafts were mixed with adipose tissue-derived stem cells (ASCs) to improve retention of adipose tissue grafts and to make the clinical outcomes of fat grafting more reliable. Adipose tissue was either injected alone (conventional group) or mixed with ASCs (stem cell group) before injection. In both groups, adipose tissue was injected at the site of contour throughout layers of tissues till visual clinical symmetry with the opposite side was achieved. The volume of injected fat graft was measured after 72 hours and 6 months using a B-mode ultrasound device connected with a 12 MH frequency probe. The percentage reduction in the volume of injected fat, physician satisfaction scores (Ph-SCs), and patient satisfaction scores (P-SCs) were also recorded. After 6 months, there was significantly lower fat absorption in the stem cell group as compared to the conventional group. Mean physician and patient satisfaction scores were significantly improved in the stem cell group. No significant adverse effects were noted in any patient. Significantly lower absorption of graft due to the use of ASCs improves the clinical outcomes of conventional fat grafting for contour deformities of the face. The current preenrichment strategy is noninvasive, safe and can be applied to other diseases that require major tissue augmentation such as breast surgery. This trial is registered with NCT02494752.
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Mujkić, Robert, Darija Šnajder Mujkić, Ivana Ilić, Edi Rođak, Antun Šumanovac, Anđela Grgić, Dalibor Divković, and Kristina Selthofer-Relatić. "Early Childhood Fat Tissue Changes—Adipocyte Morphometry, Collagen Deposition, and Expression of CD163+ Cells in Subcutaneous and Visceral Adipose Tissue of Male Children." International Journal of Environmental Research and Public Health 18, no. 7 (March 31, 2021): 3627. http://dx.doi.org/10.3390/ijerph18073627.
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Childhood obesity is a complex health problem, and not many studies have been done on adipose tissue remodeling in early childhood. The aim of this study was to examine extracellular matrix remodeling in the adipose tissue of healthy male children depending on their weight status. Subcutaneous and visceral adipose tissue was obtained from 45 otherwise healthy male children who underwent elective surgery for hernia repairs or orchidopexy. The children were divided into overweight/obese (n = 17) or normal weight groups (n = 28) depending on their body mass index (BMI) z-score. Serum was obtained for glucose, testosterone, triglyceride, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) measurements. Sections of adipose tissue were stained with hematoxylin and eosin to determine the adipocytes’ surface area, and Masson’s trichrome stain was used to detect the adipocytes’ collagen content. Immunohistochemistry for CD163+ cells was also performed. The results showed that male children in the overweight group had higher serum triglyceride levels, greater adipocyte surface area and collagen content in their subcutaneous adipose tissue, more crown-like structures in fat tissues, and more CD163+ cells in their visceral adipose tissue than males in the normal weight group. In conclusion, in male children, obesity can lead to the hypertrophy of adipocytes, increased collagen deposition in subcutaneous adipose tissues, and changes in the polarization and accumulation of macrophages.
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Gómez-Hernández, Almudena, Nuria Beneit, Sabela Díaz-Castroverde, and Óscar Escribano. "Differential Role of Adipose Tissues in Obesity and Related Metabolic and Vascular Complications." International Journal of Endocrinology 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/1216783.
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This review focuses on the contribution of white, brown, and perivascular adipose tissues to the pathophysiology of obesity and its associated metabolic and vascular complications. Weight gain in obesity generates excess of fat, usually visceral fat, and activates the inflammatory response in the adipocytes and then in other tissues such as liver. Therefore, low systemic inflammation responsible for insulin resistance contributes to atherosclerotic process. Furthermore, an inverse relationship between body mass index and brown adipose tissue activity has been described. For these reasons, in recent years, in order to combat obesity and its related complications, as a complement to conventional treatments, a new insight is focusing on the role of the thermogenic function of brown and perivascular adipose tissues as a promising therapy in humans. These lines of knowledge are focused on the design of new drugs, or other approaches, in order to increase the mass and/or activity of brown adipose tissue or the browning process of beige cells from white adipose tissue. These new treatments may contribute not only to reduce obesity but also to prevent highly prevalent complications such as type 2 diabetes and other vascular alterations, such as hypertension or atherosclerosis.
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Rosso, Renato, and Marco Lucioni. "Normal and Neoplastic Cells of Brown Adipose Tissue Express the Adhesion Molecule CD31." Archives of Pathology & Laboratory Medicine 130, no. 4 (April 1, 2006): 480–82. http://dx.doi.org/10.5858/2006-130-480-nancob.
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Abstract Context.—CD31 (platelet-endothelial cell adhesion molecule-1; PECAM-1), an adhesion molecule involved in the process of angiogenesis, is used as a marker of normal and neoplastic vascularization. During the assessment of angiogenesis and vascular invasion in a thymic carcinoid tumor, we observed unexpected immunostaining for CD31 in perithymic brown fat nests. Objective.—To determine whether CD31 is expressed by normal and neoplastic cells of brown fat, a tissue whose thermogenetic activity depends heavily on high perfusion. Design.—Formalin-fixed, paraffin-embedded archival tissues were immunostained by the labeled avidin-biotin method using antibodies against CD31 (clones JC70A and 1A10) after retrieval of heat-induced epitopes. Archival tissues included perithymic, periadrenal, axillary, and neck adipose tissue in which were embedded nests of brown fat (n = 15), hibernoma (n = 3), lipoma (n = 6), well-differentiated liposarcoma (n = 4), and myxoid liposarcoma (n = 4). Results.—Invariably, multivacuolated and univacuolated adipocytes of normal brown fat and hibernomas were intensely positive for the CD31 antigen. The immunostaining “decorated” cell membranes and the membranes of intracytoplasmic vacuoles. No expression of CD31 was found in normal adipocytes of white fat, in neoplastic cells of lipomas, or in multivacuolated lipoblasts of well-differentiated and myxoid liposarcomas. Conclusions.—The spectrum of cell types that express CD31 is expanded to include normal and neoplastic brown fat cells. We speculate that the expression of CD31 may play a role in the development and maintenance of the vascular network characterizing this specialized adipose tissue. Moreover, CD31 may inhibit the Bax-mediated apoptosis of brown fat cells. For practical purposes, CD31 may be used as an immunohistochemical marker for distinguishing between white and brown fat and for diagnosing hibernoma in paraffin sections.
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NAE, Sorin, Laura KUHLMANN, and Ion BORDEIANU. "PROCEDURES IN PLASTIC SURGERY OF SOFT TISSUES. FROM ADIPOSE TISSUE GRAFTS TO STEM CELLS." Romanian Journal of Medical Practice 12, no. 4 (December 31, 2017): 192–97. http://dx.doi.org/10.37897/rjmp.2017.4.3.
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Although significant progress has been made in recent years in plastic and reconstructive surgery procedures, there are still many issues to be solved. Thus, autologous fat transplantation is one of the promising treatments for soft tissue augmentation and facial rejuvenation, due to the lack of incisional scarring and complications associated with foreign materials. However, unpredictable problems and a low rate of graft survival due to partial necrosis occur. Recent research has led to the development of new adipose tissue transplantation techniques, with promising results, without establishing a standard protocol.
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Kouidhi, Magali, Phi Villageois, Carine M. Mounier, Corinne Ménigot, Yves Rival, David Piwnica, Jérôme Aubert, Bérengère Chignon-Sicard, and Christian Dani. "Characterization of Human Knee and Chin Adipose-Derived Stromal Cells." Stem Cells International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/592090.
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Animal study findings have revealed that individual fat depots are not functionally equivalent and have different embryonic origins depending on the anatomic location. Mouse bone regeneration studies have also shown that it is essential to match theHoxcode of transplanted cells and host tissues to achieve correct repair. However, subcutaneous fat depots from any donor site are often used in autologous fat grafting. Our study was thus carried out to determine the embryonic origins of human facial (chin) and limb (knee) fat depots and whether they had similar features and molecular matching patterns. Paired chin and knee fat depots were harvested from 11 subjects and gene expression profiles were determined by DNA microarray analyses. Adipose-derived stromal cells (ASCs) from both sites were isolated and analyzed for their capacity to proliferate, form clones, and differentiate. Chin and knee fat depots expressed a differentHOXcode and could have different embryonic origins. ASCs displayed a different phenotype, with chin-ASCs having the potential to differentiate into brown-like adipocytes, whereas knee-ASCs differentiated into white adipocytes. These results highlighted different features for these two fat sites and indicated that donor site selection might be an important factor to be considered when applying adipose tissue in cell-based therapies.
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Phillips, Kevin J. "Beige Fat, Adaptive Thermogenesis, and Its Regulation by Exercise and Thyroid Hormone." Biology 8, no. 3 (July 31, 2019): 57. http://dx.doi.org/10.3390/biology8030057.
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While it is now understood that the proper expansion of adipose tissue is critically important for metabolic homeostasis, it is also appreciated that adipose tissues perform far more functions than simply maintaining energy balance. Adipose tissue performs endocrine functions, secreting hormones or adipokines that affect the regulation of extra-adipose tissues, and, under certain conditions, can also be major contributors to energy expenditure and the systemic metabolic rate via the activation of thermogenesis. Adipose thermogenesis takes place in brown and beige adipocytes. While brown adipocytes have been relatively well studied, the study of beige adipocytes has only recently become an area of considerable exploration. Numerous suggestions have been made that beige adipocytes can elicit beneficial metabolic effects on body weight, insulin sensitivity, and lipid levels. However, the potential impact of beige adipocyte thermogenesis on systemic metabolism is not yet clear and an understanding of beige adipocyte development and regulation is also limited. This review will highlight our current understanding of beige adipocytes and select factors that have been reported to elicit the development and activation of thermogenesis in beige cells, with a focus on factors that may represent a link between exercise and ‘beiging’, as well as the role that thyroid hormone signaling plays in beige adipocyte regulation.
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TEBOUL, Lydia, Maria FEBBRAIO, Danielle GAILLARD, Ez-Zoubir AMRI, Roy SILVERSTEIN, and Paul A. GRIMALDI. "Structural and functional characterization of the mouse fatty acid translocase promoter: activation during adipose differentiation." Biochemical Journal 360, no. 2 (November 26, 2001): 305–12. http://dx.doi.org/10.1042/bj3600305.
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Fatty acid translocase (FAT/CD36) is a cell-surface glycoprotein that functions as a receptor/transporter for long-chain fatty acids (LCFAs), and interacts with other protein and lipid ligands. FAT/CD36 is expressed by various cell types, including platelets, monocytes/macrophages and endothelial cells, and tissues with an active LCFA metabolism, such as adipose, small intestine and heart. FAT/CD36 expression is induced during adipose cell differentiation and is transcriptionally up-regulated by LCFAs and thiazolidinediones in pre-adipocytes via a peroxisome-proliferator-activated receptor (PPAR)-mediated process. We isolated and analysed the murine FAT/CD36 promoter employing C2C12N cells directed to differentiate to either adipose or muscle. Transient transfection studies revealed that the 309bp upstream from the start of exon 1 confer adipose specific activity. Sequence analysis of this DNA fragment revealed the presence of two imperfect direct repeat-1 elements. Electrophoretic mobility-shift assay demonstrated that these elements were peroxisome-proliferator-responsive elements (PPREs). Mutagenesis and transfection experiments indicated that both PPREs co-operate to drive strong promoter activity in adipose cells. We conclude that murine FAT/CD36 expression in adipose tissue is dependent upon transcriptional activation via PPARs through binding to two PPREs located at −245 to −233bp and −120 to −108bp from the transcription start site.
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Bederman, Ilya, Alex DiScenna, Leigh Henderson, Aura Perez, Jeannie Klavanian, Daniel Kovtun, Olivia Collins, et al. "Small adipose stores in cystic fibrosis mice are characterized by reduced cell volume, not cell number." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 6 (December 1, 2018): G943—G953. http://dx.doi.org/10.1152/ajpgi.00096.2017.
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Cystic fibrosis (CF) is a lethal genetic disorder that affects many organ systems of the body, including various endocrine and exocrine tissues. Health and survival positively associate with body mass, and as a consequence, CF clinical care includes high-fat, high-calorie diets to maintain and increase adipose tissue stores. Such strategies have been implemented without a clear understanding of the cause and effect relationship between body mass and patients’ health. Here, we used CF mouse models, which display small adipose stores, to begin examining body fat as a prelude into mechanistic studies of low body growth in CF, so that optimal therapeutic strategies could be developed. We reasoned that low adiposity must result from reduced number and/or volume of adipocytes. To determine relative contribution of either mechanism, we quantified volume of intraperitoneal and subcutaneous adipocytes. We found smaller, but not fewer, adipocytes in CF compared with wild-type (WT) animals. Specifically, intraperitoneal CF adipocytes were one-half the volume of WT cells, whereas subcutaneous cells were less affected by the Cftr genotype. No differences were found in cell types between CF and WT adipose tissues. Adipose tissue CFTR mRNA was detected, and we found greater CFTR expression in intraperitoneal depots as compared with subcutaneous samples. RNA sequencing revealed that CF adipose tissue exhibited lower expression of several key genes of adipocyte function ( Lep, Pck1, Fas, Jun), consistent with low triglyceride storage. The data indicate that CF adipocytes contain fewer triglycerides than WT cells, and a role for CFTR in these cells is proposed. NEW & NOTEWORTHY Adipocytes in cystic fibrosis mice exhibit smaller size due to low triglyceride storage. Adipocyte cell number per fat pad is similar, implying triglyceride storage problem. The absence of CFTR function in adipose tissue has been proposed as a direct link to low triglyceride storage in cystic fibrosis.
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do Amaral, Ronaldo J. F. C., Henrique V. Almeida, Daniel J. Kelly, Fergal J. O’Brien, and Cathal J. Kearney. "Infrapatellar Fat Pad Stem Cells: From Developmental Biology to Cell Therapy." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/6843727.
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The ideal cell type to be used for cartilage therapy should possess a proven chondrogenic capacity, not cause donor-site morbidity, and should be readily expandable in culture without losing their phenotype. There are several cell sources being investigated to promote cartilage regeneration: mature articular chondrocytes, chondrocyte progenitors, and various stem cells. Most recently, stem cells isolated from joint tissue, such as chondrogenic stem/progenitors from cartilage itself, synovial fluid, synovial membrane, and infrapatellar fat pad (IFP) have gained great attention due to their increased chondrogenic capacity over the bone marrow and subcutaneous adipose-derived stem cells. In this review, we first describe the IFP anatomy and compare and contrast it with other adipose tissues, with a particular focus on the embryological and developmental aspects of the tissue. We then discuss the recent advances in IFP stem cells for regenerative medicine. We compare their properties with other stem cell types and discuss an ontogeny relationship with other joint cells and their role onin vivocartilage repair. We conclude with a perspective for future clinical trials using IFP stem cells.
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Meiliana, Anna, and Andi Wijaya. "Hypertrophic Obesity and Subcutaneous Adipose Tissue Dysfunction." Indonesian Biomedical Journal 6, no. 2 (August 1, 2014): 79. http://dx.doi.org/10.18585/inabj.v6i2.33.
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BACKGROUND: Over the past 50 years, scientists have recognized that not all adipose tissue is alike, and that health risk is associated with the location as well as the amount of body fat. Different depots are sufficiently distinct with respect to fatty-acid storage and release as to probably play unique roles in human physiology. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.CONTENT: The limited expandability of the subcutaneous adipose tissue leads to inappropriate adipose cell expansion (hypertrophic obesity) with local inflammation and a dysregulated and insulin-resistant adipose tissue. The inability to store excess fat in the subcutaneous adipose tissue is a likely key mechanism for promoting ectopic fat accumulation in tissues and areas where fat can be stored, including the intra-abdominal and visceral areas, in the liver, epi/pericardial area, around vessels, in the myocardium, and in the skeletal muscles. Many studies have implicated ectopic fat accumulation and the associated lipotoxicity as the major determinant of the metabolic complications of obesity driving systemic insulin resistance, inflammation, hepatic glucose production, and dyslipidemia.SUMMARY: In summary, hypertrophic obesity is due to an impaired ability to recruit and differentiate available adipose precursor cells in the subcutaneous adipose tissue. Thus, the subcutaneous adipose tissue may be particular in its limited ability in certain individuals to undergo adipogenesis during weight increase. Inability to promote subcutaneous adipogenesis under periods of affluence would favor lipid overlow and ectopic fat accumulation with negative metabolic consequences.KEYWORDS: obesity, adipogenesis, subcutaneous adipose tissue, visceral adipose tissue, adipocyte dysfunction
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Nascimento, Emmani B. M., Mariëtte R. Boon, and Wouter D. van Marken Lichtenbelt. "Fat Cells Gain New Identities." Science Translational Medicine 6, no. 247 (July 30, 2014): 247fs29. http://dx.doi.org/10.1126/scitranslmed.3009809.
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De Luca, Angela, Rosanna Verardi, Arabella Neva, Patrizia Benzoni, Elisabetta Crescini, Er Xia, Camillo Almici, Stefano Calza, and Patrizia Dell'Era. "Comparative Analysis of Mesenchymal Stromal Cells Biological Properties." ISRN Stem Cells 2013 (March 28, 2013): 1–9. http://dx.doi.org/10.1155/2013/674671.
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The stromal progenitors of mesodermal cells, mesenchymal stromal cells (MSCs), are a heterogeneous population of plastic adherent fibroblast-like cells with extensive proliferative capacity and differentiation potential. Human MSCs have now been isolated from various tissues including bone marrow, muscle, skin, and adipose tissue, the latter being one of the most suitable cell sources for cell therapy, because of its easy accessibility, minimal morbidity, and abundance of cells. Bone marrow and subcutaneous or visceral adipose tissue samples were collected, digested with collagenase if needed, and seeded in Iscove's medium containing 5% human platelet lysate. Nonadherent cells were removed after 2-3 days and the medium was replaced twice a week. Confluent adherent cells were detached, expanded, and analyzed for several biological properties such as morphology, immunophenotype, growth rate, senescence, clonogenicity, differentiation capacity, immunosuppression, and secretion of angiogenic factors. The results show significant differences between lines derived from subcutaneous fat compared to those derived from visceral fat, such as the higher proliferation rate of the first and the strong induction of angiogenesis of the latter. We are convinced that the identification of the peculiarities of MSCs isolated from different tissues will lead to their more accurate use in cell therapy.
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Shen, Jie‐fei, Atsunori Sugawara, Joe Yamashita, Hideo Ogura, and Soh Sato. "Dedifferentiated fat cells: an alternative source of adult multipotent cells from the adipose tissues." International Journal of Oral Science 3, no. 3 (July 2011): 117–24. http://dx.doi.org/10.4248/ijos11044.
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Vargas, Diana, Jaime Camacho, Juan Duque, Marisol Carreño, Edward Acero, Máximo Pérez, Sergio Ramirez, et al. "Functional Characterization of Preadipocytes Derived from Human Periaortic Adipose Tissue." International Journal of Endocrinology 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2945012.
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Adipose tissue can affect the metabolic control of the cardiovascular system, and its anatomic location can affect the vascular function differently. In this study, biochemical and phenotypical characteristics of adipose tissue from periaortic fat were evaluated. Periaortic and subcutaneous adipose tissues were obtained from areas surrounding the ascending aorta and sternotomy incision, respectively. Adipose tissues were collected from patients undergoing myocardial revascularization or mitral valve replacement surgery. Morphological studies with hematoxylin/eosin and immunohistochemical assay were performed in situ to quantify adipokine expression. To analyze adipogenic capacity, adipokine expression, and the levels of thermogenic proteins, adipocyte precursor cells were isolated from periaortic and subcutaneous adipose tissues and induced to differentiation. The precursors of adipocytes from the periaortic tissue accumulated less triglycerides than those from the subcutaneous tissue after differentiation and were smaller than those from subcutaneous adipose tissue. The levels of proteins involved in thermogenesis and energy expenditure increased significantly in periaortic adipose tissue. Additionally, the expression levels of adipokines that affect carbohydrate metabolism, such as FGF21, increased significantly in mature adipocytes induced from periaortic adipose tissue. These results demonstrate that precursors of periaortic adipose tissue in humans may affect cardiovascular events and might serve as a target for preventing vascular diseases.
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Sekimoto, Ryohei, Shiro Fukuda, Norikazu Maeda, Yu Tsushima, Keisuke Matsuda, Takuya Mori, Hideaki Nakatsuji, et al. "Visualized macrophage dynamics and significance of S100A8 in obese fat." Proceedings of the National Academy of Sciences 112, no. 16 (April 6, 2015): E2058—E2066. http://dx.doi.org/10.1073/pnas.1409480112.
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Chronic low-grade inflammation of adipose tissue plays a crucial role in the pathophysiology of obesity. Immunohistological microscopic analysis in obese fat tissue has demonstrated the infiltration of several immune cells such as macrophages, but dynamics of immune cells have not been fully elucidated and clarified. Here, by using intravital multiphoton imaging technique, to our knowledge for the first time, we analyzed and visualized the inflammatory processes in adipose tissue under high-fat and high-sucrose (HF/HS) diet with lysozyme M-EGFP transgenic (LysMEGFP) mice whose EGFP was specifically expressed in the myelomonocytic lineage. Mobility of LysMEGFP-positive macrophages was shown to be activated just 5 d after HF/HS diet, when the distinct hypertrophy of adipocytes and the accumulation of macrophages still have not become prominent. Significant increase of S100A8 was detected in mature adipocyte fraction just 5 d after HF/HS diet. Recombinant S100A8 protein stimulated chemotactic migration in vitro and in vivo, as well as induced proinflammatory molecules, both macrophages and adipocytes, such as TNF-α and chemokine (C-C motif) ligand 2. Finally, an antibody against S100A8 efficiently suppressed the HF/HS diet-induced initial inflammatory change, i.e., increased mobilization of adipose LysMEGFP-positive macrophages, and ameliorated HF/HS diet-induced insulin resistance. In conclusion, time-lapse intravital multiphoton imaging of adipose tissues identified the very early event exhibiting increased mobility of macrophages, which may be triggered by increased expression of adipose S100A8 and results in progression of chronic inflammation in situ.
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Mercader, Josep, Joan Ribot, Incoronata Murano, Søren Feddersen, Saverio Cinti, Lise Madsen, Karsten Kristiansen, M. Luisa Bonet, and Andreu Palou. "Haploinsufficiency of the retinoblastoma protein gene reduces diet-induced obesity, insulin resistance, and hepatosteatosis in mice." American Journal of Physiology-Endocrinology and Metabolism 297, no. 1 (July 2009): E184—E193. http://dx.doi.org/10.1152/ajpendo.00163.2009.
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Brown adipose tissue activity dissipates energy as heat, and there is evidence that lack of the retinoblastoma protein (pRb) may favor the development of the brown adipocyte phenotype in adipose cells. In this work we assessed the impact of germ line haploinsufficiency of the pRb gene (Rb) on the response to high-fat diet feeding in mice. Rb+/− mice had body weight and adiposity indistinguishable from that of wild-type (Rb+/+) littermates when maintained on a standard diet, yet they gained less body weight and body fat after long-term high-fat diet feeding coupled with reduced feed efficiency and increased rectal temperature. Rb haploinsufficiency ameliorated insulin resistance and hepatosteatosis after high-fat diet in male mice, in which these disturbances were more marked than in females. Compared with wild-type littermates, Rb+/− mice fed a high-fat diet displayed higher expression of peroxisome proliferator-activated receptor (PPAR)γ as well as of genes involved in mitochondrial function, cAMP sensitivity, brown adipocyte determination, and tissue vascularization in white adipose tissue depots. Furthermore, Rb+/− mice exhibited signs of enhanced activation of brown adipose tissue and higher expression levels of PPARα in liver and of PPARδ in skeletal muscle, suggestive of an increased capability for fatty acid oxidation in these tissues. These findings support a role for pRb in modulating whole body energy metabolism and the plasticity of the adipose tissues in vivo and constitute first evidence that partial deficiency in the Rb gene protects against the development of obesity and associated metabolic disturbances.
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Schulz, Tim J., Tian Lian Huang, Thien T. Tran, Hongbin Zhang, Kristy L. Townsend, Jennifer L. Shadrach, Massimiliano Cerletti, et al. "Identification of inducible brown adipocyte progenitors residing in skeletal muscle and white fat." Proceedings of the National Academy of Sciences 108, no. 1 (December 20, 2010): 143–48. http://dx.doi.org/10.1073/pnas.1010929108.
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Brown fat is specialized for energy expenditure and has therefore been proposed to function as a defense against obesity. Despite recent advances in delineating the transcriptional regulation of brown adipocyte differentiation, cellular lineage specification and developmental cues specifying brown-fat cell fate remain poorly understood. In this study, we identify and isolate a subpopulation of adipogenic progenitors (Sca-1+/CD45−/Mac1−; referred to as Sca-1+ progenitor cells, ScaPCs) residing in murine brown fat, white fat, and skeletal muscle. ScaPCs derived from different tissues possess unique molecular expression signatures and adipogenic capacities. Importantly, although the ScaPCs from interscapular brown adipose tissue (BAT) are constitutively committed brown-fat progenitors, Sca-1+ cells from skeletal muscle and subcutaneous white fat are highly inducible to differentiate into brown-like adipocytes upon stimulation with bone morphogenetic protein 7 (BMP7). Consistent with these findings, human preadipocytes isolated from subcutaneous white fat also exhibit the greatest inducible capacity to become brown adipocytes compared with cells isolated from mesenteric or omental white fat. When muscle-resident ScaPCs are re-engrafted into skeletal muscle of syngeneic mice, BMP7-treated ScaPCs efficiently develop into adipose tissue with brown fat-specific characteristics. Importantly, ScaPCs from obesity-resistant mice exhibit markedly higher thermogenic capacity compared with cells isolated from obesity-prone mice. These data establish the molecular characteristics of tissue-resident adipose progenitors and demonstrate a dynamic interplay between these progenitors and inductive signals that act in concert to specify brown adipocyte development.
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Ricardo-Gonzalez, Roberto R., and Richard M. Locksley. "ILC2s chew the fat." Journal of Experimental Medicine 216, no. 9 (August 12, 2019): 1972–73. http://dx.doi.org/10.1084/jem.20191098.
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In this issue of JEM, Rana et al. (https://doi.org/10.1084/jem.20190689) report that adipose tissue multipotent stromal cells (MSCs) provide multifaceted support for adipose tissue–resident ILC2s through contact-mediated proliferation and IL-33–mediated stress-induced activation.
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Sima, Aurelia, Daniel-Constantin Manolescu, and Pangala Bhat. "Retinoids and retinoid-metabolic gene expression in mouse adipose tissues." Biochemistry and Cell Biology 89, no. 6 (December 2011): 578–84. http://dx.doi.org/10.1139/o11-062.
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Vitamin A and its analogs (retinoids) regulate adipocyte differentiation. Recent investigations have demonstrated a relationship among retinoids, retinoid-binding-protein 4 (RBP4) synthesized in adipose tissues, and insulin-resistance status. In this study, we measured retinoid levels and analyzed the expression of retinoid homeostatic genes associated with retinol uptake, esterification, oxidation, and catabolism in subcutaneous (Sc) and visceral (Vis) mouse fat tissues. Both Sc and Vis depots were found to contain similar levels of all-trans retinol. A metabolite of retinol with characteristic ultraviolet absorption maxima for 9-cis retinol was observed in these 2 adipose depots, and its level was 2-fold higher in Sc than in Vis tissues. Vis adipose tissue expressed significantly higher levels of RBP4, CRBP1 (intracellular retinol-binding protein 1), RDH10 (retinol dehydrogenase), as well as CYP26A1 and B1 (retinoic acid (RA) hydroxylases). No differences in STRA6 (RBP4 receptor), LRAT (retinol esterification), CRABP1 and 2 (intracellular RA-binding proteins), and RALDH1 (retinal dehydrogenase) mRNA expressions were discerned in both fat depots. RALDH1 was identified as the only RALDH expressed in both Sc and Vis adipose tissues. These results indicate that Vis is more actively involved in retinoid metabolism than Sc adipose tissue.
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Kovsan, Julia, Matthias Blüher, Tanya Tarnovscki, Nora Klöting, Boris Kirshtein, Liron Madar, Iris Shai, et al. "Altered Autophagy in Human Adipose Tissues in Obesity." Endocrine Reviews 31, no. 6 (December 1, 2010): 945–46. http://dx.doi.org/10.1210/edrv.31.6.9993.
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Context Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. Objective We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. Setting and Patients Paired omental (Om) and sc adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). Results Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with sc, more pronounced among obese persons, particularly if with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. The increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. Conclusions Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may precede the occurrence of obesity-associated morbidity.
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Kovsan, Julia, Matthias Blüher, Tanya Tarnovscki, Nora Klöting, Boris Kirshtein, Liron Madar, Iris Shai, et al. "Altered Autophagy in Human Adipose Tissues in Obesity." Endocrine Reviews 31, no. 6 (December 1, 2010): 947. http://dx.doi.org/10.1210/edrv.31.6.9998.
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Context Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. Objective We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. Setting and Patients Paired omental (Om) and sc adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). Results Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with sc, more pronounced among obese persons, particularly if with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. The increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. Conclusions Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may precede the occurrence of obesity-associated morbidity.
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Kovsan, Julia, Matthias Blüher, Tanya Tarnovscki, Nora Klöting, Boris Kirshtein, Liron Madar, Iris Shai, et al. "Altered Autophagy in Human Adipose Tissues in Obesity." Molecular Endocrinology 24, no. 12 (December 1, 2010): 2406. http://dx.doi.org/10.1210/mend.24.12.9998.
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Abstract Context: Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. Objective: We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. Setting and Patients: Paired omental (Om) and sc adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). Results: Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with sc, more pronounced among obese persons, particularly if with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. The increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. Conclusions: Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may precede the occurrence of obesity-associated morbidity.
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Kovsan, Julia, Matthias Blüher, Tanya Tarnovscki, Nora Klöting, Boris Kirshtein, Liron Madar, Iris Shai, et al. "Altered Autophagy in Human Adipose Tissues in Obesity." Endocrinology 151, no. 12 (December 1, 2010): 5973–74. http://dx.doi.org/10.1210/endo.151.12.9995.
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Context: Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. Objective: We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. Setting and Patients: Paired omental (Om) and sc adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). Results: Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with sc, more pronounced among obese persons, particularly if with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. The increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. Conclusions: Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may precede the occurrence of obesity-associated morbidity.
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Crisp, Ms, C. Lane, M. Halliwell, D. Wynford-Thomas, and M. Ludgate. "Thyrotropin Receptor Transcripts in Human Adipose Tissue." Journal of Clinical Endocrinology & Metabolism 82, no. 6 (June 1, 1997): 2003–5. http://dx.doi.org/10.1210/jcem.82.6.2003.
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Abstract Thyroid associated ophthalmopathy (TAO) is generally considered to have an autoimmune pathogenesis but the target antigen has yet to be identified. It is most frequently associated with Graves’ disease and there is some logic in assuming that the same antigen, the thyrotropin receptor (TSHR), is the common link. Previous studies, mostly PCR based, aimed at investigating TSHR transcripts in the orbit, have yielded conflicting results, although there is circumstantial evidence for their presence in orbital fat. In this study, we have examined adult human adipose and muscle tissues from various locations, initially by PCR and subsequently by northern blot. We obtained the expected 610bp product in normal intestinal and orbital fat but not skeletal muscle, following two rounds of PCR amplification but only when reverse transcription used a TSHR specific primer. In northern blots, despite loading all of the RNA obtained from total normal orbital fat contents, TSHR transcripts were at the limit of detection and similarly for large samples of intestinal fat. The exception was RNA obtained from TAO orbital fat, in which TSHR transcripts of 4.6 and 1.7kb were clearly visible, as in the thyroid. We conclude that normal adult adipose tissues contain low levels of TSHR transcripts. In TAO, TSHR transcripts are elevated probably due to an increased number of cells, in particular of preadipocytes in orbital adipose tissue.
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Gorwood, Jennifer, Tina Ejlalmanesh, Christine Bourgeois, Matthieu Mantecon, Cindy Rose, Michael Atlan, Delphine Desjardins, et al. "SIV Infection and the HIV Proteins Tat and Nef Induce Senescence in Adipose Tissue and Human Adipose Stem Cells, Resulting in Adipocyte Dysfunction." Cells 9, no. 4 (April 1, 2020): 854. http://dx.doi.org/10.3390/cells9040854.
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Background: Aging is characterized by adipose tissue senescence, inflammation, and fibrosis, with trunk fat accumulation. Aging HIV-infected patients have a higher risk of trunk fat accumulation than uninfected individuals—suggesting that viral infection has a role in adipose tissue aging. We previously demonstrated that HIV/SIV infection and the Tat and Nef viral proteins were responsible for adipose tissue fibrosis and impaired adipogenesis. We hypothesized that SIV/HIV infection and viral proteins could induce adipose tissue senescence and thus lead to adipocyte dysfunctions. Methods: Features of tissue senescence were evaluated in subcutaneous and visceral adipose tissues of SIV-infected macaques and in human adipose stem cells (ASCs) exposed to Tat or Nef for up to 30 days. Results: p16 expression and p53 activation were higher in adipose tissue of SIV-infected macaques than in control macaques, indicating adipose tissue senescence. Tat and Nef induced higher senescence in ASCs, characterized by higher levels of senescence-associated beta-galactosidase activity, p16 expression, and p53 activation vs. control cells. Treatment with Tat and Nef also induced oxidative stress and mitochondrial dysfunction. Prevention of oxidative stress (using N-acetyl-cysteine) reduced senescence in ASCs. Adipocytes having differentiated from Nef-treated ASCs displayed alterations in adipogenesis with lower levels of triglyceride accumulation and adipocyte marker expression and secretion, and insulin resistance. Conclusion: HIV/SIV promotes adipose tissue senescence, which in turn may alter adipocyte function and contribute to insulin resistance.
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Choi, Won-Il, Jae-Hyun Yoon, Seo-Hyun Choi, Bu-Nam Jeon, Hail Kim, and Man-Wook Hur. "Proto-oncoprotein Zbtb7c and SIRT1 repression: implications in high-fat diet-induced and age-dependent obesity." Experimental & Molecular Medicine 53, no. 5 (May 2021): 917–32. http://dx.doi.org/10.1038/s12276-021-00628-5.
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AbstractZbtb7c is a proto-oncoprotein that controls the cell cycle and glucose, glutamate, and lipid metabolism. Zbtb7c expression is increased in the liver and white adipose tissues of aging or high-fat diet-fed mice. Knockout or knockdown of Zbtb7c gene expression inhibits the adipocyte differentiation of 3T3-L1 cells and decreases adipose tissue mass in aging mice. We found that Zbtb7c was a potent transcriptional repressor of SIRT1 and that SIRT1 was derepressed in various tissues of Zbtb7c-KO mice. Mechanistically, Zbtb7c interacted with p53 and bound to the proximal promoter p53RE1 and p53RE2 to repress the SIRT1 gene, in which p53RE2 was particularly critical. Zbtb7c induced p53 to interact with the corepressor mSin3A-HADC1 complex at p53RE. By repressing the SIRT1 gene, Zbtb7c increased the acetylation of Pgc-1α and Pparγ, which resulted in repression or activation of Pgc-1α or Pparγ target genes involved in lipid metabolism. Our study provides a molecular target that can overexpress SIRT1 protein in the liver, pancreas, and adipose tissues, which can be beneficial in the treatment of diabetes, obesity, longevity, etc.
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Raclot, T., E. Mioskowski, A. C. Bach, and R. Groscolas. "Selectivity of fatty acid mobilization: a general metabolic feature of adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 5 (November 1, 1995): R1060—R1067. http://dx.doi.org/10.1152/ajpregu.1995.269.5.r1060.
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This study extends our earlier work (T. Raclot and R. Groscolas. J. Lipid Res. 34: 1515-1526, 1993), which showed that, under norepinephrine-stimulated lipolysis, fatty acids of rat retroperitoneal fat cells are selectively mobilized. The present study examines whether this selective mobilization of fatty acids 1) is based on their proportions in adipose tissue, 2) is a metabolic feature common to all adipose tissues, and/or 3) depends on the lipolysis-stimulating agent. Rat fat cells with two markedly different fatty acid compositions were isolated from four white adipose tissues and treated with three lipolytic agents. Fatty acid composition of in vitro released free fatty acids was compared with that of fat cell triacylglycerols, the ratio of percent in free fatty acid to percent in triacylglycerol being defined as the relative mobilization rate (RMR). The RMR of individual fatty acids was related to their molecular structure. It increased exponentially with unsaturation for a given chain length and decreased with increasing chain length for a given unsaturation. The selectivity of fatty acid mobilization was similar regardless of the fatty acid composition of adipose tissue, the tissue location, and the lipolytic agent used. Under conditions of stimulated lipolysis, the selectivity of fatty acid mobilization is therefore a general metabolic feature of adipose tissue. Fatty acids with 16-20 carbon atoms and 4 or 5 double bonds had the highest RMR (from 1.4 to > 5), whereas fatty acids with 20-22 carbon atoms and 0 or 1 double bond had the lowest RMR (from 0.3 to 0.7). For the other fatty acids, RMR was close to unity.(ABSTRACT TRUNCATED AT 250 WORDS)
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Xie, Zongyan, Yu Cheng, Qi Zhang, Haojie Hao, Yaqi Yin, Li Zang, Xuhong Wang, and Yiming Mu. "Anti-obesity effect and mechanism of mesenchymal stem cells influence on obese mice." Open Life Sciences 16, no. 1 (January 1, 2021): 653–66. http://dx.doi.org/10.1515/biol-2021-0061.
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Abstract Mesenchymal stem cells (MSCs) can be obtained from almost all tissues and present promising therapeutic effects for metabolic diseases. Human adipose-derived MSCs (hASCs) have recently been widely studied due to their easy access and low immunity. Thus, we intended to figure out the effects and potential mechanism of hASCs on obesity in high-fat-diet (HFD)-induced obese mice. Following 16 weeks of being fed HFD, hASCs were intravenously injected. Two weeks later, body weight, body composition, and energy expenditure were evaluated. Additionally, the phenotypes of macrophages infiltrating adipose tissue were analyzed. The results revealed that hASCs administration significantly reduced adipose tissue weight, adipocyte size, and fat mass and exerted beneficial effects in serum lipid profile. This anti-obesity effect was mediated by the increased O2 consumption, CO2 production, and energy expenditure, which was further evidenced by the upregulation of uncoupling protein-1 (UCP-1) and metabolism-associated genes. Furthermore, hASCs infusion increased the amount of alternatively activated (M2) macrophages in adipose tissue, and the expression of pro-inflammatory cytokines-related genes was reduced. Taken together, these results indicated that hASCs suppressed obesity by increasing UCP-1 expression and enhancing energy expenditure, and this effect might be due to the increased M2 macrophages.
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Jiang, Aimei, Ming Li, Wenjing Duan, Yilong Dong, and Yanmei Wang. "Improvement of the Survival of Human Autologous Fat Transplantation by Adipose-Derived Stem-Cells-Assisted Lipotransfer Combined with bFGF." Scientific World Journal 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/968057.
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Adipose-derived stem cells (ASCs) transplanted along with autologous adipose tissue may improve fat graft survival; however, the efficacy of ASCs has been diluted by low vascularization. This study was designed to test the hypothesis that basic fibroblast growth factor (bFGF) may improve the effects of ASCs because it owns the property to boost angiogenesis. In the present study, human fat tissues were mixed with ASCs, ASCs plus 100 U bFGF, or medium as the control and then injected subcutaneously into immunologically compromised nude mice for 12 weeks. Our findings demonstrated that mixture with the ASCs significantly increased the weight and volume of the fat grafts compared to control grafts, and histological analysis revealed that both ASCs and ASCs plus bFGF grafts consisted predominantly of adipose tissue and had significantly less fibrosis but greater microvascular density compared with control and also grafts mixed with ASCs had a high expression of angiogenic factors. More importantly, the bFGF treated fat grafts shown elevate in survival, vascularization, and angiogenic factors expression when compared with the grafts that received ASCs alone. These results indicated that bFGF together with ASCs can enhance the efficacy of autologous fat transplantation and increase blood vessel generation involved in the benefits from bFGF.
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Fukai, Nozomi, Takanobu Yoshimoto, Toru Sugiyama, Naoko Ozawa, Ryuji Sato, Masayoshi Shichiri, and Yukio Hirata. "Concomitant expression of adrenomedullin and its receptor components in rat adipose tissues." American Journal of Physiology-Endocrinology and Metabolism 288, no. 1 (January 2005): E56—E62. http://dx.doi.org/10.1152/ajpendo.00586.2003.
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Adrenomedullin (AM) expressed by and secreted from a variety of cells plays pluripotent roles in an autocrine/paracrine fashion. The present study was undertaken to explore the expression of AM and its receptor genes in adipose tissues, their changes during the development of obesity, and the process of preadipocyte differentiation. Both mature adipocytes and stromal vascular cells constituting adipose tissue expressed AM transcript. AM and its receptor component [calcitonin receptor-like receptor and receptor activity-modifying protein-2 (CRLR/RAMP2)] mRNAs were expressed in a variety of rat adipose tissues, including epididymal, mesenteric, retroperitoneal, and subcutaneous adipose tissue. AM mRNA levels in rat and human epididymal adipose tissue were about one-tenth of those in the kidney. Steady-state mRNA levels of AM and CRLR/RAMP2 in epididymal, mesenteric, and retroperitoneal adipose tissues in rats fed a high-fat diet for 4 wk were far greater than those in rats with normal diet accompanied by increased plasma AM levels, whereas steady-state AM mRNA levels conversely decreased in other organs, such as kidney and liver. AM mRNA expressed in a mouse preadipocyte cell line (3T3-L1) transiently decreased by day 3, returned to basal level by day 6, and then increased by day 9 during preadipocyte differentiation, which paralleled AM secretion from the cells. However, the addition of either exogenous AM or AM receptor antagonist calcitonin gene-related peptide-(8–37), to block endogenous AM did not affect lipid droplet accumulation during preadipocyte differentiation. The present study demonstrates for the first time that AM and its receptor component (CRLR/RAMP2) mRNAs were concomitantly expressed in various adipose tissues, whose tissue-specific upregulation was induced during the development of obesity. These data suggest that AM may act as a new member of adipokines, although its functional role, as well as its pathophysiological significance in obesity, remains to be determined.
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Hong, Yeon-Hee, Yukihiko Nishimura, Daisuke Hishikawa, Hiroaki Tsuzuki, Hisae Miyahara, Chizu Gotoh, Ki-Choon Choi, et al. "Acetate and Propionate Short Chain Fatty Acids Stimulate Adipogenesis via GPCR43." Endocrinology 146, no. 12 (December 1, 2005): 5092–99. http://dx.doi.org/10.1210/en.2005-0545.
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It has recently been discovered that G protein-coupled receptors (GPCR) 41 and 43 are characterized by having the short chain fatty acids acetate and propionate as their ligands. The objective of this study was to investigate the involvement of GPCR41, GPCR43, and their ligands in the process of adipogenesis. We measured the levels of GPCR41 and GPCR43 mRNA in both adipose and other tissues of the mouse. GRP43 mRNA expression was higher in four types of adipose tissue than in other tissues, whereas GPCR41 mRNA was not detected in any adipose tissues. A high level of GPCR43 expression was found in isolated adipocytes, but expression level was very low in stromal-vascular cells. Expression of GPCR43 was up-regulated in adipose tissues of mice fed a high-fat diet compared with those fed a normal-fat diet. GPCR43 mRNA could not be detected in confluent and undifferentiated 3T3-L1 adipocytes; however, the levels rose with time after the initiation of differentiation. GPCR41 expression was not detected in confluent and differentiated adipocytes. Acetate and propionate treatments increased lipids present as multiple droplets in 3T3-L1 adipocytes. Propionate significantly elevated the level of GPCR43 expression during adipose differentiation, with up-regulation of PPAR-γ2. Small interfering RNA mediated a reduction of GPCR43 mRNA in 3T3-L1 cells and blocked the process of adipocyte differentiation. In addition, both acetate and propionate inhibited isoproterenol-induced lipolysis in a dose-dependent manner. We conclude that acetate and propionate short chain fatty acids may have important physiological roles in adipogenesis through GPCR43, but not through GPCR41.
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Liu, Lulu, Mei Mei, Shumin Yang, and Qifu Li. "Roles of Chronic Low-Grade Inflammation in the Development of Ectopic Fat Deposition." Mediators of Inflammation 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/418185.
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Pattern of fat distribution is a major determinant for metabolic homeostasis. As a depot of energy, the storage of triglycerides in adipose tissue contributes to the normal fat distribution. Decreased capacity of fat storage in adipose tissue may result in ectopic fat deposition in nonadipose tissues such as liver, pancreas, and kidney. As a critical biomarker of metabolic complications, chronic low-grade inflammation may have the ability to affect the process of lipid accumulation and further lead to the disorder of fat distribution. In this review, we have collected the evidence linking inflammation with ectopic fat deposition to get a better understanding of the underlying mechanism, which may provide us with novel therapeutic strategies for metabolic disorders.
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Boquest, Andrew C., Aboulghassem Shahdadfar, Katrine Frønsdal, Olafur Sigurjonsson, Siv H. Tunheim, Philippe Collas, and Jan E. Brinchmann. "Isolation and Transcription Profiling of Purified Uncultured Human Stromal Stem Cells: Alteration of Gene Expression after In Vitro Cell Culture." Molecular Biology of the Cell 16, no. 3 (March 2005): 1131–41. http://dx.doi.org/10.1091/mbc.e04-10-0949.
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Stromal stem cells proliferate in vitro and may be differentiated along several lineages. Freshly isolated, these cells have been too few or insufficiently pure to be thoroughly characterized. Here, we have isolated two populations of CD45-CD34+CD105+ cells from human adipose tissue which could be separated based on expression of CD31. Compared with CD31+ cells, CD31- cells overexpressed transcripts associated with cell cycle quiescence and stemness, and transcripts involved in the biology of cartilage, bone, fat, muscle, and neural tissues. In contrast, CD31+ cells overexpressed transcripts associated with endothelium and the major histocompatibility complex class II complex. Clones of CD31- cells could be expanded in vitro and differentiated into cells with characteristics of bone, fat, and neural-like tissue. On culture, transcripts associated with cell cycle quiescence, stemness, certain cytokines and organ specific genes were down-regulated, whereas transcripts associated with signal transduction, cell adhesion, and cytoskeletal components were up-regulated. CD31+ cells did not proliferate in vitro. CD45-CD34+CD105+CD31- cells from human adipose tissue have stromal stem cell properties which may make them useful for tissue engineering.
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Cousin, B., L. Casteilla, C. Dani, P. Muzzin, J. P. Revelli, and L. Penicaud. "Adipose tissues from various anatomical sites are characterized by different patterns of gene expression and regulation." Biochemical Journal 292, no. 3 (June 15, 1993): 873–76. http://dx.doi.org/10.1042/bj2920873.
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We have shown previously the presence of brown adipocytes among white fat pads, and proposed the existence of a spectrum of adipose depots according to the abundance of brown fat cells [Cousin, Cinti, Morroni, Raimbault, Ricquier, Pénicaud and Casteilla (1992) J. Cell Sci. 103, 931-942]. In this study, we tried to characterize this spectrum better. We determined in several adipose depots (i) the richness of pre-adipose cells, as assessed by A2COL6 mRNA levels; (ii) whether a fat pad was characterized by a pattern of mRNA expression; (iii) whether this pattern was close related to abundance of brown adipocytes, and (iv) whether the regulation of this pattern by catecholamines under cold exposure or beta-agonist treatment was similar in the different pads. This was achieved by studying proteins involved in glucose and lipid metabolism such as insulin-sensitive glucose transporter (GLUT4), fatty acid synthase, lipoprotein lipase and fatty acid binding protein aP2, as well as beta 3-adrenergic-receptor expression. Among white adipose depots, the periovarian fat pad was characterized by the highest content of pre-adipocytes and of brown adipocytes, and inguinal fat by the highest lipogenic activity potential. There was no close correlation between beta 3-adrenergic-receptor expression and brown adipocyte content in the tissues, as measured by the degree of uncoupling protein (UCP) gene expression. However, in pads expressing UCP mRNA, mRNA levels of beta 3-adrenergic receptor and other markers were increased in parallel. Under cold exposure or beta 3-agonist treatment, a specific up-regulation of GLUT4 expression was observed in interscapular brown adipose tissue. The regional difference described in this study, could participate in preferential fat-pad growth under physiological conditions as well as in pathological situations.
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Bonnet, Muriel, Nicolas Kaspric, Kimberly Vonnahme, Didier Viala, Christophe Chambon, and Brigitte Picard. "Prediction of the Secretome and the Surfaceome: A Strategy to Decipher the Crosstalk between Adipose Tissue and Muscle during Fetal Growth." International Journal of Molecular Sciences 21, no. 12 (June 19, 2020): 4375. http://dx.doi.org/10.3390/ijms21124375.
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Crosstalk between adipose and muscular tissues is hypothesized to regulate the number of muscular and adipose cells during fetal growth, with post-natal consequences on lean and fat masses. Such crosstalk largely remains, however, to be described. We hypothesized that a characterization of the proteomes of adipose and muscular tissues from bovine fetuses may enhance the understanding of the crosstalk between these tissues through the prediction of their secretomes and surfaceomes. Proteomic experiments have identified 751 and 514 proteins in fetal adipose tissue and muscle. These are mainly involved in the regulation of cell proliferation or differentiation, but also in pathways such as apoptosis, Wnt signalling, or cytokine-mediated signalling. Of the identified proteins, 51 adipokines, 11 myokines, and 37 adipomyokines were predicted, together with 26 adipose and 13 muscular cell surface proteins. Analysis of protein–protein interactions suggested 13 links between secreted and cell surface proteins that may contribute to the adipose–muscular crosstalk. Of these, an interaction between the adipokine plasminogen and the muscular cell surface alpha-enolase may regulate the fetal myogenesis. The in silico secretome and surfaceome analyzed herein exemplify a powerful strategy to enhance the elucidation of the crosstalk between cell types or tissues.
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Perruchot, Marie-Hélène, Louis Lefaucheur, Corinne Barreau, Louis Casteilla, and Isabelle Louveau. "Age-related changes in the features of porcine adult stem cells isolated from adipose tissue and skeletal muscle." American Journal of Physiology-Cell Physiology 305, no. 7 (October 1, 2013): C728—C738. http://dx.doi.org/10.1152/ajpcell.00151.2013.
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A better understanding of the control of body fat distribution and muscle development is of the upmost importance for both human and animal physiology. This requires a better knowledge of the features and physiology of adult stem cells in adipose tissue and skeletal muscle. Thus the objective of the current study was to determine the type and proportion of these cells in growing and adult pigs. The different cell subsets of stromal vascular cells isolated from these tissues were characterized by flow cytometry using cell surface markers (CD11b, CD14, CD31, CD34, CD45, CD56, and CD90). Adipose and muscle cells were predominantly positive for the CD34, CD56, and CD90 markers. The proportion of positive cells changed with age especially in intermuscular adipose tissue and skeletal muscle where the percentage of CD90+ cells markedly increased in adult animals. Further analysis using coimmunostaining indicates that eight populations with proportions ranging from 12 to 30% were identified in at least one tissue at 7 days of age, i.e., CD90+/CD34+, CD90+/CD34−, CD90+/CD56+, CD90+/CD56−, CD90−/CD56+, CD56+/CD34+, CD56+/CD34−, and CD56−/CD34+. Adipose tissues appeared to be a less heterogeneous tissue than skeletal muscle with two main populations (CD90+/CD34− and CD90+/CD56−) compared with five or more in muscle during the studied period. In culture, cells from adipose tissue and muscle differentiated into mature adipocytes in adipogenic medium. In myogenic conditions, only cells from muscle could form mature myofibers. Further studies are now needed to better understand the plasticity of those cell populations throughout life.
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Lee, Hyo-Geun, Yu An Lu, Xining Li, Ji-Min Hyun, Hyun-Soo Kim, Jeong Jun Lee, Tae Hee Kim, Hye Min Kim, Min-Cheol Kang, and You-Jin Jeon. "Anti-Obesity Effects of Grateloupia elliptica, a Red Seaweed, in Mice with High-Fat Diet-Induced Obesity via Suppression of Adipogenic Factors in White Adipose Tissue and Increased Thermogenic Factors in Brown Adipose Tissue." Nutrients 12, no. 2 (January 24, 2020): 308. http://dx.doi.org/10.3390/nu12020308.
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Obesity is a serious metabolic syndrome characterized by high levels of cholesterol, lipids in the blood, and intracellular fat accumulation in adipose tissues. It is known that the suppression of adipogenic protein expression is an effective approach for the treatment of obesity, and regulates fatty acid storage and transportation in adipose tissues. The 60% ethanol extract of Grateloupia elliptica (GEE), a red seaweed from Jeju Island in Korea, was shown to exert anti-adipogenic activity in 3T3-L1 cells and in mice with high-fat diet (HFD)-induced obesity. GEE inhibited intracellular lipid accumulation in 3T3-L1 cells, and significantly reduced expression of adipogenic proteins. In vivo experiments indicated a significant reduction in body weight, as well as white adipose tissue (WAT) weight, including fatty liver, serum triglycerides, total cholesterol, and leptin contents. The expression of the adipogenic proteins, SREBP-1 and PPAR-γ, was significantly decreased by GEE, and the expression of the metabolic regulator protein was increased in WAT. The potential of GEE was shown in WAT, with the downregulation of PPAR-γ and C/EBP-α mRNA; in contrast, in brown adipose tissue (BAT), the thermogenic proteins were increased. Collectively, these research findings suggest the potential of GEE as an effective candidate for the treatment of obesity-related issues via functional foods or pharmaceutical agents.
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Roth, Christel L., Filippo Molica, and Brenda R. Kwak. "Browning of White Adipose Tissue as a Therapeutic Tool in the Fight against Atherosclerosis." Metabolites 11, no. 5 (May 14, 2021): 319. http://dx.doi.org/10.3390/metabo11050319.
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Despite continuous medical advances, atherosclerosis remains the prime cause of mortality worldwide. Emerging findings on brown and beige adipocytes highlighted that these fat cells share the specific ability of non-shivering thermogenesis due to the expression of uncoupling protein 1. Brown fat is established during embryogenesis, and beige cells emerge from white adipose tissue exposed to specific stimuli like cold exposure into a process called browning. The consecutive energy expenditure of both thermogenic adipose tissues has shown therapeutic potential in metabolic disorders like obesity and diabetes. The latest data suggest promising effects on atherosclerosis development as well. Upon cold exposure, mice and humans have a physiological increase in brown adipose tissue activation and browning of white adipocytes is promoted. The use of drugs like β3-adrenergic agonists in murine models induces similar effects. With respect to atheroprotection, thermogenic adipose tissue activation has beneficial outcomes in mice by decreasing plasma triglycerides, total cholesterol and low-density lipoproteins, by increasing high-density lipoproteins, and by inducing secretion of atheroprotective adipokines. Atheroprotective effects involve an unaffected hepatic clearance. Latest clinical data tend to find thinner atherosclerotic lesions in patients with higher brown adipose tissue activity. Strategies for preserving healthy arteries are a major concern for public health.
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Zacharia, Anish, Daniel Saidemberg, Chanchal Thomas Mannully, Natalya M. Kogan, Alaa Shehadeh, Reut Sinai, Avigail Zucker, et al. "Distinct infrastructure of lipid networks in visceral and subcutaneous adipose tissues in overweight humans." American Journal of Clinical Nutrition 112, no. 4 (August 7, 2020): 979–90. http://dx.doi.org/10.1093/ajcn/nqaa195.
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ABSTRACT Background Adipose tissue plays important roles in health and disease. Given the unique association of visceral adipose tissue with obesity-related metabolic diseases, the distribution of lipids between the major fat depots located in subcutaneous and visceral regions may shed new light on adipose tissue–specific roles in systemic metabolic perturbations. Objective We sought to characterize the lipid networks and unveil differences in the metabolic infrastructure of the 2 adipose tissues that may have functional and nutritional implications. Methods Paired visceral and subcutaneous adipose tissue samples were obtained from 17 overweight patients undergoing elective abdominal surgery. Ultra-performance LC-MS was used to measure 18,640 adipose-derived features; 520 were putatively identified. A stem cell model for adipogenesis was used to study the functional implications of the differences found. Results Our analyses resulted in detailed lipid metabolic maps of the 2 major adipose tissues. They point to a higher accumulation of phosphatidylcholines, triacylglycerols, and diacylglycerols, although lower ceramide concentrations, in subcutaneous tissue. The degree of unsaturation was lower in visceral adipose tissue (VAT) phospholipids, indicating lower unsaturated fatty acid incorporation into adipose tissue. The differential abundance of phosphatidylcholines we found can be attributed at least partially to higher expression of phosphatidylethanolamine methyl transferase (PEMT). PEMT-deficient embryonic stem cells showed a dramatic decrease in adipogenesis, and the resulting adipocytes exhibited lower accumulation of lipid droplets, in line with the lower concentrations of glycerolipids in VAT. Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways. Conclusions Our work unveils differential infrastructure of the lipid networks in visceral and subcutaneous adipose tissues and suggests an integrative pathway, with a discriminative flux between adipose tissues.
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Ocón-Grove, Olga M., Susan M. Krzysik-Walker, Sreenivasa R. Maddineni, Gilbert L. Hendricks, and Ramesh Ramachandran. "Adiponectin and its receptors are expressed in the chicken testis: influence of sexual maturation on testicular ADIPOR1 and ADIPOR2 mRNA abundance." REPRODUCTION 136, no. 5 (November 2008): 627–38. http://dx.doi.org/10.1530/rep-07-0446.
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Adiponectin is an adipokine hormone that influences glucose utilization, insulin sensitivity, and energy homeostasis by signaling through two distinct receptors, ADIPOR1 and ADIPOR2. While adipose tissue is the primary site of adiponectin expression in the chicken, we previously reported that adiponectin and its receptors are expressed in several other tissues. The objectives of the present study are to characterize adiponectin, ADIPOR1, and ADIPOR2 expressions in the chicken testis and to determine whether sexual maturation affects the abundance of testicular adiponectin,ADIPOR1, andADIPOR2mRNAs. By RT-PCR and nucleotide sequencing, testicular adiponectin,ADIPOR1, andADIPOR2mRNAs were found to be identical to that expressed in the abdominal fat pad. Using anti-chicken adiponectin, ADIPOR1, or ADIPOR2 antibodies and immunohistochemistry, adiponectin-immunoreactive (ir) and ADIPOR1-ir cells were found exclusively in the peritubular cells as well as in Leydig cells. However, ADIPOR2-ir cells were found in the adluminal and luminal compartments of the seminiferous tubules as well as in interstitial cells. In particular, Sertoli cell syncytia, round spermatids, elongating spermatids, spermatozoa, and Leydig cells showed strong ADIPOR2 immunoreactivity. Using quantitative real-time PCR analyses, testicularADIPOR1andADIPOR2mRNA abundance were found to be 8.3- and 9-fold higher (P<0.01) in adult chickens compared with prepubertal chickens respectively, suggesting that sexual maturation is likely to be associated with an up-regulation of testicularADIPOR1andADIPOR2gene expressions. Collectively, our results indicate that adiponectin and its receptors are expressed in the chicken testis, where they are likely to influence steroidogenesis, spermatogenesis, Sertoli cell function as well as spermatozoa motility.