Relevant bibliographies by topics / Brown Adipocytes

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Brown Adipocytes'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Brown Adipocytes"

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Okamatsu-Ogura, Yuko, Junko Nio-Kobayashi, Kazuki Nagaya, Ayumi Tsubota, and Kazuhiro Kimura. "Brown adipocytes postnatally arise through both differentiation from progenitors and conversion from white adipocytes in Syrian hamster." Journal of Applied Physiology 124, no. 1 (January 1, 2018): 99–108. http://dx.doi.org/10.1152/japplphysiol.00622.2017.

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To investigate the postnatal development of brown adipose tissue (BAT) in Syrian hamsters, we histologically examined interscapular fat tissue from 5–16-day-old pups, focusing on how brown adipocytes arise. Interscapular fat of 5-day-old hamsters mainly consisted of white adipocytes containing large unilocular lipid droplets, as observed in typical white adipose tissue (WAT). On day 7, clusters of small, proliferative nonadipocytes with a strong immunoreactivity for Ki67 appeared near the edge of the interscapular fat tissue. The area of the Ki67-positive regions expanded to ~50% of the total tissue area by day 10. The interscapular fat showed the typical BAT feature by day 16. A brown adipocyte-specific marker, uncoupling protein-1, was clearly detected on day 10 and thereafter, while not detected on day 7. During conversion of interscapular fat from WAT to BAT, unilocular adipocytes completely and rapidly disappeared without obvious apoptosis. Dual immunofluorescence staining for Ki67 and monocarboxylate transporter 1 (MCT1), another selective marker for brown adipocytes, revealed that most of the proliferating cells were of the brown adipocyte lineage. Electron microscopic examination showed that some of the white adipocytes contained small lipid droplets in addition to the large droplet and expressed MCT1 as do progenitor and mature brown adipocytes, implying a direct conversion from white to brown adipocytes. These results suggest that BAT of Syrian hamsters develops postnatally through two different pathways: the proliferation and differentiation of brown adipocyte progenitors and the conversion of unilocular adipocytes to multilocular brown adipocytes. NEW & NOTEWORTHY Brown and white adipose tissues (BAT and WAT, respectively) are quite different in morphological features and function; however, the boundary between these tissues is obscure. In this study, we histologically evaluated the process of BAT development in Syrian hamsters, which shows postnatal conversion of WAT to BAT. Our results suggest that brown adipocytes arise through two different pathways: the proliferation and differentiation of brown adipocyte progenitors and the conversion from white adipocytes.
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Rakhshandehroo, Maryam, Arjen Koppen, and Eric Kalkhoven. "Pref-1 preferentially inhibits heat production in brown adipose tissue." Biochemical Journal 443, no. 3 (April 16, 2012): e3-e5. http://dx.doi.org/10.1042/bj20120382.

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In mammals there are two types of adipocytes with opposing functions. Brown adipocytes are characterized by a high number of mitochondria and are specialized for heat production (thermogenesis), expressing thermogenic genes such as UCP1 (uncoupling protein 1). White adipocytes, on the other hand, store energy. Although many key regulators in the differentiation of white adipocytes have been established, our current knowledge on the same proteins in brown adipogenesis is lagging behind. One example is Pref-1 (pre-adipocyte factor-1), which maintains white pre-adipocytes in an undifferentiated state, but is only poorly characterized in the brown pre-adipocyte lineage. In this issue of the Biochemical Journal, Armengol et al. now shed new light on the role and regulation of Pref-1 in brown pre-adipocytes. First, Pref-1 specifically inhibits the thermogenic gene programme in brown pre-adipocytes. Secondly, they identified the transcription factor C/EBPδ (CCAAT/enhancer-binding protein δ) as a direct positive regulator of Pref-1 expression, whereas this protein does not fulfil this role in white adipogenesis. Taken together, these findings indicate that specific manipulation of brown adipocyte differentiation and/or function without interfering with their white adipocyte counterparts may be possible, which may open up new therapeutic ways to combat obesity-associated health problems.
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Gburcik, Valentina, William P. Cawthorn, Jan Nedergaard, James A. Timmons, and Barbara Cannon. "An essential role for Tbx15 in the differentiation of brown and “brite” but not white adipocytes." American Journal of Physiology-Endocrinology and Metabolism 303, no. 8 (October 15, 2012): E1053—E1060. http://dx.doi.org/10.1152/ajpendo.00104.2012.

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The transcription factor Tbx15 is expressed predominantly in brown adipose tissue and in those white adipose depots that are capable of giving rise to brown-in-white (“brite”/“beige”) adipocytes. Therefore, we have investigated a possible role here of Tbx15 in brown and brite adipocyte differentiation in vitro. Adipocyte precursors were isolated from interscapular and axilliary brown adipose tissues, inguinal white (“brite”) adipose tissue, and epididymal white adipose tissue in 129/Sv mouse pups and differentiated in culture. Differentiation was enhanced by chronic treatment with the PPARγ agonist rosiglitazone plus the sympathetic neurotransmitter norepinephrine. Using short interfering RNAs (siRNA) directed toward Tbx15 in these primary adipocyte cultures, we decreased Tbx15 expression >90%. This resulted in reduced expression levels of adipogenesis markers (PPARγ, aP2). Importantly, Tbx15 knockdown reduced the expression of brown phenotypic marker genes (PRDM16, PGC-1α, Cox8b/Cox4, UCP1) in brown adipocytes and even more markedly in inguinal white adipocytes. In contrast, Tbx15 knockdown had no effect on white adipocytes originating from a depot that is not brite competent in vivo (epididymal). Therefore, Tbx15 may be essential for the development of the adipogenic and thermogenic programs in adipocytes/adipomyocytes capable of developing brown adipocyte features.
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Saggerson, E. D., and Z. Jamal. "Differences in the properties of A1-type adenosine receptors in rat white and brown adipocytes." Biochemical Journal 269, no. 1 (July 1, 1990): 157–61. http://dx.doi.org/10.1042/bj2690157.

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1. White adipocytes were found to be more responsive than brown adipocytes to inhibition of lipolysis by the A1 adenosine receptor agonist phenylisopropyladenosine. 2. Radioligand binding studies with plasma membranes isolated from the two adipocyte types indicated differences in the properties of the A1 receptors. Kd values (high and low affinity) for phenylisopropyladenosine were higher in membranes from brown adipocytes. The Kd values for the antagonist dipropylcyclopentylxanthine were also higher in brown adipocyte membranes. 3. The effects of guanine nucleotides in converting adipocyte A1 receptors into a low-affinity state were enhanced by dithiothreitol.
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Giralt, Marta, and Francesc Villarroya. "White, Brown, Beige/Brite: Different Adipose Cells for Different Functions?" Endocrinology 154, no. 9 (June 19, 2013): 2992–3000. http://dx.doi.org/10.1210/en.2013-1403.

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Brown adipose tissue (BAT) is a major site of nonshivering thermogenesis in mammals. Rodent studies indicated that BAT thermogenic activity may protect against obesity. Recent findings using novel radiodiagnosis procedures revealed unanticipated high activity of BAT in adult humans. Moreover, complex processes of cell differentiation leading to the appearance of active brown adipocytes have been recently identified. The brown adipocytes clustered in defined anatomical BAT depots of rodents arise from mesenchymal precursor cells common to the myogenic cell lineage. They are being called “classical” or “developmentally programmed” brown adipocytes. However, brown adipocytes may appear after thermogenic stimuli at anatomical sites corresponding to white adipose tissue (WAT). This process is called the “browning” of WAT. The brown adipocytes appearing in WAT derive from precursor cells different from those in classical BAT and are closer to the white adipocyte cell lineage. The brown adipocytes appearing in WAT are often called “inducible, beige, or brite.” The appearance of these inducible brown adipocytes in WAT may also involve transdifferentiation processes of white-to-brown adipose cells. There is no evidence that the ultimate thermogenic function of the beige/brite adipocytes differs from that of classical brown adipocytes, although some genetic data in rodents suggest a relevant role of the browning process in protection against obesity. Although the activation of classical BAT and the browning process share common mechanisms of induction (eg, noradrenergic-mediated induction by cold), multiple novel adrenergic-independent endocrine factors that activate BAT and the browning of WAT have been identified recently. In adult humans, BAT is mainly composed of beige/brite adipocytes, although recent data indicate the persistence of classical BAT at some anatomical sites. Understanding the biological processes controlling brown adipocyte activity and differentiation could help the design of BAT-focused strategies to increase energy expenditure and fight against obesity.
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Dowal, Louisa, Pooja Parameswaran, Sarah Phat, Syamala Akella, Ishita Deb Majumdar, Jyoti Ranjan, Chahan Shah, et al. "Intrinsic Properties of Brown and White Adipocytes Have Differential Effects on Macrophage Inflammatory Responses." Mediators of Inflammation 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/9067049.

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Obesity is marked by chronic, low-grade inflammation. Here, we examined whether intrinsic differences between white and brown adipocytes influence the inflammatory status of macrophages. White and brown adipocytes were characterized by transcriptional regulation of UCP-1, PGC1α, PGC1β, and CIDEA and their level of IL-6 secretion. The inflammatory profile of PMA-differentiated U937 and THP-1 macrophages, in resting state and after stimulation with LPS/IFN-gamma and IL-4, was assessed by measuring IL-6 secretion and transcriptional regulation of a panel of inflammatory genes after mono- or indirect coculture with white and brown adipocytes. White adipocyte monocultures show increased IL-6 secretion compared to brown adipocytes. White adipocytes cocultured with U937 and THP-1 macrophages induced a greater increase in IL-6 secretion compared to brown adipocytes cocultured with both macrophages. White adipocytes cocultured with macrophages increased inflammatory gene expression in both types. In contrast, macrophages cocultured with brown adipocytes induced downregulation or no alterations in inflammatory gene expression. The effects of adipocytes on macrophages appear to be independent of stimulation state. Brown adipocytes exhibit an intrinsic ability to dampen inflammatory profile of macrophages, while white adipocytes enhance it. These data suggest that brown adipocytes may be less prone to adipose tissue inflammation that is associated with obesity.
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Giordano, A., M. Morroni, F. Carle, R. Gesuita, G. F. Marchesi, and S. Cinti. "Sensory nerves affect the recruitment and differentiation of rat periovarian brown adipocytes during cold acclimation." Journal of Cell Science 111, no. 17 (September 1, 1998): 2587–94. http://dx.doi.org/10.1242/jcs.111.17.2587.

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Rat periovarian adipose tissue contains a low number of uncoupling protein-expressing brown adipocytes scattered into lobules of white fat. Their increase following cold acclimation is matched by a major increase in noradrenergic and neuropeptide Y-, substance P- and calcitonin gene-related peptide-containing nerves. To ascertain whether periovarian fat is provided with sensory nerves, and whether any relationship exists between such nerves (in particular the calcitonin gene-related peptide-containing fibers found in cold-acclimated rats in close association with brown adipocytes) and brown fat recruitment, the effects of capsaicin desensitization on neuropeptide-containing nerves and brown adipocyte density were studied in the periovarian tissue of rats kept at 20 degrees C and on a group acclimated to 4 degrees C for 14 days. In both groups, systemic capsaicin administration considerably reduced the expression of substance P and calcitonin gene-related peptide in vascular-nerve bundles and parenchyma. In cold-acclimated rats, the increase in brown adipocyte density was significantly checked by capsaicin administration (21.11 versus 7.96 brown adipocytes/mm2, P<0.05). Finally, ultrastructural investigation showed the occurrence of brown adipocyte precursors filled with aggregates of glycogen and poorly differentiated multilocular adipocytes in capsaicin-treated cold-acclimated rats. These data suggest that periovarian adipose tissue is indeed provided with sensory neuropeptide-containing nerves and that they play a role in the recruitment and differentiation of brown adipocytes.
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Lizcano, Fernando, and Diana Vargas. "Biology of Beige Adipocyte and Possible Therapy for Type 2 Diabetes and Obesity." International Journal of Endocrinology 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/9542061.

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All mammals own two main forms of fat. The classical white adipose tissue builds up energy in the form of triglycerides and is useful for preventing fatigue during periods of low caloric intake and the brown adipose tissue instead of inducing fat accumulation can produce energy as heat. Since adult humans possess significant amounts of active brown fat depots and their mass inversely correlates with adiposity, brown fat might play an important role in human obesity and energy homeostasis. New evidence suggests two types of thermogenic adipocytes with distinct developmental and anatomical features: classical brown adipocytes and beige adipocytes. Beige adipocyte has recently attracted special interest because of its ability to dissipate energy and the possible ability to differentiate itself from white adipocytes. Importantly, adult human brown adipocyte appears to be mainly composed of beige-like adipocytes, making this cell type an attractive therapeutic target for obesity and obesity-related diseases. Because many epigenetic changes can affect beige adipocyte differentiation, the knowledge of the circumstances that affect the development of beige adipocyte cells may be important for therapeutic strategies. In this review we discuss some recent observations arising from the great physiological capacity of these cells and their possible role as ways to treat obesity and diabetes mellitus type 2.
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Rajan, Sujith, Kripa Shankar, Muheeb Beg, Salil Varshney, Abhishek Gupta, Ankita Srivastava, Durgesh Kumar, et al. "Chronic hyperinsulinemia reduces insulin sensitivity and metabolic functions of brown adipocyte." Journal of Endocrinology 230, no. 3 (September 2016): 275–90. http://dx.doi.org/10.1530/joe-16-0099.

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The growing pandemics of diabetes have become a real threat to world economy. Hyperinsulinemia and insulin resistance are closely associated with the pathophysiology of type 2 diabetes. In pretext of brown adipocytes being considered as the therapeutic strategy for the treatment of obesity and insulin resistance, we have tried to understand the effect of hyperinsulinemia on brown adipocyte function. We here with for the first time report that hyperinsulinemia-induced insulin resistance in brown adipocyte is also accompanied with reduced insulin sensitivity and brown adipocyte characteristics. CI treatment decreased expression of brown adipocyte-specific markers (such as PRDM16, PGC1α, and UCP1) and mitochondrial content as well as activity. CI-treated brown adipocytes showed drastic decrease in oxygen consumption rate (OCR) and spare respiratory capacity. Morphological study indicates increased accumulation of lipid droplets in CI-treated brown adipocytes. We have further validated these findings in vivo in C57BL/6 mice implanted with mini-osmotic insulin pump for 8weeks. CI treatment in mice leads to increased body weight gain, fat mass and impaired glucose intolerance with reduced energy expenditure and insulin sensitivity. CI-treated mice showed decreased BAT characteristics and function. We also observed increased inflammation and ER stress markers in BAT of CI-treated animals. The above results conclude that hyperinsulinemia has deleterious effect on brown adipocyte function, making it susceptible to insulin resistance. Thus, the above findings have greater implication in designing approaches for the treatment of insulin resistance and diabetes via recruitment of brown adipocytes.
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Baht, H. S., and E. D. Saggerson. "Comparison of triacylglycerol synthesis in rat brown and white adipocytes. Effects of hypothyroidism and streptozotocin-diabetes on enzyme activities and metabolic fluxes." Biochemical Journal 250, no. 2 (March 1, 1988): 325–33. http://dx.doi.org/10.1042/bj2500325.

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1. Adipocytes were isolated from the interscapular brown fat and the epididymal white fat of normal, streptozotocin-diabetic and hypothyroid rats. 2. Measurements were made of the maximum rate of triacylglycerol synthesis by monitoring the incorporation of [U-14C]glucose into acylglycerol glycerol in the presence of palmitate (1 mM) and insulin (4 nM) and of the activities of the following triacylglycerol-synthesizing enzymes: fatty acyl-CoA synthetase (FAS), mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), dihydroxyacetonephosphate acyltransferase (DHAPAT), monoacylglycerol phosphate acyltransferase (MGPAT), Mg2+-dependent phosphatidate phosphohydrolase (PPH) and diacylglycerol acyltransferase (DGAT). 3. FAS activity in brown adipocytes was predominantly localized in the mitochondrial fraction, whereas a microsomal localization of this enzyme predominated in white adipocytes. Subcellular distributions of the other enzyme activities in brown adipocytes were similar to those shown previously with white adipocytes [Saggerson, Carpenter, Cheng & Sooranna (1980) Biochem. J. 190, 183-189]. 4. Relative to cell DNA, brown adipocytes had lower activities of triacylglycerol-synthesizing enzymes and showed lower rates of metabolic flux into acylglycerols than did white adipocytes isolated from the same animals. 5. Diabetes decreased both metabolic flux into acylglycerols and the activities of triacylglycerol-synthesizing enzymes in white adipocytes. By contrast, although diabetes decreased metabolic flux into brown-adipocyte acylglycerols by 80%, there were no decreases in the activities of triacylglycerol-synthesizing enzymes, and the activity of PPH was significantly increased. 6. Hypothyroidism increased metabolic flux into acylglycerols in both cell types, and increased activities of all triacylglycerol-synthesizing enzymes in brown adipocytes. By contrast, in white adipocytes, although hypothyroidism increased the activities of FAS, microsomal GPAT and DGAT, this condition decreased the activities of mitochondrial GPAT and PPH. 7. It was calculated that the maximum capabilities for fatty acid oxidation and esterification are approximately equal in brown adipocytes. In white adipocytes esterification is predominant by approx. 100-fold. 8. Diabetes almost abolished incorporation of [U-14C]glucose into fatty acids in both adipocyte types. Hypothyroidism increased fatty acid synthesis in white and brown adipocytes by 50% and 1000% respectively.
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Dissertations / Theses on the topic "Brown Adipocytes"

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Dimitri, Federica. "MicroRNAs in brown and white adipocytes." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/99123/.

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The adipose tissue has an important role in maintaining the energy homeostasis balance. Understanding its physiology is important for the development of treatments against diseases where this equilibrium is compromised, such as obesity and associated metabolic disorders. MicroRNAs (miRNAs) are important gene regulators and an increasing body of evidence suggests their involvement in adipogenesis and adipose metabolism. MiRNAs can also be secreted into the extracellular environment and be taken up by distal cells, mediating cell-to-cell communication. However, very little is known about adipose tissue-derived circulating miRNAs. Through miRNA PCR array analysis we identified several miRNAs that are differentially secreted among mouse undifferentiated and differentiated brown and white adipocytes, among which, miR-196a and miR-378a-3p showed a conservative pattern of secretion in different adipocyte models. MiR-138-5p was identified as the unique miRNA differentially secreted between human brown and white adipocytes. Bioinformatics target prediction revealed that these miRNAs are potentially involved in important processes regulating the functioning of adipose tissue and its cross-talk with distal cells. By ultracentrifugation of adipose conditioned media and Nanosight technology, we investigated vesicle and vesicle-free miRNA carriers and characterized adipose derived vesicles. Finally, through microRNA array and mRNA sequencing we identified genes, miRNAs and pathways differentially enriched in human brown and white adipocytes contributing to improve the knowledge on the nature of human adipocytes, hampered by the scarce availability of human brown adipose samples. Through integration of the two analyses, we identify poorly known or novel miRNAs, potentially involved in the pathways associated with the genes differentially expressed between human brown and white adipocytes. Among the significantly downregulated miRNAs in brown versus white adipocytes we highlighted miR-513a-3p, miR-4511 and miR-4328. While, among the significantly upregulated miRNAs in brown versus white we highlighted miR-4698, miR-4516, miR-4531, miR-29a-3p and miR-3915.
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Chernogubova, Ekaterina. "Adrenergic stimulation of glucose uptake in brown adipocytes." Doctoral thesis, Stockholm : The Wenner-Gren institute, Stockholm university, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-549.

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Min, So Yun. "The Origin of Human White, Brown, and Brite/Beige Adipocytes." eScholarship@UMMS, 2016. http://escholarship.umassmed.edu/gsbs_diss/878.

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During embryonic development, adipocytes emerge from microvasculature. Lineage-­‐tracing studies in mice have shown that adipocyte progenitors reside in the adipose tissue capillaries. However, the direct evidence of an association between adipocyte progenitors and vasculature in humans is lacking. A specific class of adipocytes (brown and beige/brite) expresses the uncoupling protein 1 (UCP1), which consumes glucose and fatty acids to generate heat. The abundance of UCP1- containing adipocytes correlates with a lean metabolically healthy phenotype in human. However, a causal relationship between the presence of these cells and metabolic benefits in human is not clear. In this thesis, I report human adipocyte progenitors proliferate in response to pro-angiogenic factors in association with adipose capillary networks in-vitro. The capillary-derived adipocytes transform from being UCP1-negative to positive upon adenylate cyclase activation, a defining feature of the brite/beige phenotype. Activated cells have denser, round mitochondria with UCP1 protein, and display uncoupled respiration. When implanted into NOD-scid IL2rgnull (NSG) mice, the adipocytes can form a vascularized fat pad that induces vascularization and becomes integrated into mouse circulatory system. In normal or high fat diet-fed NSG mice, activated brite/beige adipocytes enhance systemic glucose tolerance and improved hepatic steatosis, thus providing evidence for their potential therapeutic use. The adipocytes also express neuroendocrine and secretory factors such as Interleukin-33, proprotein convertase PCSK1 and proenkephalin PENK, which are correlated with human obesity. Finally, analyses on single-cell clones of capillary-sprout cells reveal the existence of diverse adipogenic progenitor populations. Further characterization of the clones will define the identifying features of the diverse adipocyte progenitor types that exist in human adipose tissue.
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Wikström, Jakob D. "Mitochondrial form and function in pancreatic β-cells and brown adipocytes." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-39336.

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This thesis is focused on the role of mitochondria in pancreatic β-cells and brown adipose tissue (BAT). Two main aspects of mitochondria were explored; mitochondrial functional efficiency and the interrelationship between mitochondrial shape and function. Mitochondria in β-cells were found to exhibit heterogeneity in mitochondrial membrane potential. This functional diversity decreased when cells were challenged with glucose stimuli, suggesting that at higher fuel levels low-activity mitochondria are recruited into a pool of high-activity mitochondria. Glucolipotoxic conditions increased the functional diversity suggesting that this may be of importance for diabetes pathophysiology. To examine mitochondrial efficiency in intact islets a high throughput islet respirometry method was developed. Due to increased uncoupling, islets from a diabetic animal model exhibit lower respiratory efficiency. Glucose, free fatty acids and amino acids all decreased respiratory efficiency. A large portion of the respiratory efficiency was mediated by reactive oxygen species and the adenine nucleotide translocase. In β-cells mitochondria were found to undergo cycles of fusion and fission. During glucolipotoxicity mitochondria fragmented and lost their fusion ability. Knock down of the fission protein Fis1 rescued the β-cells from glucolipotoxic induced cell death. BAT mitochondria also showed fusion and fission. The mitochondrial dynamics proteins Mfn2 and Drp1 were shown to strongly affect BAT mitochondrial morphology. In response to a combination of adrenergic and free fatty acid stimuli mitochondria drastically changed from long filamentous structures to fragmented spheres. Inhibiting fission by the negative form of Drp1 decreased BAT response to adrenergic stimuli by half. In conclusion, mitochondrial efficiency may be of importance for normal as well as compromised β-cell and islet function. Mitochondrial morphology appears critical for mitochondrial function in β-cells and BAT.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.
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Rockstroh, Denise, Kathrin Landgraf, Isabel Viola Wagner, Julia Gesing, Roy Tauscher, Nicole Lakowa, Wieland Kiess, et al. "Direct evidence of brown adipocytes in different fat depots in children." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-161428.

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Recent studies suggested the persistence of brown adipocytes in adult humans, as opposed to being exclusively present in infancy. In this study, we investigated the presence of brown-like adipocytes in adipose tissue (AT) samples of children and adolescents aged 0 to 18 years and evaluated the association with age, location, and obesity. For this, we analysed AT samples from 131 children and 23 adults by histological, immunohistochemical and expression analyses. We detected brown-like and UCP1 positive adipocytes in 10.3% of 87 lean children (aged 0.3 to 10.7 years) and in one overweight infant, whereas we did not find brown adipocytes in obese children or adults. In our samples, the brown-like adipocytes were interspersed within white AT of perirenal, visceral and also subcutaneous depots. Samples with brown-like adipocytes showed an increased expression of UCP1 (>200fold), PRDM16 (2.8fold), PGC1α and CIDEA while other brown/beige selective markers, such as PAT2, P2RX5, ZIC1, LHX8, TMEM26, HOXC9 and TBX1 were not significantly different between UCP1 positive and negative samples. We identified a positive correlation between UCP1 and PRDM16 within UCP1 positive samples, but not with any other brown/beige marker. In addition, we observed significantly increased PRDM16 and PAT2 expression in subcutaneous and visceral AT samples with high UCP1 expression in adults. Our data indicate that brown-like adipocytes are present well beyond infancy in subcutaneous depots of non-obese children. The presence was not restricted to typical perirenal locations, but they were also interspersed within WAT of visceral and subcutaneous depots.
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Giroud, Maude. "Implication des microARNs dans la conversion des adipocytes blancs en adipocytes thermogéniques." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4082/document.

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La découverte récente d'adipocytes bruns fonctionnels chez les humains adultes a conduit à envisager leur utilisation afin d’augmenter la dépense énergétique dans de potentiels traitements contre l'obésité et les maladies associées. Par ailleurs, des ilots d’adipocytes bruns, appelés adipocytes "brite" (brown in white), émergent dans le tissu adipeux blanc après une exposition au froid ou une stimulation des récepteurs β3-adrénergiques. En utilisant les cellules hMADS, nous avons identifié plusieurs miARNs régulés pendant le « britening ». miR-125b et let-7i ont des niveaux d’expression plus bas dans les adipocytes « brites ». Des analyses fonctionnelles utilisant un « mimic » de miR-125b ou un inhibiteur ont révélé que miR-125b agit comme un frein sur le « brunissage » des cellules hMADS en altérant leur respiration ainsi que leur contenu mitochondrial. In vivo, nous avons montré que miR-125b et let-7i sont moins exprimés dans le tissu adipeux brun par rapport au tissu adipeux blanc. La stimulation des récepteurs β3-adrénergiques ou l'exposition au froid induit une diminution d’expression des miARNs dans les deux tissus et est associée à l'activation du tissu adipeux brun et au recrutement des adipocytes « brites ». Nous avons constaté que l’injection de miR-125b ou let-7i dans le tissu adipeux blanc sous-cutané inhibait l’expression de gènes du « brunissage » induite par la stimulation de la voie β3-adrénergique. En conclusion, nos observations ont montré que miR-125b et let-7i jouaient un rôle important dans la modulation des adipocytes « brites » et des adipocytes « bruns » en ciblant l’expression de gènes mitochondriaux et en diminuant la biogenèse mitochondriale
The recent discovery of functional brown adipocytes in adult humans has led to the consideration of their use to increase energy expenditure in the treatment of obesity and associated metabolic disorders. Furthermore, in rodents and humans, islands of thermogenic adipocytes, termed “brite” (brown in white) adipocytes, emerge within white adipose tissue after cold exposure or β3-adrenergic receptor stimulation. Using hMADS cells, we identified several miRNAs regulated during “britening” including miR-125b and let-7i which showed lower levels in brite adipocytes. Functional analysis using miR-125b mimic or miR-125b inhibitor transfection revealed that miR-125b-5p acts as a brake of the browning of hMADS cells by impairing respiration rate as well as their mitochondrial content. miR-125b and let-7i levels were lower in brown compared to white adipose tissue. In vivo, we showed that both miRNAs levels were down regulated in mice sub-cutaneous white and brown adipose tissues upon β3-adrenergic receptors stimulation or cold exposure, which is associated with BAT activation and brite adipocyte recruitment. We found that injection of both miRNA mimics in subcutaneous white adipose tissue inhibited β3-adrenergic-induced brown adipocyte markers expression. Altogether, our observations showed that miR-125b and let-7i played an important role in the modulation of brite and brown adipocytes function targeting oxygen consumption and mitochondrial gene expression
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Kohlie, Rose [Verfasser]. "Dopamine directly increases mitochondrial mass and thermogenesis in brown adipocytes / Rose Kohlie." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2018. http://d-nb.info/116222861X/34.

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Waldén, Tomas B. "Regulatory Factors that Reveal Three Distinct Adipocytes : The Brown, the White and the Brite." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-38362.

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Adipose tissues have long been considered to derive from a common origin. Even the functionally different brown and white adipose tissues were generalized to share a common origin. Brown adipose tissue is a highly innervated and vascularised tissue containing multilocular and multimitochondrial brown adipocytes. Brown adipose tissue expends energy through sympathetic nervous system-mediated non-shivering thermogenesis, where uncoupling protein 1 (UCP1) is the key player. In contrast, white adipose tissue consists of unilocular white adipocytes with a main role to store energy in the form of the lipid droplet. We know today that this generalisation is exaggerated since adipocytes can derive from more than one origin and not only be brown or white. We and others have demonstrated that the brown adipocyte has a dermomyotomal origin and derives from the adipomyocyte, the precursor cell that can also become a myocyte, whereas white adipocytes are suggested to derive from pericytes, cells that are embedded within the vascular vessel walls. For a long time there has been evidence that energy-expending adipocytes reside within certain white adipose tissues, based on the fact that cold exposure, by switching on the sympathetic nervous system, leads to levels of UCP1 that are not detectable in mice housed at thermoneutrality. We demonstrated that these cells have a molecular signature that is distinct from brown and white adipocytes. Since these energy-expending cells reside within certain white adipose tissues, we chose to name them brite (brown in white) adipocytes. Moreover, we also identified regulatory factors that were specifically expressed in each adipocyte type, thus, facilitating the possibility to identify the three adipocytes: the brown, the white and the brite.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 4: Manuscript. Paper 5: Manuscript.
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Hu, Jiamiao. "The effects of short-chain fatty acid acetate on brown adipocytes differentiation and metabolism." Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/81114/.

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Short-chain fatty acids (SCFA) are a sub-group of fatty acids including formic acid, acetic acid, propionic acid, isobutyric acid, butyric acid, isovaleric acid and valeric acid. Acetate, propionate and butyrate are three major shortchain fatty acids, which are mainly formed in the gastrointestinal tract via colonic bacteria fermentation of carbohydrates, especially resistant starches and dietary fibre. There has been increasing interest in the idea that the short-chain fatty acids play crucial roles in a range of physiological functions. Recently, increasing evidence suggested there is a strong link between short-chain fatty acids and energy homeostasis. Several studies highlighted the protective effects of the short-chain fatty acids on high-fat diet induced obesity and other harmful metabolic disorders in mice. However, the coherent understanding of the multi-level network in which short-chain fatty acids exert their effects still needs to be elucidated. Up to date, it has been demonstrated that short-chain fatty acids can mediate energy balance via affecting appetite control in brain, increasing adipogenesis in white adipocyte, and regulating insulin sensitivities in white adipose tissue and muscle, etc. However, the effects of short-chain fatty acids on brown adipocytes have not been fully investigated. In this study, we examined the roles of short-chain fatty acid acetate and its receptor(s) in the regulation of brown adipocyte differentiation and metabolism. Firstly, we identified the expression of short-chain fatty acids sensing GPR43 in brown adipose tissue and immortalized brown adipocytes by real-time PCR, Western blots and immunohistochemistry. Moreover, GPR43 expression was found to increase during the adipogenesis of cultured brown adipocytes. Pro-adipogenic reagent PPARγ agonist stimulation led to a further augment of GPR43 expression while antiadipogenic reagents such as PPARγ antagonist, RXR antagonist and STAT5 inhibitor played the opposite role on GPR43 expression. Transcription factors such as XBP1 and STAT5 were identified to be involved in GPR43 expression regulation in brown adipocytes. Furthermore, we also examined the role of acetate in the regulation of brown adipogenesis. Our results showed that acetate treatment during adipogenesis up-regulated AP2, PGC-1α and UCP1 expression and affected the morphological changes of brown adipocytes. Moreover, an increase in mitochondrial biogenesis was observed after acetate treatment. Acetate also elicited the activation of ERK and CREB, and these responses were sensitive to G(i/o)-type G-protein inactivator, Gβγ-subunit inhibitor, PLC inhibitor and MEK inhibitor, indicating a role for the G(i/o)βγ/PLC/PKC/MEK signalling pathway in these responses. These effects of acetate were mimicked by treatment with 4-CMTB, a synthetic GPR43 agonist, and were impaired in GPR43 knock-down cells, further supported the hypothesis that GPR43 mediates the pro-adipogenic effects of acetate in brown adipocytes. Furthermore, the effects of acetate treatment on brown adipose tissue were also measured in vivo. Mice fed with acetate demonstrated increased PGC-1α in brown adipose tissue, which was in agreement with the results obtained from immortalized brown adipocytes. In addition, we also measured the effects of acetate on lipid metabolism in differentiated brown adipocytes. The results showed effects of acetate treatment on lipolysis were different in white adipocytes and brown adipocytes. Acetate treatment significantly decreased the lipolysis in white adipocytes while had little effects on lipolysis in brown adipocytes. Besides, acetate treatment was also found to decrease TF2-C12 fatty acid uptake in differentiated IM-BAT cells, suggesting acetate may affect many aspects of lipid metabolism in brown adipocytes. Collectively, our results indicated that acetate might have important physiological roles in brown adipocytes. Short-chain fatty acids may serve to regulate brown adipose tissue functions and therefore improve metabolic health.
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Schinzel, Robert [Verfasser]. "The culture and differentiation of human pluripotent cells into brown and white adipocytes / Robert Schinzel." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/103029092X/34.

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Book chapters on the topic "Brown Adipocytes"

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Bi, Sheng. "Role of NPY in Brown Adipocytes and Obesity." In Angiogenesis in Adipose Tissue, 169–86. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8069-3_9.

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Darcy, Justin, Chih-Hao Wang, and Yu-Hua Tseng. "Analyzing Mitochondrial Function in Brown Adipocytes with a Bioenergetic Analyzer." In Methods in Molecular Biology, 289–96. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0471-7_20.

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Lee, Yun-Hee. "Gene Expression and Histological Analysis of Activated Brown Adipocytes in Adipose Tissue." In Thermogenic Fat, 89–98. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_9.

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Ricquier, Daniel, and Anne-Marie Cassard-Doulcier. "The biochemistry of white and brown adipocytes analysed from a selection of proteins." In EJB Reviews 1993, 227–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78757-7_17.

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Steinbring, Jochen, Antonia Graja, Anne-Marie Jank, and Tim J. Schulz. "Flow Cytometric Isolation and Differentiation of Adipogenic Progenitor Cells into Brown and Brite/Beige Adipocytes." In Thermogenic Fat, 25–36. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_4.

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Puerta, Marisa. "Sympathetic Tone and Noradrenaline Responsiveness of Brown Adipocytes from Rats with High Levels of Sexual Steroids." In Temperature Regulation, 253–60. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-8491-4_41.

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Uchida, Y., K. Irie, F. Tsukahara, K. Ohba, T. Nomoto, and T. Muraki. "Effect of Tumor Necrosis Factor on the Lipoprotein Lipase Gene Expression in Brown Adipocytes Differentiated in Culture." In Thermal Balance in Health and Disease, 121–27. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7429-8_16.

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Christian, Mark. "In Vitro Models for Study of Brown Adipocyte Biology." In Brown Adipose Tissue, 85–96. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_122.

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Yao, Xi, Barbara Salingova, and Christian Dani. "Brown-Like Adipocyte Progenitors Derived from Human iPS Cells: A New Tool for Anti-obesity Drug Discovery and Cell-Based Therapy?" In Brown Adipose Tissue, 97–105. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_115.

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Hafner, Anne-Laure, Tala Mohsen-Kanson, and Christian Dani. "Differentiation of Brown Adipocyte Progenitors Derived from Human Induced Pluripotent Stem Cells." In Adipose-Derived Stem Cells, 31–39. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7799-4_4.

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Conference papers on the topic "Brown Adipocytes"

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Worschech, Andrea, Melissa Kazantzis, Remy Thomas, Martin Wabitsch, Daniel Tews, Mouaadh Abdelkarim, Vladimir Zilberfarb, A. Donny Strosberg, and Lotfi Chouchane. "Molecular Characterization Of White And Brown Adipocytes Reveals Complex Phenotypes." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0328.

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Aleksic, Marija. "Changes in peroxisomal pool of rat brown adipocytes in hypothyroidism." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.359.

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Frille, Armin, Hartmut Kuhn, Claudia Hänel, Thomas Ebert, Hans-Jürgen Seyfarth, and Hubert Wirtz. "Cocultured brown or white adipocytes can reduce efficacy of targeted therapy in lung cancer cells." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1764.

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Li, Juanjuan, Qi Wu, Zhiyu Li, Si Sun, Shan Zhu, Lijun Wang, Juan Wu, et al. "Abstract 1986: Breast cancer-secreted exosomes stimulate beige/brown differentiation and reprogram metabolism in stromal adipocytes to promote tumor progression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1986.

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Li, Juanjuan, Qi Wu, Zhiyu Li, Si Sun, Shan Zhu, Lijun Wang, Juan Wu, et al. "Abstract 1986: Breast cancer-secreted exosomes stimulate beige/brown differentiation and reprogram metabolism in stromal adipocytes to promote tumor progression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1986.

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Gohlke, S., F. Garcia-Carrizo, and TJ Schulz. "Role of mast cells in age-related brown adipocyte dysfunction." In Abstracts der Adipositastage 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1693609.

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Mancini, C., S. Gohlke, and TJ Schulz. "Analysis of the effects of age-related changes in the microenvironment on brown adipocyte formation and function." In Abstracts der Adipositastage 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1693599.

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