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Relevant bibliographies by topics / Diet-induced

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Academic literature on the topic 'Diet-induced'

Author: Grafiati

Published: 3 June 2025

Last updated: 22 June 2025

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Journal articles on the topic "Diet-induced"

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Mercer, Julian G., and Zoë A. Archer. "Putting the diet back into diet-induced obesity: Diet-induced hypothalamic gene expression." European Journal of Pharmacology 585, no. 1 (2008): 31–37. http://dx.doi.org/10.1016/j.ejphar.2007.11.077.

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GE, Chang-rong, Si-zheng GAO, Jun-jing JIA, and Mark Jois. "Diet-Induced Thermogenesis." Agricultural Sciences in China 7, no. 9 (2008): 1133–39. http://dx.doi.org/10.1016/s1671-2927(08)60156-x.

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Mansell, P. I., I. A. Macdonald, and I. W. Fellows. "Diet-induced thermogenesis." Clinical Science 72, no. 2 (1987): 259–60. http://dx.doi.org/10.1042/cs0720259.

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Millichap, J. Gordon. "Ketogenic Diet-Induced Cardiomyopathy." Pediatric Neurology Briefs 14, no. 7 (2000): 50. http://dx.doi.org/10.15844/pedneurbriefs-14-7-3.

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Clark, Barbara, Mohammad Wisam Baqdunes, and Gregory M. Kunkel. "Diet-induced oxalate nephropathy." BMJ Case Reports 12, no. 9 (2019): e231284. http://dx.doi.org/10.1136/bcr-2019-231284.

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Oxalate nephropathy is a rare condition and may be overlooked due to lack of recognition and understanding of triggers. An 81-year-old man was sent to nephrologist because of significantly increased creatinine (1.5–1.9 mg/dL) noted for 3 months. He had well-controlled diabetes but no history of kidney disease. He had no chronic diarrhoea or intestinal surgery. He was a health-minded individual who had read extensively about benefit of antioxidants. Initial work-up was unrevealing. Within a few weeks after first visit, he developed acute symptomatic worsening kidney injury with nausea, vomiting and creatinine up to 6.8 mg/dL. Repeat examination of the urine sediment revealed casts containing calcium oxalate crystals. A deeper dietary history revealed widespread oxalate precursor consumption. A kidney biopsy confirmed oxalate nephropathy. Restriction of oxalate consumption combined with adequate hydration, oral calcium acetate resulted in partial renal recovery without need for haemodialysis.

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Adeva, María M., and Gema Souto. "Diet-induced metabolic acidosis." Clinical Nutrition 30, no. 4 (2011): 416–21. http://dx.doi.org/10.1016/j.clnu.2011.03.008.

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Galef, Bennett G. "Socially induced diet preference can partially reverse a LiCl-induced diet aversion." Animal Learning & Behavior 13, no. 4 (1985): 415–18. http://dx.doi.org/10.3758/bf03208018.

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Briggs, D. I., M. B. Lemus, E. Kua, and Z. B. Andrews. "Diet-Induced Obesity Attenuates Fasting-Induced Hyperphagia." Journal of Neuroendocrinology 23, no. 7 (2011): 620–26. http://dx.doi.org/10.1111/j.1365-2826.2011.02148.x.

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Marcos, Rafael, M. Teresa Macarulla, J. Alfredo Martinez, and Jesús Larralde. "Hormonal diet-induced changes in a pea based diet." International Journal of Food Sciences and Nutrition 45, no. 1 (1994): 41–47. http://dx.doi.org/10.3109/09637489409167016.

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Seaman, David R. "The diet-induced proinflammatory state:." Journal of Manipulative and Physiological Therapeutics 25, no. 3 (2002): 168–79. http://dx.doi.org/10.1067/mmt.2002.122324.

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Dissertations / Theses on the topic "Diet-induced"

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Gao, Yuanqing. "Hypothalamic Glial Cells in Diet Induced Obesity." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447071648.

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Blackman, James R. "Diet-induced thermogenesis in the domestic chicken." Diss., Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/54737.

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Four experiments were conducted to examine the energetic responses of chicks from lines divergently selected for 56-day body weight to caloric intake. Caloric overconsumption or calorie-protein imbalances were induced by providing glucose solutions (16% w/v) in lieu of water in the first experiment, and by force-feeding the diet to crop capacity in the subsequent trials. Feed restriction was accomplished by providing 75% of ad libitum intake each day. Both low-weight (LN) and high-weight (HN) chicks reduced their voluntary feed intake when glucose solutions were provided; caloric intake was reduced by 25% and 10% in LN and HN chicks, respectively. Weight gain and the deposition of protein and ash in the carcass were reduced by the glucose treatment, but carcass lipid deposition was increased. The efficiency of energy deposition was improved in HN but unchanged in LN chicks. Feed restriction reduced feed intake, energetic efficiency, and gain of body weight, carcass dry matter, protein, lipid and ash. The suppression of lipid deposition was more severe in the LN chicks than in the HNs. Overfeeding of a complete diet increased body weight, the deposition of all carcass constituents, and energetic efficiency. Feed restriction exerted an opposite effect, with the LN chicks exhibiting more pronounced responses than the HNs. Determined metabolizable energy values of the diet differed among feeding treatments and between lines, and line by feeding treatment interactions were observed. Body core and surface temperatures demonstrated that the LN chicks were less able than the HNs to maintain homeothermy under treatments imposed. Heat production tended to be increased by overfeeding and reduced by feed restriction. Metabolic rates were higher in LN than in HN chicks when the chicks were fed ad libitum or subjected to restricted feeding, but not when force-fed. The latter observations were attributed to differences in physical activity. Plasma triiodothyronine (T₃) of LN chicks was increased by force-feeding and reduced by restricted feeding, but no significant differences in plasma T₃ occurred in HNs. Thyroxine (T₄) and the T₃:T₄ ratios were unchanged by feed intake, although LNs exhibited higher plasma T₃ and T₃:T₄ ratios than HNs. Although endocrinological changes to caloric consumption analogous to those observed in mammals occurred, energy balance did not confirm the existence of diet-induced thermogenesis in the fowl.<br>Ph. D.

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Eastgard, Rebecca Lugar. "Diet-induced hyperhomocysteinemia in a mouse model /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6601.

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Soltis, Anthony Robert. "Systems biology of diet-induced hepatic insulin resistance." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111272.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2017.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis.<br>Includes bibliographical references (pages 192-205).<br>Human obesity is a world-wide health crisis that promotes insulin resistance and type 2 diabetes. Obesity increases intracellular free fatty acid concentrations in peripheral tissues, particularly the liver, which disrupts molecular mechanisms that maintain normal glycemia in response to fasting and feeding. The progression towards outright pathology in response to obesity is a highly complex process that involves coordinated dysregulation of a variety of molecular processes across multiple regulatory levels. The goal of this thesis was to apply a quantitative, multi-omic systems biology approach to the study of obesity-induce hepatic insulin resistance. We fed male C57BL/6J mice high-fat diets (HFD) to induce obesity and insulin resistance. In the first presented study, our group collected datasets to profile the hepatic epigenomes, transcriptomes, proteomes, and metabolomes of chow diet (CD) control and HFD-fed mice. I extended and applied an established computational modeling algorithm, namely the prize-collecting Steiner forest (PCSF), to simultaneously integrate these molecular data with protein-protein and protein-metabolite interactions into a tractable network model of hepatic dysregulation. This model uncovered a variety of dysregulated pathways and processes, some of which are not well-established aspects of insulin resistance. We further tested and validated some of these model predictions, finding that HFD induces serious architectural defects in the liver and enhances hepatocyte apoptosis. In the next study, we focused more specifically on hepatic transcription. We fed mice short and long-term HFDs and treated them with the type 2 diabetes drug metformin. Compared to non-treated CD controls, diet exerted the strongest effect on transcription, progressively inducing changes as HFD duration increased. We additionally stimulated mice with insulin and collected temporal transcriptomic profiles. We found that long-term HFD almost completely blunted normal insulin-induced transcriptional changes, but also found a small set of genes that are specifically insulin-responsive in HFD livers. We further characterized one of these genes and provided evidence supporting the notion that aspects of hepatic insulin signaling are intact during insulin resistance. In another study, we collected transcriptomic and epigenomic data from mice fed a calorie-restricted (CR) diet. Interestingly, we found a small set of genes altered in the same direction by both CR and HFD. We then used chromatin accessibility experiments to infer regulators associated with these gene expression changes and found roles for PPAR[alpha] and RXR[alpha]. We performed ChIP-Seq experiments for these factors and treated mice and primary hepatocytes with a PPAR[alpha] activator, uncovering a role for PPARα in the regulation of anaerobic glycolysis. We also validated novel predicted target genes of PPAR[alpha] involved in glucose metabolism. Finally, we profiled hepatic miRNAs in CD and HFD livers, finding that HFD progressively alters their expression levels. We implemented an enrichment procedure and a network modeling approach to analyze these data. We integrated additional mRNA and epigenetic data to infer miRNAs that may play regulatory roles during insulin resistance. In total, this thesis presents a unique comprehensive approach to the study of diet-induced hepatic insulin resistance that revealed new insights into pathology.<br>by Anthony Robert Soltis.<br>Ph. D.

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Burrage, Lindsay. "Genetic Resistance to Diet-Induced Obesity in Mice." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1151680415.

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Robey, Ian Forrest. "Examining the relationship between diet-induced acidosis and cancer." BioMed Central, 2012. http://hdl.handle.net/10150/610226.

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Increased cancer risk is associated with select dietary factors. Dietary lifestyles can alter systemic acid-base balance over time. Acidogenic diets, which are typically high in animal protein and salt and low in fruits and vegetables, can lead to a sub-clinical or low-grade state of metabolic acidosis. The relationship between diet and cancer risk prompts questions about the role of acidosis in the initiation and progression of cancer. Cancer is triggered by genetic and epigenetic perturbations in the normal cell, but it has become clear that microenvironmental and systemic factors exert modifying effects on cancer cell development. While there are no studies showing a direct link between diet-induced acidosis and cancer, acid-base disequilibrium has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion. In short, diet-induced acidosis may influence molecular activities at the cellular level that promote carcinogenesis or tumor progression. This review defines the relationship between dietary lifestyle and acid-base balance and discusses the potential consequences of diet-induced acidosis and cancer occurrence or progression.

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Blackmore, Heather Louise. "Programming of cardiovascular disease by maternal diet-induced obesity." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648545.

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Yang, Tianxu. "Diet-Induced Obesity in Growth Hormone Receptor Antagonist Mice." Ohio University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1288987144.

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Alexander, Lindsey Ann. "The Role of Inflammation in Diet-Induced Insulin Resistance." University of Toledo / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1260808416.

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Kogan, Sophia. "Role of Inflammation in Diet-Induced Obesity: A Dissertation." eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/647.

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Obesity results from expansion of white adipose tissue. The inability of white adipose tissue to adequately store lipids leads to ectopic deposition of lipids in non-adipose tissue that can lead to systemic insulin resistance. It is well known that insulin resistance correlates with inflammation of adipose tissue in obese animals and humans. Decreasing inflammation in the adipose tissue has been proven as a therapeutic strategy for improvement of insulin sensitivity in vivo. Numerous factors secreted by immune cells, including macrophages, have been suggested as regulating adipose tissue insulin sensitivity. In the first part of my thesis, I describe the role of one such factor, CD40 in adipose tissue inflammation. The CD40-CD40L dyad acts as co-stimulation in the interaction of antigen-presenting cells, such as macrophages and dendritic cells, with effector cells, such as T cells, in adaptive immunity. We found that CD40 knockout mice were smaller but surprisingly more insulin resistant and glucose intolerant compared to wild-type mice when fed a high fat diet. Consistent with their metabolic phenotype, knockout mice displayed increased adipose tissue inflammation with infiltration of immune cells including macrophages and T cells. Consistent with increased inflammation, CD40 knockout adipose tissue displayed decreased lipid storage. Deficiency of CD40 also led to increased lipid deposition in liver, which may be due to increased lipid release into circulation from the adipose tissue as well as increased lipid synthesis in the liver. CD40 knockout mice had increased hepatic insulin resistance and increased gluconeogensis despite decreased hepatic inflammation. These findings suggest that CD40 is a novel regulator of adipose tissue inflammation in diet-induced obesity. In the second part of this thesis we examined perivascular adipose tissue and brown adipose tissue for the presence of inflammation. In contrast to visceral adipose tissue, macrophage infiltration was absent in perivascular and brown adipose tissue as defined by reduced F480+ cells by flow cytometry and immunohistochemistry. We also found that perivascular adipose tissue was similar to brown adipose tissue as shown by gross morphology and gene expression pattern. Inflammatory gene expression was not increased in brown or perivascular adipose tissue in obese mice as determined by microarray gene expression analysis. These findings suggest that perivascular adipose tissue is more similar to brown adipose tissue than white adipose tissue and that both perivascular and brown adipose tissue are resistant to inflammation. We conclude that, (1) CD40 protects against adipose tissue inflammation in diet-induced obesity, (2) the CD40 knockout mouse is an interesting model of hepatic steatosis with decreased inflammation and (3) perivascular adipose tissue is almost identical to brown adipose tissue in obese mice and that both are resistant to inflammation.

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Books on the topic "Diet-induced"

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Stulen, Richard H., and Michael L. Knotek, eds. Desorption Induced by Electronic Transitions DIET III. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73728-2.

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Burns, Alan R., Ellen B. Stechel, and Dwight R. Jennison, eds. Desorption Induced by Electronic Transitions DIET V. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78080-6.

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Brenig, Wilhelm, and Dietrich Menzel, eds. Desorption Induced by Electronic Transitions DIET II. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82547-7.

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Betz, Gerhard, and Peter Varga, eds. Desorption Induced by Electronic Transitions DIET IV. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-84145-3.

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Shiratori, Sanae. Kyōi no DIT daietto: Diet induced thermogenesis. Bukkuman Sha, 2003.

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Kushi, Michio. Crime & diet: The macrobiotic approach. Japan Publications, 1987.

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K, Carroll K., and Royal Society of Canada, eds. Diet, nutrition, and health. Published for the Royal Society of Canada by McGill-Queen's University Press, 1989.

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P, Robitaille Francis, ed. Diet therapy research trends. Nova Biomedical Books, 2007.

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P, Robitaille Francis, ed. Diet therapy research trends. Nova Biomedical Books, 2007.

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Baroody, Theodore A. Alkalize or die: Superior health through proper alkaline-acid balance. Eclectic, 1991.

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Book chapters on the topic "Diet-induced"

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Assifi, M. Mura, and Guido Eibl. "Western Diet-Induced Pancreatic Cancer." In Nutrition, Diet and Cancer. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2923-0_14.

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Farage, Najla Elias, and Milena Barcza Stockler-Pinto. "Hyperhidrosis and Diet-Induced Thermogenesis." In Hyperhidrosis. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89527-7_10.

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Engin, Atilla. "Circadian Rhythms in Diet-Induced Obesity." In Obesity and Lipotoxicity. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48382-5_2.

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Collins, Cian E. "Diet- and Mercury-induced Visual Loss." In Handbook of Behavior, Food and Nutrition. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-92271-3_175.

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Yamazaki, Tomomi. "Calculating Diet-Induced Thermogenesis in Mice." In Thermogenic Fat. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3167-6_11.

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Nedergaard, Jan, and Barbara Cannon. "Diet-Induced Thermogenesis: Principles and Pitfalls." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2087-8_12.

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AbstractConcerning diet-induced thermogenesis, methodological issues relate mainly to the interpretation of measurements, rather than to the technical methodology as such. In the following, we point to a series of issues where the analysis often suggests the occurrence of UCP1-related diet-induced thermogenesis but where the observations are often the consequences of a process that has induced leanness rather than being the cause of them. We particularly emphasize the necessity of focusing on the total organism when interpreting biochemical and molecular data, where the concept of total tissue values rather than relative data better reflects physiologically important alterations. We stress the importance of performing experiments at thermoneutrality in order to obtain clinically relevant data and stress that true thermogenic agents may be overlooked if this is not done.

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Menzel, D. "Some Recent Developments in DIET." In Desorption Induced by Electronic Transitions DIET III. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73728-2_1.

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Nielsen, H. B., J. Reif, E. Matthias, E. Westin, and A. Rosén. "Multiphoton-Induced Desorption from BaF2(111)." In Desorption Induced by Electronic Transitions DIET III. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73728-2_39.

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Stechel, E. B., D. R. Jennison, and A. R. Burns. "Dynamics in Neutral DIET from Chemisorbed Molecules." In Desorption Induced by Electronic Transitions DIET III. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73728-2_19.

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Bell, Roma R. "Exercise and Diet-Induced Obesity in Mice." In Animal Models — Disorders of Eating Behaviour and Body Composition. Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9662-6_6.

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Conference papers on the topic "Diet-induced"

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Calco, Gina, Becky Proskocil, David Jacoby, Allison Fryer, and Zhenying Nie. "Sex differences in bronchoconstriction in diet-induced obese rats." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4065.

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Plataki, M., L. Fan, M. Imamura, E. Sanchez, S. M. Cloonan, and A. M. K. Choi. "Impact of Diet Induced Obesity on Hyperoxic Lung Injury." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1157.

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TSUJI, TAKAO, Ashley M. Houghton, Adriana S. Leme, Atsushi Nagai, and Steven D. Shapiro. "High Fat Diet Ameliorates Cigarette Smoke-induced Weight Loss." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5436.

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Mayr, L., J. Schwärzler, M. Philipp, et al. "A role of autophagy in diet-induced metabolic enteritis." In 55. Jahrestagung & 32. Fortbildungskurs der Österreichischen Gesellschaft für Gastroenterologie & Hepatologie–ÖGGH (Hybrid Veranstaltung). Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1755724.

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Hülser, M. L., C. Schreiyaeck, Y. Luo, et al. "OP0108 Diet induced metabolic changes in an osteoarthritis mouse model." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3082.

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Hendrawan, Thressia, Nurul Paramita, Dewi Irawati, and Ani Retno Prijanti. "Diabetes Sprague-Dawley Model Induced With Fat Diet And Streptozotocin." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007337902920293.

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Pereira, T., C. Dias, P. Cassanelli, et al. "Effects of Diet Induced Obesity in Lung Alterations in Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2225.

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nie, zhenying, David B. Jacoby, and Allison D. Fryer. "Decreased Airway Parasympathetic Nerve Control In Diet-induced Obese Rats." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5549.

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Henkel-Oberländer, Janin, Katja Buchheim-Dieckow, JosèP Castro, Thomas Laeger, Korinna Jöhrens, and GerhardP Püschel. "Role of endurance training in diet-induced steatohepatitis in rats." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740740.

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Angelotti, Austin, Rachel Cole, Amy Webb, Maciej Pietrzak, and Martha Belury. "Diet-induced Gene Expression Changes of Cachectic Muscle, Adipose, and Liver." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/gvbe2596.

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Cancer cachexia is a systemic disease characterized by muscle and adipose loss that cannot be reversed by increasing caloric intake. Our previous research has shown insulin resistance precedes cancer cachexia in the C26 mouse model of cachexia, and a diet high in linoleic acid, the essential omega-6 polyunsaturated fatty acid, attenuates the C26-induced insulin resistance. Therefore, to better understand how dietary linoleic acid is improving insulin sensitivity, we characterized gene expression changes in three major tissues responsible for controlling insulin sensitivity: skeletal muscle, adipose, and liver. To do this male CD2F1 (Charles River, MA) were randomized to semi-purified diet (24% fat by weight) containing fat prominently from lard, or containing fat prominently from safflower oil (a linoleic acid-rich oil). One week after diet randomization, mice were inoculated with colon-26 (C26) adenocarcinoma cells (1.0E6 cells). 13 days after inoculation mice were euthanized and gastrocnemius skeletal muscle, epididymal white adipose tissue, and liver tissue were collected for total transcriptome analysis using poly-A enriched next generation RNA-sequencing. Differentially expressed genes were selected based on p-values < 0.05. There were no detectable differences in body weight or food intake between the two diets in mice with C26 tumors. Between the two diets 12 genes were differentially expressed in the muscle, while 57 genes were differentially expressed in the liver, and 314 genes were differentially expressed in adipose. A linoleic acid enriched diet had little effect on the skeletal muscle transcriptome but induced larger transcriptome changes in liver and adipose. This could suggest dietary linoleic acid increases insulin sensitivity through affecting metabolism in adipose and liver, rather than skeletal muscle. Determining these diet-induced transcriptome changes allows us to better target tissue-specific molecular mechanisms of linoleic acid in future research.

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Reports on the topic "Diet-induced"

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Deng, Yingjun, ShengJing Liu, Ming Zhao, Feng Zhao, Jun Guo, and Bin Yan. Diet-induced male infertility in mice models: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0116.

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Review question / Objective: In order to compare the different high energy diet such as high-fat diet and high sugar diet how to damage the male mice model in metabolize and fertility,and explore a reliable mice model method in the study of obesity with male infertility. P：obesity mice model with male infertility. I: High energy diet such as High-fat or High-sugar diet. C:High-fat diet,High-sugar diet, compared with normal diet in mice model. O:High energy diet induce male mice obesity model and damage their fertility. S: Use network meta-analysis. Condition being studied: The relationship between obesity and male infertility attacth more and more attention at present.So many animal expriments are carried out on this problem,there are enough exprimental article to support this meta analysis.

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Ma, Jianming. Effect Evaluation of Transfat Decoction on Obesity Mice Induced by High-Fat Diet. Science Repository, 2019. http://dx.doi.org/10.31487/j.jfnm.2019.01.01.

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Lawanprasert, Somsong, Chaiyo Chaichantipyuth, Supatra Srichairat, Nuansri Niwattisaiwong, and Laddawal Phivthong-ngam. Subchronic exposure of Pueraria mirifica in normal - and high cholesterol diet fed rats : influence on hepatic cytochrome P450, lipid profile and toxicity. Chulalongkorn University, 2004. https://doi.org/10.58837/chula.res.2004.28.

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Pueraria mirifica airy shaw and suvatabandhu, know locally as Kwao Keur, is a plant in family Leguminosae. In this study, effects of P.mirifica on hepatic cytochrome P450 (CYP), serum lipid profile and subchronic toxicity were investigated in male Wistar rats. Rats were randomly divided into four treatment groups as following: normal diet-fed group; normal diet-fed supplemented with P.mirifica group; high cholesterol diet-fed group; high cholesterol diet-fed supplemented with P.mirifica group. Each group comprised 10 rats. P.mirifica was administered orally at a dosage of 100 mg/kg/day for 90 consecutive days. At the end of the treatment, animals were anesthesized. Blood samples were collected by heart puncture and serum sample were prepared for determination of hematology and clinical blood chemistry, respectively. Microsomes were prepared from livers for enzyme assays. The results showed that body weight of rats given P.mirifica in either normal diet or high cholesterol diet conditions were significantly lower than their corresponding control groups. There was no significant difference of these following hematology and clinical blood chemistry: hemoglobin, hemotocrit, WBC count, %differential WBC, platelet count, RBC morphology, glucose, BUN, SCr, total bilirubin, and direct bilirubin in all experimental groups. P.mirifica did not affect serum level of AST, ALT, and ALP in normal diet-fed condition. High cholesterol diet-fed condition caused a significant increase of AST, ALT, and ALP but P.mirifica attenuated these effects. P.mirifica significantly decreased serum total cholesterol and LDL-C in either normal diet-fed or high cholesterol diet-fed rats. Serum triglyceride was increased in normal diet-fed rats but decreased in high cholesterol diet-fed rats. P.mirifica caused a significant decrease of HDL-C in both normal and high cholesterol diet-fed rats whereas its improvement in the LDL-C/HDL-C ratio was shown only in high cholesterol diet-fed rats. Concerning the effects on CYPs, P.mirifica significantly inhibited CYP2B1&B2 in either normal diet or high cholesterol diet-fed rats. Its inhibitory effect of CYP1A2 and CYP2E1 was found only in normal diet-fed rats. No effect of P.mirifica was found on CYP1A1 and CYP3A. Inhibitory effects of P.mirifica on CYP2B1&2B2 and CYP2E1 were also found in the in vitro study. Although, P.mirifica demonstrated a benefit on lipid profile and did not show any toxic effects on liver, kidney, and blood system in this study, an increment of serum triglyceride in normal rat receiving P.mirifica, howerer, is not favorable. Inhibitory effects of P.mirifica on CYP1A2, CYP2B1&2B2 and CYP2E1 indicated a beneficial potential of this plant regarding the chemical-induced carcinogenesis as well as a possible potential of this plant regarding drug-drug interaction with other medicines that are metabolized by these CYPs. Effects of P.mirifica at various doses, long term used as well as mechanism of effects should be further investigated. Effects of P.mirifica on other isoforms of CYP in human should also be explored.

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Hristov, Milen, Boycho Landzhov, Kalina Kamenova, and Krassimira Yakimova. Diet-induced Obese Rats Are Associated with Leptin Resistance in the Medial Preoptic Area of the Anterior Hypothalamus. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2020. http://dx.doi.org/10.7546/crabs.2020.05.17.

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Kanner, Joseph, Dennis Miller, Ido Bartov, John Kinsella, and Stella Harel. The Effect of Dietary Iron Level on Lipid Peroxidation of Muscle Food. United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7604282.bard.

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Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.

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Shpigel, Muki, Allen Place, William Koven, Oded (Odi) Zmora, Sheenan Harpaz, and Mordechai Harel. Development of Sodium Alginate Encapsulation of Diatom Concentrates as a Nutrient Delivery System to Enhance Growth and Survival of Post-Larvae Abalone. United States Department of Agriculture, 2001. http://dx.doi.org/10.32747/2001.7586480.bard.

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The major bottlenecks in rearing the highly priced gastropod abalone (Haliotis spp.) are the slow growth rate and the high mortality during the first 8 to 12 weeks following metamorphosis and settling. The most likely reason flor these problems is related to nutritional deficiencies in the diatom diet on which the post larvae (PL) feed almost exclusively in captivity. Higher survival and improved growth rate will reduce the considerable expense of hatchery-nursery resisdence time and thereflore the production costs. BARD supported our research for one year only and the support was given to us in order to prove that "(1) Abalone PL feed on encapsulated diatoms, and (2) heterotrophic diatoms can be mass produced." In the course of this year we have developed a novel nutrient delivery system specifically designed to enhance growth and survival of post-larval abalone. This approach is based on the sodium-alginate encapsulation of heterotrophically grown diatoms or diatom extracts, including appetite-stimulating factors. Diatom species that attract the PL and promote the highest growth and survival have been identified. These were also tested by incorporating them (either intact cells or as cell extracts) into a sodium-alginate matrix while comparing the growth to that achieved when using diatoms (singel sp. or as a mixture). A number of potential chemoattractants to act as appetite-stimulating factors for abalone PL have been tested. Preliminary results show that the incorporation of the amino acid methionine at a level of 10-3M to the sodim alginate matrix leads to a marked enhancement of growth. The results ol these studies provided basic knowledge on the growth of abalone and showed that it is possible to obtain, on a regular basis, survival rates exceeding 10% for this stage. Prior to this study the survival rates ranged between 2-4%, less than half of the values achieved today. Several diatom species originated from the National Center for Mariculture (Nitzchia laevis, Navicula lenzi, Amphora T3, and Navicula tennerima) and Cylindrotheca fusiformis (2083, 2084, 2085, 2086 and 2087 UTEX strains, Austin TX) were tested for heterotrophic growth. Axenic colonies were initially obtained and following intensive selection cycles and mutagenesis treatments, Amphora T3, Navicula tennerima and Cylindrotheca fusiformis (2083 UTEX strain) were capable of growing under heterotrophic conditions and to sustain highly enriched mediums. A highly efficient selection procedure as well as cost effective matrix of media components were developed and optimized. Glucose was identified as the best carbon source for all diatom strains. Doubling times ranging from 20-40 h were observed, and stable heterotroph cultures at a densities range of 103-104 were achieved. Although current growth rates are not yet sufficient for full economical fermentation, we estimate that further selections and mutagenesis treatments cycles should result in much faster growing colonies suitable for a fermentor scale-up. As rightfully pointed out by one of the reviewers, "There would be no point in assessing the optimum levels of dietary inclusions into micro-capsules, if the post-larvae cannot be induced to consume those capsules in the first place." We believe that the results of the first year of research provide a foundationfor the continuation of this research following the objectives put forth in the original proposal. Future work should concentrate on the optimization of incorporation of intact cells and cell extracts of the developed heterotrophic strains in the alginate matrix, as well as improving this delivery system by including liposomes and chemoattractants to ensure food consumption and enhanced growth.

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Brosh, Arieh, David Robertshaw, Yoav Aharoni, Zvi Holzer, Mario Gutman, and Amichai Arieli. Estimation of Energy Expenditure of Free Living and Growing Domesticated Ruminants by Heart Rate Measurement. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7580685.bard.

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Research objectives were: 1) To study the effect of diet energy density, level of exercise, thermal conditions and reproductive state on cardiovascular function as it relates to oxygen (O2) mobilization. 2) To validate the use of heart rate (HR) to predict energy expenditure (EE) of ruminants, by measuring and calculating the energy balance components at different productive and reproductive states. 3) To validate the use of HR to identify changes in the metabolizable energy (ME) and ME intake (MEI) of grazing ruminants. Background: The development of an effective method for the measurement of EE is essential for understanding the management of both grazing and confined feedlot animals. The use of HR as a method of estimating EE in free-ranging large ruminants has been limited by the availability of suitable field monitoring equipment and by the absence of empirical understanding of the relationship between cardiac function and metabolic rate. Recent developments in microelectronics provide a good opportunity to use small HR devices to monitor free-range animals. The estimation of O2 uptake (VO2) of animals from their HR has to be based upon a consistent relationship between HR and VO2. The question as to whether, or to what extent, feeding level, environmental conditions and reproductive state affect such a relationship is still unanswered. Studies on the basic physiology of O2 mobilization (in USA) and field and feedlot-based investigations (in Israel) covered a , variety of conditions in order to investigate the possibilities of using HR to estimate EE. In USA the physiological studies conducted using animals with implanted flow probes, show that: I) although stroke volume decreases during intense exercise, VO2 per one heart beat per kgBW0.75 (O2 Pulse, O2P) actually increases and measurement of EE by HR and constant O2P may underestimate VO2unless the slope of the regression relating to heart rate and VO2 is also determined, 2) alterations in VO2 associated with the level of feeding and the effects of feeding itself have no effect on O2P, 3) both pregnancy and lactation may increase blood volume, especially lactation; but they have no effect on O2P, 4) ambient temperature in the range of 15 to 25°C in the resting animal has no effect on O2P, and 5) severe heat stress, induced by exercise, elevates body temperature to a sufficient extent that 14% of cardiac output may be required to dissipate the heat generated by exercise rather than for O2 transport. However, this is an unusual situation and its affect on EE estimation in a freely grazing animal, especially when heart rate is monitored over several days, is minor. In Israel three experiments were carried out in the hot summer to define changes in O2P attributable to changes in the time of day or In the heat load. The animals used were lambs and young calves in the growing phase and highly yielding dairy cows. In the growing animals the time of day, or the heat load, affected HR and VO2, but had no effect on O2P. On the other hand, the O2P measured in lactating cows was affected by the heat load; this is similar to the finding in the USA study of sheep. Energy balance trials were conducted to compare MEI recovery by the retained energy (RE) and by EE as measured by HR and O2P. The trial hypothesis was that if HR reliably estimated EE, the MEI proportion to (EE+RE) would not be significantly different from 1.0. Beef cows along a year of their reproductive cycle and growing lambs were used. The MEI recoveries of both trials were not significantly different from 1.0, 1.062+0.026 and 0.957+0.024 respectively. The cows' reproductive state did not affect the O2P, which is similar to the finding in the USA study. Pasture ME content and animal variables such as HR, VO2, O2P and EE of cows on grazing and in confinement were measured throughout three years under twenty-nine combinations of herbage quality and cows' reproductive state. In twelve grazing states, individual faecal output (FO) was measured and MEI was calculated. Regression analyses of the EE and RE dependent on MEI were highly significant (P<0.001). The predicted values of EE at zero intake (78 kcal/kgBW0.75), were similar to those estimated by NRC (1984). The EE at maintenance condition of the grazing cows (EE=MEI, 125 kcal/kgBW0.75) which are in the range of 96.1 to 125.5 as presented by NRC (1996 pp 6-7) for beef cows. Average daily HR and EE were significantly increased by lactation, P<0.001 and P<0.02 respectively. Grazing ME significantly increased HR and EE, P<0.001 and P<0.00l respectively. In contradiction to the finding in confined ewes and cows, the O2P of the grazing cows was significantly affected by the combined treatments (P<0.00l ); this effect was significantly related to the diet ME (P<0.00l ) and consequently to the MEI (P<0.03). Grazing significantly increased O2P compared to confinement. So, when EE of grazing animals during a certain season of the year is estimated using the HR method, the O2P must be re measured whenever grazing ME changes. A high correlation (R2>0.96) of group average EE and of HR dependency on MEI was also found in confined cows, which were fed six different diets and in growing lambs on three diets. In conclusion, the studies conducted in USA and in Israel investigated in depth the physiological mechanisms of cardiovascular and O2 mobilization, and went on to investigate a wide variety of ruminant species, ages, reproductive states, diets ME, time of intake and time of day, and compared these variables under grazing and confinement conditions. From these combined studies we can conclude that EE can be determined from HR measurements during several days, multiplied by O2P measured over a short period of time (10-15 min). The study showed that RE could be determined during the growing phase without slaughtering. In the near future the development microelectronic devices will enable wide use of the HR method to determine EE and energy balance. It will open new scopes of physiological and agricultural research with minimizes strain on animals. The method also has a high potential as a tool for herd management.

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Effects of silica inhalation on metabolic obesity in a western diet-induced F344 rat model; silica inhibits adipose function and diet-induced inflammation (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2021. http://dx.doi.org/10.26616/nioshrd-1019-2021-0.

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High-fat Western diet consumption exacerbates silica-induced pulmonary inflammation and fibrosis (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2022. http://dx.doi.org/10.26616/nioshrd-1032-2022-0.

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High-fat Western diet alters silica-induced airway epithelium ion exchange but not airway smooth muscle reactivity (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2023. http://dx.doi.org/10.26616/nioshrd-1068-2023-0.

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