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Sofianos Andrikopoulos, Christine M Massa, Kathryn Aston-Mourney, Alexandra Funkat, Barbara C Fam, Rebecca L Hull, Steven E Kahn, and Joseph Proietto

a ). For example, obesity or energy-rich (high fat) diets can exacerbate metabolic defects associated with type 2 diabetes, such as an impairment in insulin secretion ( Lee et al. 1995 , Paolisso et al. 1995 , Zraika et al. 2002 , Zraika et

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Jie Wei, Xia Sun, Yajie Chen, Yuanyuan Li, Liqiong Song, Zhao Zhou, Bing Xu, Yi Lin, and Shunqing Xu

findings supported this hypothesis and further indicated that perinatal exposure to BPA coupled with the postweaning high-fat diet (HFD) significantly initiated hepatic oxidative stress, thereby predisposing offspring to hepatic inflammation and early

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Yu Wu, Tingting Wu, Jun Wu, Lei Zhao, Qing Li, Zac Varghese, John F Moorhead, Stephen H Powis, Yaxi Chen, and Xiong Z Ruan

hyperglycemia in high-fat diet (HFD)-fed C57BL/6J mice and to explore its underlying mechanism. Materials and methods Animal model Animal care and experimental procedures were performed with approval from the Animal Care Committee of Chongqing Medical University

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Andrew T Templin, Christine Schmidt, Meghan F Hogan, Nathalie Esser, Richard N Kitsis, Rebecca L Hull, Sakeneh Zraika, and Steven E Kahn

first to show that ARC is required for β-cell survival and sufficient insulin secretion in vivo in response to a genetic model of diabetogenic stress. The role of ARC in β-cell adaptation to high fat diet (HFD) feeding, a physiologically relevant

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G Tulipano, A V Vergoni, D Soldi, E E Muller, and D Cocchi

-resistant (OR) rats selected from a large number of rats fed on a moderate high-fat (HF) diet. Reportedly, leptin also mediates adaptive responses of hypothalamo–pituitary function to changes of the nutritional status ( Barash et al. 1996 , Chehab et al

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Joshua Columbus, YuTing Chiang, Weijuan Shao, Nina Zhang, Dingyan Wang, Herbert Y Gaisano, Qinghua Wang, David M Irwin, and Tianru Jin

, we observed the expression of Tcf7 and Tcf7l1 in the pancreas of rodent species. In addition, we found that the expression of Tcf7 , Tcf7l1 , and Tcf7l2 in the rodent pancreas can be significantly downregulated by insulin treatment or high-fat

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Jacob C Garza, Chung Sub Kim, Jing Liu, Wei Zhang, and Xin-Yun Lu

results show that MC4R knockdown in PVN neurons increases food intake and body weight gain in response to a high-fat diet, suggesting that MC4R signaling in PVN neurons may protect against overeating and obesity under the dietary challenge. Materials and

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The influence of the diet on the levels of insulin was studied in rats on a high-fat diet. Plasma and glucose insulin concentrations of a control group and of rats on a high-fat diet were compared, and so was the insulin concentration in the pancreas of the two groups.

The mean plasma insulin concentration in the control group was 40 μ-u./ml. and that of insulin extracted from the pancreas was 2·5 μg./100 mg. tissue; plasma glucose was 156 mg./100 ml.

The animals fed on a high-fat diet showed diabetic features. The mean plasma insulin level was 9 μ-u./ml., and plasma glucose increased to 210 mg./100 ml. The insulin concentration in the pancreas was not significantly different from that in the controls. In vitro the epididymal fat and the diaphragm of the high-fat-diet group were less sensitive to insulin than the same tissues in the control group.

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Andréa M Caricilli, Paula H Nascimento, José R Pauli, Daniela M L Tsukumo, Lício A Velloso, José B Carvalheira, and Mário J A Saad

-activated signal transduction, through TLR2 activation ( Senn 2006 ). However, the role of TLR2 in insulin resistance induced by a high-fat diet in animals has not yet been investigated. The aims of the present study were to investigate the expression of TLR2 in

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R Vinayagamoorthi, Zachariah Bobby, and M G Sridhar

( Phillips et al . 1996 , Pan et al . 1997 , Krssak et al . 1999 ). Insulin resistance and several defects in insulin signaling have been reported in rats fed with high-fat diet. The high-fat diet-fed rodent is a model of research interest because it