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Greg M Kowalski, Michael J Kraakman, Shaun A Mason, Andrew J Murphy and Clinton R Bruce

Introduction With the increasing prevalence of obesity and insulin resistance, the reliance on mouse models of metabolic disease has increased dramatically over the last decade ( Kowalski & Bruce 2014 ). The high-fat, high-sucrose-fed C57Bl/6

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Holly M Johnson, Erin Stanfield, Grace J Campbell, Erica E Eberl, Gregory J Cooney and Kim S Bell-Anderson

is almost always prescribed and is easily manipulated. Increased energy intake from either fat or carbohydrate, resulting in a positive energy balance, produces insulin resistance in rodents and humans ( Small et al. 2018 ). High-fat feeding in

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Eliana H Akamine, Anderson C Marçal, João Paulo Camporez, Mara S Hoshida, Luciana C Caperuto, Estela Bevilacqua and Carla R O Carvalho

to analyze the effect of high-fat diet-induced obesity on the insulin signaling in the ovary. We also verified if insulin signaling impairment is time dependent in relation to the period during which the ovary was submitted to adverse effects of

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Tomoaki Hayakawa, Tomomi Minemura, Toshiharu Onodera, Jihoon Shin, Yosuke Okuno, Atsunori Fukuhara, Michio Otsuki and Iichiro Shimomura

, Japan) or a high-fat/high-sucrose diet (HFHSD; protein, 17.2%; lipid, 54.5%; carbohydrate, 28.3% (sucrose, 16.6%) by calories; Oriental Yeast) from 5 weeks of age. All the mice were individually housed. There were eleven MR flox/flox (control) mice aged

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Rebecca L Hull, Joshua R Willard, Matthias D Struck, Breanne M Barrow, Gurkirat S Brar, Sofianos Andrikopoulos and Sakeneh Zraika

low or high fat feeding to determine whether in vitro findings translate to responses in a whole-body setting where complex interactions among various hormones and tissues influence the metabolic phenotype. Our findings call for caution in

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Juliane K Czeczor, Amanda J Genders, Kathryn Aston-Mourney, Timothy Connor, Liam G Hall, Kyoko Hasebe, Megan Ellis, Kirstie A De Jong, Darren C Henstridge, Peter J Meikle, Mark A Febbraio, Ken Walder and Sean L McGee

) were maintained on either a standard rodent diet or a high-fat diet (HFD) consisting of 43% of calories from fat (23.5% by weight; SF04-001 Rodent Diet, Research Diets D12451 Equivalent; Specialty Feeds) for 14 weeks. Throughout the experiment, three

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Bo Ahrén, Maria Sörhede Winzell and Giovanni Pacini

2003 ). Whether the upregulation of insulin secretion also involves the incretin effect is, however, not known. To study this possibility, incretin contribution to the insulin response to oral glucose was examined in the animal model of high-fat feeding

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Hamza Amine, Yacir Benomar, Adil Haimeur, Hafida Messaouri, Nadia Meskini and Mohammed Taouis

during a high fat diet in rats ( Storlien et al . 1991 ). Indeed, the substitution of omega-3 fatty acids (w-3 FAs) from fish oil for other types of lipids prevents insulin resistance ( Kraegen et al . 1991 , Jucker et al . 1999 ) and has been

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Anshu Gupta, Malathi Srinivasan, Supaporn Thamadilok and Mulchand S Patel

establishment of adverse programming effects in the offspring. The present study evaluated the maternal and fetal environments during pregnancy complicated by obesity in rats fed a high-fat (HF) diet. We investigated the signaling pathways of insulin and leptin

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Shibin Ding, Ying Fan, Nana Zhao, Huiqin Yang, Xiaolei Ye, Dongliang He, Xin Jin, Jian Liu, Chong Tian, Hongyu Li, Shunqing Xu and Chenjiang Ying

be really safe. In recent years, life styles dominated by an increase in the consumption of high-fat diets have contributed to the accelerated diabetes epidemic ( Hu 2011 ), and consumption of fat-rich products favors co-exposure to BPA and HFD