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Kishor Devalaraja-Narashimha and Babu J Padanilam

exist in susceptibility to diet-induced obesity in humans ( Comuzzie & Allison 1998 ) as well as among various inbred strains of mice ( Brockmann & Bevova 2002 ). Both mono- and polygenic variations contribute to the development of obesity phenotype in

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Mirian A Kurauti, José M Costa-Júnior, Sandra M Ferreira, Gustavo J dos Santos, André O P Protzek, Tarlliza R Nardelli, Luiz F de Rezende, and Antonio C Boschero

-Hay et al. 2011 ). In addition, diet-induced obese (DIO) rodents display hyperinsulinemia as well as glucose and insulin intolerance ( Ropelle et al. 2009 , Brandimarti et al. 2013 ). The hyperinsulinemia observed in DIO mice was associated with

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Stefan O Krechowec, Mark Vickers, Arieh Gertler, and Bernhard H Breier

and endocrine homeostasis may create a predisposition to a range of metabolic disorders, including diet-induced obesity and type-2 diabetes in adult life ( Ozanne 2001 , Barker 2004 , McMillen & Robinson 2005 ). The etiology of obesity is

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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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Andreas Nygaard Madsen, Gitte Hansen, Sarah Juel Paulsen, Kirsten Lykkegaard, Mads Tang-Christensen, Harald S Hansen, Barry E Levin, Philip Just Larsen, Lotte Bjerre Knudsen, Keld Fosgerau, and Niels Vrang

pathophysiology of the human obesity syndrome, and in the search of novel anti-obesity agents, polygenetic animal models closely mimicking the human obesity syndrome are crucial. One such polygenetic model is the diet-induced obese (DIO) and diet-resistant (DR

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

liver TG content also tended to decrease, whereas the expression levels of lipogenic genes were not affected in AdipoMR-KO mice. The data were partially consistent with those of previous studies. In high-fat diet-induced obese animals, treatment with

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Xiao-Bing Cui, Jun-Na Luan, Jianping Ye, and Shi-You Chen

demonstrate that high-fat diet (HFD) dramatically induces RGC32 expression in the adipose tissue. RGC32 deficiency attenuates HFD-induced obesity and insulin resistance in mice. The beneficial effect of RGC32 deficiency is due to the decreased adipose tissue

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Bettina A Ikenasio-Thorpe, Bernhard H Breier, Mark H Vickers, and Mhoyra Fraser

, to assess whether increased susceptibility to diet-induced obesity in offspring of undernourished mothers is related to alterations in neuroendocrine gene expression involved in the regulation of energy homeostasis. Materials and Methods

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Min Liu, Shuo Xie, Weiwei Liu, Jingjin Li, Chao Li, Wei Huang, Hexin Li, Jinghai Song, and Hong Zhang

that SEMA3G knockdown may antagonize the changes in serum levels of adiponectin and leptin, and alleviate obesity induced by HFD. Figure 3 Effect of SEMA3G knockdown on SEMA3G, adiponectin, and leptin levels in chow diet- and HFD-fed mice (A

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Gabriel Forn-Cuní, Monica Varela, Conrado M Fernández-Rodríguez, Antonio Figueras, and Beatriz Novoa

mammalian NASH features. Furthermore, NAFLD can be induced in healthy zebrafish both chemically, with tamoxifen ( Anezaki et al . 2009 ), and with a high-fat content diet ( Oka et al . 2010 ). The diet-induced obesity (DIO) approach allows the modeling of