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Yanjun Liu, Yuichi Nakagawa, Ying Wang, Limei Liu, Hongwei Du, Wei Wang, Xiuhai Ren, Kabirullah Lutfy and Theodore C Friedman

obesity and insulin resistance have not yet been reported. Here, we evaluated the effects of CBX on the expression of GR and H6PDH in diet-induced obese (DIO) mice that are insulin resistant. We also assessed whether CBX would limit the corticosterone

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Yousheng Xu, Yongshun Wang, Jingjin Liu, Wei Cao, Lili Li, Hongwei Du, Enbo Zhan, Ruoxi Zhang, Huimin Liu, Maoen Xu, Tao Chen, Yilin Qu and Bo Yu

autotaxin mRNA levels were increased by about four-fold in db/db mice when compared to lean littermates ( Boucher et al. 2005 ). In contrast, depletion of autotaxin could protect against high-fat diet (HFD)-induced obesity, insulin resistance and glucose

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Edra London, Maria Nesterova and Constantine A Stratakis

Differentially regulated protein kinase A (PKA) activity in adipose tissue and liver is associated with resistance to diet-induced obesity and glucose intolerance in mice that lack PKA regulatory subunit type IIalpha . Endocrinology 155 3397 – 3408 . ( doi

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N T Lam, S D Covey, J T Lewis, S Oosman, T Webber, E C Hsu, A T Cheung and T J Kieffer

regulation must be outside of leptin-responsive hypothalamic neurons, since elimination of these in PTP1B −/− mice has no effect on the insulin hypersensitivity of the animals and only partially reverses the protection from diet-induced obesity. If indeed

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Li Hu, Fengli He, Meifeng Huang, Meihua Peng, Zhiguang Zhou, Feng Liu and Yan-Shan Dai

diet-induced obesity. We showed that reduced M1 macrophage polarization in AT and improved insulin sensitivity in Nfatc3−/− mice fed with HFD. We had identified NFATc3 as a positive regulator of obesity-induced inflammation and insulin resistance. This

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Julika Lietzow, Janine Golchert, Georg Homuth, Uwe Völker, Wenke Jonas and Josef Köhrle

published study, chronic treatment with 3,5-T 2 (2.5 µg/g body weight (bw)) in diet-induced obese euthyroid mice resulted in reduction of body fat mass and improvement of hepatic lipid status. But in contrast to these beneficial effects, an undesired

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Ji Seon Park, Su Jung Bae, Sik-Won Choi, You Hwa Son, Sung Bum Park, Sang Dal Rhee, Hee Youn Kim, Won Hoon Jung, Seung Kyu Kang, Jin Hee Ahn, Seong Hwan Kim and Ki Young Kim

al . 2012 ). Here, we have explored whether KR-67500 can improve glucose tolerance and insulin sensitivity in diet-induced obese (DIO)-C57BL/6 mice. Additionally, we accessed the effect of KR-67500 on the cortisone-induced adipogenesis in 3T3-L1 cells

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Kayla A Boortz, Kristen E Syring, Lynley D Pound, Huan Mo, Lisa Bastarache, James K Oeser, Owen P McGuinness, Joshua C Denny and Richard M O’Brien

the food intake study. References Almind K Kahn CR 2004 Genetic determinants of energy expenditure and insulin resistance in diet-induced obesity in mice . Diabetes 53 3274 – 3285 . ( doi:10.2337/diabetes.53.12.3274 ) Arden

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Farhana Naznin, Koji Toshinai, T M Zaved Waise, Tadashi Okada, Hideyuki Sakoda and Masamitsu Nakazato

( Kohno et al . 2003 , Hardie 2004 ). Previous studies showed that neither central nor peripheral ghrelin administration induced feeding in diet-induced obese (DIO) mice fed a high-fat diet (HFD, 60% of energy from fat) for 12 or 16 weeks ( Perreault et

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Haoyong Yu, Mingliang Zhang, Yunqin Ma, Junxi Lu, Jiemin Pan, Pan Pan, Haibing Chen and Weiping Jia

regular chow diet (Shanghai Laboratory Animal Co. Ltd, Shanghai, China). For the diet-induced obesity model, mice at 8 weeks of age were fed a high-fat diet (HFD) containing 60% kcal of fat (D12492; Research Diets, Inc., NJ, USA) for 18 weeks. 5-ALA