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Sujith Rajan, Kripa Shankar, Muheeb Beg, Salil Varshney, Abhishek Gupta, Ankita Srivastava, Durgesh Kumar, Raj K Mishra, Zakir Hussain, Jiaur R Gayen, and Anil N Gaikwad

2013 ). Numerous studies, on both animals and humans, have inferred negative correlation between body weight and insulin sensitivity ( Cinti 2012 ). Weight gain in the body is largely due to accumulation of white adipose tissue (WAT); thus, insulin

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Hiranya Pintana, Wanpitak Pongkan, Wasana Pratchayasakul, Nipon Chattipakorn, and Siriporn C Chattipakorn

-insulin resistance, but also impaired brain insulin sensitivity, brain mitochondrial dysfunction and cognitive decline ( Pintana et al . 2012 , 2013 , Pipatpiboon et al . 2013 ). Testosterone is an androgenic steroid hormone, which plays an important role in the

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Sandra Pereira, Wen Qin Yu, María E Frigolet, Jacqueline L Beaudry, Yaniv Shpilberg, Edward Park, Cristina Dirlea, B L Grégoire Nyomba, Michael C Riddell, I George Fantus, and Adria Giacca

in hepatic and peripheral insulin resistance ( Cai et al . 2005 ). Hepatocyte-specific IKKB knockout (KO) mice show improved hepatic insulin sensitivity when challenged with high-fat feeding ( Arkan et al . 2005 ). Salicylates ameliorate glucose

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Elena Maneschi, Linda Vignozzi, Annamaria Morelli, Tommaso Mello, Sandra Filippi, Ilaria Cellai, Paolo Comeglio, Erica Sarchielli, Alessandra Calcagno, Benedetta Mazzanti, Roberto Vettor, Gabriella Barbara Vannelli, Luciano Adorini, and Mario Maggi

high-carbohydrate diet, and develop peripheral insulin resistance ( Sinal et al . 2000 ). Three independent reports have linked FXR deficiency to impaired insulin sensitivity ( Cariou et al . 2006 , Ma et al . 2006 , Zhang et al . 2006 ). In

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Sun-O Ka, Mi-Young Song, Eun Ju Bae, and Byung-Hyun Park

and decreases insulin sensitivity ( Kanda et al . 2006 ). In contrast, genetic deletion of C-C chemokine ligand 2 ( Ccl2 )/ Mcp1 or its receptor, C-C chemokine receptor 2 ( Ccr2 ), protects mice from high-fat-diet (HFD)-induced inflammation and

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Simon Klebanov, Clinton M Astle, Olga DeSimone, Vitaly Ablamunits, and David E Harrison

procedure itself did not have any long-lasting effect on insulin levels. To confirm that insulin sensitivity was improved in WAT-transplanted mice, we performed insulin tolerance tests, 4 weeks after WAT transplantation, on a separate group of 14

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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

( Perreault & Marette 2001 , Yuan et al . 2001 , Hirosumi et al . 2002 , Lee et al . 2003 , Carvalho-Filho et al . 2005 ) pathways is related to the reduction in insulin sensitivity, but it has only recently been shown that these pathways may be

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Yanbin Zheng, Wenshuo Zhang, Elisha Pendleton, Sanhua Leng, Jiong Wu, Ridong Chen, and Xiao Jian Sun

plasma dyslipidemia, and reduce oxidative stress, leading to improved insulin sensitivity ( Ugochukwu & Figgers 2007 ). The underlying molecular mechanisms mediating these effects are not very clear. It has been observed that an elevation in the ratio of

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P Ebeling, U-H Stenman, M Seppälä, and V A Koivisto


The acute effects of hyperinsulinemia on androgen homeostasis and a possible association of androgens to insulin sensitivity, serum lipids and lipoproteins and to lipid oxidation were examined in 19 healthy males (27 ± 1 yrs, body mass index 24 ± 1 kg/m2). In each subject, a 240 min euglycemic hyperinsulinemic clamp was performed and glucose and lipid oxidation were determined by indirect calorimetry. During hyperinsulinemia serum sex hormone-binding globulin (SHBG) concentration decreased by 5% (P<0·01), insulin-like growth factor binding protein (IGFBP-1) by 88% (P<0·001) and dehydroepiandrosterone sulphate (DHEAS) by 12% (P<0·001), with no change in total or free testosterone concentrations. In the basal state, IGFBP-1 and C-peptide were inversely related (r= −0·54, P<0·05). Fasting concentrations of serum free testosterone (r=0·59, P<0·01) and DHEAS (r=0·47, P<0·05) correlated positively with serum free fatty acid (FFA) concentrations during hyperinsulinemia, but not with fasting FFA level. Lipid oxidation rate in the basal state correlated positively to the decline in SHBG (r=0·61, P<0·01) and DHEAS concentrations (r=0·62, P<0·01) during hyperinsulinemia. While the fasting serum high density lipoprotein cholesterol level correlated positively with the insulin-induced decline in DHEAS level (r=0·58, P<0·01), no associations were found between serum androgens and total cholesterol, low density lipoprotein cholesterol or triglyceride concentrations. Insulin sensitivity was not related to SHBG, IGFBP-1, DHEAS or testosterone concentrations. It is concluded that, in the healthy man with normal androgen homeostasis, (1) acute hyperinsulinemia decreases SHBG, IGFBP-1 and DHEAS concentrations, (2) the relative insulin-induced decline of IGFBP-1 level is 18-fold greater than that of the SHBG level, (3) androgens may maintain lipolysis during hyperinsulinemia and (4) there is no association between physiological androgen concentrations and insulin sensitivity.

Journal of Endocrinology (1995) 146, 63–69

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A fixed dose of glucose, irrespective of body weight, used for i.v. glucose tolerance tests in rats with hypothalamic obesity and in non-obese control rats caused almost identical blood glucose increments in both kinds of rats, and the K values (coefficients of glucose assimilation) were not significantly different. Glucose doses proportional to body weight caused much larger increments of blood glucose in the obese animals but the K value was not significantly different from that for the controls.

On the other hand, the insulin sensitivity of obese rats was found to be less than that of control rats when a fixed dose of the hormone was given. When the insulin dosage was proportional to body weight, the fall of fasting blood glucose produced in the obese animals was not significantly different from that in the control group. In vitro, the diaphragm muscle of the obese animals was insensitive to the action of insulin as compared with controls. There was no evidence of insulin insensitivity of the obese animals' adipose tissue; the very low metabolic activity of the adipose tissue of both the control and obese animals may have been responsible. The interpretation of these findings is discussed in the light of similar work in human obesity.