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Anna Krook

insulin resistance have not been fully clarified. In a study published in this issue of Journal of Endocrinology , Okamoto et al . (2011) present evidence that the degree of insulin sensitivity in a rat model of type 1 diabetes presents as a bell

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C Gonzalez, A Alonso, N Alvarez, F Diaz, M Martinez, S Fernandez, and AM Patterson

The mechanism for the development of insulin resistance in normal pregnancy is complex and is associated with serum levels of both progesterone and 17beta-estradiol. However, it remains unclear whether estrogens alone or progestins alone can cause insulin resistance, or whether it is a combination of both which produces this effect. We attempted to determine the role played by progesterone and/or 17beta-estradiol on the phenomena of sensitivity to insulin action that take place during pregnancy in the rat. Ovariectomized rats were treated with different doses of progesterone and/or 17beta-estradiol in order to simulate the plasma levels in normal pregnant rats. A euglycemic/hyperinsulinemic clamp was used to measure insulin sensitivity. At days 6 and 11, vehicle (V)- and progesterone (P)-treated groups were more insulin resistant than 17beta-estradiol (E)- and 17beta-estradiol+progesterone (EP)-treated groups. Nevertheless, at day 16, the V, EP and E groups were more resistant to insulin action than the P group. On the other hand, the V, EP and E groups were more insulin resistant at day 16 than at day 6, whereas the P group was more insulin resistant at day 6 than at day 16. Our results seem to suggest that the absence of female steroid hormones gives rise to a decreased insulin sensitivity. The rise in insulin sensitivity during early pregnancy, when the plasma concentrations of 17beta-estradiol and progesterone are low, could be due to 17beta-estradiol. However, during late pregnancy when the plasma concentrations of 17beta-estradiol and progesterone are high, the role of 17beta-estradiol could be to antagonize the effect of progesterone, diminishing insulin sensitivity.

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Antonella Amato, Sara Baldassano, and Flavia Mulè

–33), a GLP2R antagonist used to reveal the physiological actions of GLP2 ( Shin et al . 2005 , Nelson et al . 2008 , Iakoubov et al . 2009 , Baldassano et al . 2013 ), does not affect glycaemic parameters, glucose tolerance, insulin sensitivity or

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Sujith Rajan, Ganesh Panzade, Ankita Srivastava, Kripa Shankar, Rajesh Pandey, Durgesh Kumar, Sanchita Gupta, Abhishek Gupta, Salil Varshney, Muheeb Beg, Raj Kumar Mishra, Ravi Shankar, and Anil Gaikwad

insulin sensitivity via regulating adiponectin expression. Figure 6 Inhibition of miR-876-3p in CI-induced IR adipocytes increased adiponectin level and restored insulin signaling. CI-treated adipocytes were either transduced with Lenti-con inhibitor

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Dario A Gutierrez and Alyssa H Hasty

not affect macrophage recruitment to AT or insulin sensitivity during HFD-induced obesity. Materials and Methods Mice and diets All animal care and experimental procedures were performed with approval from the Institutional Animal Care and Use

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C Gonzalez, A Alonso, F Diaz, and AM Patterson

Numerous studies have suggested that ovarian hormones are able to modulate insulin sensitivity, but their exact role remains unclear. We have investigated whether different doses of 17beta-oestradiol mediate changes in insulin sensitivity and if these changes could be related to modifications of insulin receptor substrate-1 (IRS-1). Female rats were ovariectomized and later separated into three groups: untreated; treated with a dose of 17beta-oestradiol sufficient to reproduce gestational plasma concentrations of 17beta-oestradiol (group E); and treated with a dose 100 times greater than that given to group E (group E2). A euglycaemic-hyperinsulinaemic clamp was used to measure insulin sensitivity. Changes in IRS-1 were analysed by Western blotting and RT-PCR assays. In group E we found a decrease in insulin sensitivity between days 11 and 16 of treatment as in late gestation, whereas in the untreated group and group E2, development of insulin resistance was observed throughout the treatment. In contrast, whereas in group E2 insulin resistance throughout the hormonal treatment was related to diminished expression and phosphorylation of IRS-1, in group E the decrease in insulin sensitivity between days 11 and 16 of treatment was not related to a decrease in IRS-1 expression. Our results suggest that the effects of oestradiol on insulin sensitivity were dose-dependent and that the insulin resistance associated with a high dose of 17beta-oestradiol was related to downregulation of IRS-1 expression.

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M Furuhashi, N Ura, H Murakami, M Hyakukoku, K Yamaguchi, K Higashiura, and K Shimamoto

We investigated the effect of fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, on insulin sensitivity including lipid metabolism in skeletal muscle. Six-week-old male Sprague-Dawley rats were divided into two groups: those fed a standard chow (control) or a fructose-rich chow (fructose-fed rats (FFRs)) for 6 weeks. FFRs were treated either with a vehicle or with 30 mg/kg per day of fenofibrate for the last 2 weeks. Insulin sensitivity (M-value) was estimated by the euglycemic hyperinsulinemic glucose clamp method. Fatty acid-binding protein (FABP) in skeletal muscle was measured by ELISA, and the expression of FABP mRNA was analyzed by semi-quantitative RT-PCR. The serum and muscle triglyceride (sTG and mTG) levels and the activity of 3-hydroxyacyl-CoA dehydrogenase (HADH), a beta-oxidation enzyme, in muscle were also determined. FFRs showed a lower M-value and higher blood pressure, sTG and mTG than did the control group. The mTG was correlated positively with sTG and negatively with the M-value. Fenofibrate treatment for 2 weeks did not change blood pressure but significantly improved the M-value, sTG and mTG. FABP content and mRNA in the soleus muscle were significantly elevated in FFRs compared with those in the control group. Fenofibrate treatment further increased FABP. The HADH activity was comparable between the control group and FFRs, but significantly increased by fenofibrate treatment. These results suggest that fenofibrate improves insulin sensitivity not only by lowering serum lipids and subsequent influx of fatty acids into muscles but also by reducing intramuscular lipid content via further induction of FABP and stimulation of beta-oxidation in muscles.

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L M McShane, N Irwin, D O’Flynn, Z J Franklin, C M Hewage, and F P M O’Harte

end of the treatment period, oral and i.p. (18mmol/kg bw) glucose tolerance tests were performed in overnight-fasted mice. In addition, an insulin sensitivity (10U/kgbw) test was also performed in non-fasted mice. At termination, pancreatic tissue was

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Li Feng, Ling Gao, Qingbo Guan, Xiaolei Hou, Qiang Wan, Xiangdong Wang, and Jiajun Zhao

Introduction The high-fat (HF) diet with a high ratio of saturated fatty acid is considered as a risk factor for insulin resistance, while moderate ethanol drinking was reported to have beneficial effect on insulin sensitivity ( Kiechl et al . 1996

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Tetsuya Kouno, Nobuteru Akiyama, Takahito Ito, Tomohiko Okuda, Isamu Nanchi, Mitsuru Notoya, Shogo Oka, and Hideo Yukioka

concentration during the OGTT was dramatically decreased ( Fig. 5 F and H), indicating that GOAT KO mice showed increased insulin sensitivity. Moreover, ITT revealed that GOAT KO mice exhibited improved insulin response ( Fig. 6 C and D). Importantly, KO mice