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Rubén Marín-Juez, Susanne Jong-Raadsen, Shuxin Yang and Herman P Spaink

resistance is a common aspect of a number of these metabolic pathologies, such as type 2 diabetes, and also a powerful parameter for predicting the incidence of cardiovascular diseases and cancer ( Shanik et al . 2008 ). Hyperinsulinemia is the hallmark of

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Nicole M Templeman, Søs Skovsø, Melissa M Page, Gareth E Lim and James D Johnson

associated with excessive insulin production. Hyperinsulinemia, which for the purpose of this review will broadly refer to elevated basal and/or stimulated insulin secretion, is associated with obesity, and is nearly universal in the early stages of type 2

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E Bucris, A Beck, S Boura-Halfon, R Isaac, Y Vinik, T Rosenzweig, S R Sampson and Y Zick

oxidative stress than other cell types. Several studies indicate that treatment of cultured cells with insulin, or hyperinsulinemia induced in animal models, promotes the generation of reactive oxygen species (ROS) ( Mukherjee et al . 1978 , May & de Haen

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Sarit Ben-Shmuel, Eyal J Scheinman, Rola Rashed, Zila Shen Orr, Emily J Gallagher, Derek LeRoith and Ran Rostoker

, Larsson et al . 2007 ). Hyperglycemia, insulin resistance, and subsequently hyperinsulinemia, key features of T2D, have been suggested as potential molecular mechanisms underlying this association ( Novosyadlyy & LeRoith 2010 , Xu et al . 2014

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Sheree D Martin and Sean L McGee

to drive aberrant growth and proliferation. We will specifically examine the mechanisms by which type 2 diabetes might promote the development of breast cancer, with an emphasis on the role of hyperinsulinemia in this process. Finally, we will

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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

et al showed that hyperinsulinemia precedes insulin resistance in mice lacking pancreatic leptin signaling ( Gray et al . 2010 ). This was further confirmed in obese human by Alemzadeh and coworkers in which authors have shown beneficial effect of

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

Abstract

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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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

Introduction Hyperinsulinemia is often associated with obesity and type 2 diabetes mellitus (T2DM) ( Kahn et al. 2006 ). Chronic hyperinsulinemia impairs insulin receptor function, leading to insulin resistance ( Kanety et al. 1994

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Caitlin S Wyrwoll, Peter J Mark, Trevor A Mori and Brendan J Waddell

) or carbenoxolone, an inhibitor of 11β-hydroxysteroid dehydrogenase, increases fetal glucocorticoid exposure and leads to offspring hyperglycemia, glucose intolerance, hyperinsulinemia, and insulin resistance ( Nyirenda et al . 1998 , Cleasby et al

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Victoria E DeMambro, Masanobu Kawai, Thomas L Clemens, Keertik Fulzele, Jane A Maynard, Caralina Marín de Evsikova, Kenneth R Johnson, Ernesto Canalis, Wesley G Beamer, Clifford J Rosen and Leah Rae Donahue

subjected to a (D) ITT as described in the Materials and Methods. Females were tested at the same time and they showed a similar pattern of significance ( n =10 per genotype * P ≤0.05). GTT and ITT To investigate whether the mild hyperinsulinemia in Irs1