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R H Rao

Abstract

The metabolic effects of angiotensin II (AII) were studied under steady-state conditions of euglycaemic hyperinsulinaemia in anaesthetized rats. Pressor doses of AII (50 and 400 ng/kg per min) had dose-dependent hypertensive and hyperglycaemic effects during glucose clamp studies. Glucose turnover measurements showed that hepatic glucose output (HGO) increased equally at both pressor doses compared with either saline infusion or AII infusion at a dose without a pressor effect (20 ng/kg per min); however, glucose disposal increased significantly only at 50 ng/kg per min. Infusion of the AII receptor antagonist, saralasin, did not itself alter glucose output or disposal significantly, but it abolished the effects of a simultaneous infusion of All. It is concluded that pressor doses of AII increase HGO by a receptor-mediated mechanism that is not related to the pressor response to the hormone. The hyperglycaemic reaction to this metabolic effect of AII is partially offset by increased glucose disposal at lower doses. The physiological significance of these metabolic actions of AII remains to be established, but they raise the possibility that AII could potentially play a role in glucose homeostasis in vivo.

Journal of Endocrinology (1996) 148, 311–318

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Alex Rafacho, Henrik Ortsäter, Angel Nadal, and Ivan Quesada

first-degree relatives of diabetic patients ( Van Raalte et al . 2009 ). The ability of GCs to produce peripheral IR is central to explain their impact on glucose homeostasis. It is well known that any reduction in peripheral insulin sensitivity, e

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E. BLÁZQUEZ and C. LÓPEZ QUIJADA

SUMMARY

The administration of a high-protein diet to rats, from the end of lactation until they reached a weight of 150 g., produced significant changes in the concentrations of insulin in the plasma and pancreas. Compared with controls, the animals receiving this diet had higher plasma glucose and insulin concentrations and a higher hormone content in the pancreas.

The levels of hepatic glycogen were similar to those in the control rats, but the muscle glycogen was significantly lower. Adipose tissue in vitro was less sensitive to the action of insulin on glucose uptake.

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FP Dominici, S Hauck, DP Argentino, A Bartke, and D Turyn

In the present study we have used hypopituitary Ames dwarf mice, which lack GH, prolactin and TSH, to investigate the consequences of the deficiency of these hormones on glucose homeostasis and on the initial components of the insulin signal transduction pathway in the liver. Ames dwarf mice displayed hypersensitivity to insulin since they maintained lower fasting glucose concentrations (73% of control values), had significantly reduced amounts of insulin (58% of control values), and exhibited an increased hypoglycemic response to exogenous insulin. Probably as a result of reduced insulin production, Ames dwarf mice displayed intolerance to glucose. The insulin-stimulated phosphorylation of the insulin receptor (IR) tended to be increased in the liver of Ames dwarf mice, while IR receptor protein content was increased by 38%. Insulin-stimulated phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 was increased by 61 and 72% respectively, while IRS-1 and IRS-2 protein levels were increased by 76 and 95%. The insulin-stimulated association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 was increased by 28%, but unaltered with IRS-2. Interestingly, while the insulin-stimulated phosphotyrosine-derived PI 3-kinase activity was not changed, insulin-stimulated protein kinase B activation was increased by 41% in this tissue. These alterations may account for the insulin hypersensitivity exhibited by these animals. The present findings in long-lived Ames dwarf mice add to the evidence that insulin signaling is importantly related to the regulation of aging and life span.

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R De Matteo, D J Hodgson, T Bianco-Miotto, V Nguyen, J A Owens, R Harding, B J Allison, G Polglase, M J Black, and K L Gatford

type 2 diabetes (T2D) in adult life ( Lawlor et al . 2006 , Kaijser et al . 2009 , Kajantie et al . 2010 , 2014 , Pilgaard et al . 2010 ), with poorer insulin sensitivity implicated as an underlying mechanism ( Tinnion et al . 2013 ). Direct

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R Vinayagamoorthi, Zachariah Bobby, and M G Sridhar

, there is an inverse relationship between fasting plasma triglyceride concentration and insulin sensitivity ( Perseghin et al . 1997 ). There is an even stronger relationship between the accumulation of intracellular triglycerides and insulin resistance

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Camilla Alexanderson, Elias Eriksson, Elisabet Stener-Victorin, Malin Lönn, and Agneta Holmäng

in a predisposition to metabolic and endocrine disease in adulthood ( Barker 1990 , Lucas 1991 , Barker et al . 1993 ). In humans and animals, perinatal programming may contribute to inappropriate insulin sensitivity by affecting glucose and lipid

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Jiali Liu, Yue Li, Xiaoyan Zhou, Xi Zhang, Hao Meng, Sanyuan Liu, Lei Zhang, Juntao He, Qian He, and Yan Geng

-body improvements of insulin sensitivity ( Wu et al . 2000 , Hook & Means 2001 , Lee et al . 2014 ). CaMKIV, also known as CaMK4, has been shown to regulate various cellular events through phosphorylated transcription factors. It plays an essential role in

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Sergio Caja, Izaskun Martínez, María Abelenda, and Marisa Puerta

insulin in 3T3-L1 cells ( Haugen et al. 2001 , Shojima et al. 2002 ) has cast doubt on the role of resistin in the development of insulin resistance. Additionally, in some physiological states related with an altered insulin sensitivity, no changes in

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M Fraenkel, J Caloyeras, S-G Ren, and S Melmed

. 1978 , Maclaren et al. 1980 , Kava et al. 1992 , Shi et al. 1994 , Weksler-Zangen et al. 2001 ). Removal of testosterone from the sex-steroid milieu of the male animal improved insulin sensitivity in most studies, and thus was protective