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Nigel Irwin, Pamela Frizelle, Finbarr P M O'Harte, and Peter R Flatt

conditions is of value. This study indicates that (pGlu-Gln)-CCK-8 exerts beneficial effects on body weight regulation and insulin sensitivity with no obvious signs of malaise or harmful effects on behavior. Materials and methods Peptides synthesis (pGlu

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I. Guéritault, J. Simon, B. Chevalier, M. Derouet, M. Tixier-Boichard, and P. Mérat


The effects of the recessive and sex-linked dw gene on insulin sensitivity and liver insulin receptors were compared in normal (Dw-dw) and dwarf (dw-dw) brother or half-brother chickens. At 3·5 weeks of age, following an overnight fast, exogenous insulin (0–6·9 nmol/kg body weight) was slightly but significantly more hypoglycaemic in dwarf chickens. At 4 weeks of age, following an oral glucose load (2 g/kg), glucose tolerance was the same in both genotypes, whereas plasma insulin levels were greatly decreased in dwarf chickens. At 5 weeks of age, plasma concentrations of glucose and insulin were the same in both genotypes in the fasting state and decreased in the fed state in dwarf chickens. In liver membranes prepared from fasted chickens, insulin binding was increased in dwarf chickens, while the affinity of insulin receptors and the insulin-degrading activity of the membranes were the same in both genotypes. Following solubilization with Triton X-100, liver receptors were successively purified on lentil then wheat germ lectins. Autophosphorylation of the β-subunit did not differ between either the genotype or the nutritional (fed or fasted) state. In the basal state (in the absence of insulin) the tyrosine kinase activity of the receptor towards artificial substrate poly(Glu,Tyr)4:1 was significantly decreased in dwarf chickens by fasting. However, the change in tyrosine kinase activity of the receptor in response to insulin was similar, irrespective of the genotype and the nutritional state. Therefore, the slight increase in insulin sensitivity observed in vivo in dwarf chickens is accounted for, at least partly, by a slight increase in liver insulin receptor number, but not by a change in the kinase activity of liver insulin receptors. In addition, post-insulin receptor kinase events and/or GH-dependent counter-regulatory mechanisms may superimpose and increase the insulin sensitivity of dwarf chickens.

Journal of Endocrinology (1990) 126, 67–74

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An investigation was made of the interactions between insulin and cortisol on carbohydrate, fat and protein metabolism in the marsupial brush-tailed opossum Trichosurus vulpecula (Kerr).

Intravenous injection of 0·15 i.u. regular insulin/kg caused a prompt fall in plasma glucose concentration to 33–54% of the control value, in the first 30 min, with complete recovery within 4 h. This was associated with a slow fall in plasma amino acid concentration and a moderate rise in plasma free fatty acid (FFA) concentration. Plasma cortisol concentration was increased 1·5 h after insulin injection to maximum values of 1·24–4·44 μg/100 ml, which were approximately proportional to the degree of hypoglycaemia.

Pretreatment with five daily i.m. injections of 1 mg cortisol acetate/kg caused a marked reduction in insulin sensitivity of three out of four opossums, and increasing the dose to 5 mg/kg caused a similar reduction in insulin sensitivity of the remaining opossum. Cortisol pretreatment raised the control plasma amino acid and FFA concentrations and enhanced the effect of insulin injection on these variables. There was a linear relationship between the control plasma cortisol concentration, within the physiological range, and sensitivity to insulin.

It is concluded that, in contrast to the red kangaroo, the interactions between insulin and glucocorticoids in Trichosurus resemble those reported for eutherian mammals. However, the unusual increase in plasma FFA after insulin injection is unexplained.

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NJ Lewis-Barned, WH Sutherland, RJ Walker, SA de Jong, HL Walker, EA Edwards, V Markham, and A Goulding

This study was designed to determine the effect of menopause and hormone replacement therapy (HRT) on plasma cholesteryl ester fatty acid (CEFA) composition and insulin sensitivity and the relationships between these variables in perimenopausal women (aged 40-55 years) including 49 who were premenopausal and 32 who were postmenopausal. Plasma cholesteryl ester proportions of dihomo-gamma-linolenic acid (20:3 n-6) were correlated significantly with insulin sensitivity index (r=-0.319, P=0.005), fasting serum insulin levels (r=0.230, P=0.038), body mass index (r=0.242, P=0.03) and per cent body fat (r=0.329, P=0.003) in perimenopausal women (n=81). Similar associations were observed in premenopausal women. Regression analysis suggested the relationships between 20:3 n-6 proportions and indices of insulin action may be partly mediated by levels of adiposity. In postmenopausal women, 6 months of HRT significantly (P=0.008) increased the ratio of arachidonic acid (20:4 n-6) to linoleic acid (18:2 n-6), which is an indicator of activity in the pathway of 20:4 n-6 synthesis, compared with placebo. These findings suggest that the type of fat in the diet indicated by plasma CEFA composition is linked to adiposity and insulin action. They also suggest that in postmenopausal women, HRT may increase the synthesis of 20:4 n-6, which is the precursor for eicosanoids with important cardiovascular functions.

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Tianxue Zhao, Qian Li, Qianyun Mao, Kaida Mu, and Chen Wang

Neuronal nitric oxide synthase (nNOS) interacts with its adaptor protein NOS1AP through its PZD domain in the neurons. Previously, we had reported that NOS1AP enhanced hepatic insulin sensitivity through its PZD-binding domain, which suggested that nNOS might mediate the effect of NOS1AP. This study aimed to examine the role and underlying mechanisms of nNOS in regulating hepatic insulin sensitivity. nNOS co-localized with NOS1AP in mouse liver. The overexpression of NOS1AP in mouse liver decreased the level of phosphorylated nNOS (p-nNOS (Ser1417)), the active form of nNOS. Conversely, the liver-specific deletion of NOS1AP increased the level of p-nNOS (Ser1417). The overexpression of nNOS in the liver of high-fat diet-induced obese mice exacerbated glucose intolerance, enhanced intrahepatic lipid accumulation, decreased glycogen storage, and blunted insulin-induced phosphorylation of IRβ and Akt in the liver. Similarly, nNOS overexpression increased triglyceride production, decreased glucose utilization, and downregulated insulin-induced expression of p-IRβ, p-Akt, and p-GSK3β in the HepG2 cells. In contrast, treatment with Nω-propyl-L-arginine (L-NPA), a selective nNOS inhibitor, improved glucose tolerance and upregulated insulin-induced phosphorylation of IRβ and Akt in the liver of ob/ob mice. Furthermore, overexpression of nNOS increased p38MAPK phosphorylation in the HepG2 cells. In contrast, inhibition of p38MAPK with SB203580 significantly reversed the nNOS-induced inhibition of insulin signaling activity (all P < 0.05). This indicated that hepatic nNOS inhibited the insulin-signaling pathway through the activation of p38MAPK. These findings suggest that nNOS is involved in the development of hepatic insulin resistance and that nNOS might be a potential therapeutic target for diabetes.

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Rodrigo Martins Pereira, Kellen Cristina da Cruz Rodrigues, Chadi Pellegrini Anaruma, Marcella Ramos Sant’Ana, Thaís Dantis Pereira de Campos, Rodrigo Stellzer Gaspar, Raphael dos Santos Canciglieri, Diego Gomes de Melo, Rania A Mekary, Adelino Sanchez Ramos da Silva, Dennys Esper Cintra, Eduardo Rochete Ropelle, José Rodrigo Pauli, and Leandro Pereira de Moura

insulin sensitivity The ipPTT was carried out 8 h after the last strength session for HGP control evaluation. Initially, we observed that the glycemic values of OB group were higher than CTL group at all times of the test ( Fig. 4A ). Moreover, obese

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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