Phosphatidylinositol-3-kinase is involved in the antihyperglycemic effect induced by resveratrol in streptozotocin-induced diabetic rats

Chi, Tzong‐Cherng; Chen, Win-Pin; Chi, Tsung-Li; Kuo, Ting‐Shen; Lee, Shoei‐Sheng; Cheng, Juei‐Tang; Su, Ming‐Jai

doi:10.1016/j.lfs.2007.02.002

Cited by 139 publications

(121 citation statements)

References 28 publications

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“…Though, recently, we reported that one bout of exercise reduced protein tyrosine phosphatase 1B (PTP1B) activity and IRS-1 serine phosphorylation (two molecular mechanisms mediating insulin resistance), leading to restored insulin sensitivity in the gastrocnemius muscle of DIO rats , the role of acute exercise on PTP1B activity and IRS1 serine phosphorylation in the hepatic tissue was not investigated and could be involved in the improvement on insulin signaling but these mechanisms remain uncertain and deserve further investigations. In the hepatic tissue, insulin resistance is related as reduced insulin stimulation of tyrosine phosphorylation of the IR and its major substrates (Michael et al, 2000;Pagliassotti et al, 2002) and as an increase in gluconeogenesis and hepatic glucose output (Boden et al, 2001), as a result of the inability of PI 3-K to inhibit the activation of glucose-6-phosphatase (G6Pase) and PEPCK (Kotani et al, 1999;Chi et al, 2007). Exercise has been shown to improve insulin action in the liver (Gao et al, 1994); physical exercise ameliorated the insulin-signaling response in diabetes-prone Psammomys obesus and inhibited PEPCK activity (Heled et al, 2004).…”

Section: Journal Of Cellular Physiologymentioning

confidence: 99%

Acute exercise reduces insulin resistance‐induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice

Lima

Ropelle

Pauli

et al. 2009

Journal Cellular Physiology

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TRB3 (a mammalian homolog of Drosophila) is emerging as an important player in the regulation of insulin signaling. TRB3 can directly bind to Ser/Thr protein kinase Akt, the major downstream kinase of insulin signaling. Conversely, physical exercise has been linked to improved glucose homeostasis and enhanced insulin sensitivity; however, the molecular mechanisms by which exercise improves glucose homeostasis, particularly in the hepatic tissue, are only partially known. Here, we demonstrate that acute exercise reduces fasting glucose in two models diabetic mice. Western blot analysis showed that 8 h after a swimming protocol, TRB3 expression was reduced in the hepatic tissue from diet-induced obesity (Swiss) and leptin-deficient (ob/ob) mice, when compared with respective control groups at rest. In parallel, there was an increase in insulin responsiveness in the canonical insulin-signaling pathway in hepatic tissue from DIO and ob/ob mice after exercise. In addition, the PEPCK expression was reduced in the liver after the exercise protocol, suggesting that acute exercise diminished hepatic glucose production through insulin-signaling restoration. Thus, these results provide new insights into the mechanism by which physical activity improves glucose homeostasis in type 2 diabetes.

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Section: Journal Of Cellular Physiologymentioning

confidence: 99%

Acute exercise reduces insulin resistance‐induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice

Lima

Ropelle

Pauli

et al. 2009

Journal Cellular Physiology

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“…Recently, the direct inhibitory effect of resveratrol on insulin secretion from pancreatic islets of normal rats was described [18][19][20]. Resveratrol was also found to affect blood insulin concentrations [20][21][22][23] and to exert an insulin-like effect in diabetic rats [21,23]. The other beneficial effects of resveratrol, including enhanced glucose uptake by soleus muscle, hepatocytes and adipocytes [21] and the decreased blood glucose and glycosylated haemoglobin, were demonstrated in diabetic rats [24].…”

Section: Introductionmentioning

confidence: 99%

The inhibitory effect of resveratrol on leptin secretion from rat adipocytes

Szkudelska

Nogowski

Szkudelski

2009

Eur J Clin Investigation

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Background Resveratrol was found to alleviate consequences of some metabolic disturbances which may be due to inappropriate dietary habits. It decreases mortality, increases insulin sensitivity and improves motor functions; these effects are accompanied by reduced plasma leptin and insulin. Leptin plays a significant role in the regulation of food intake and energy expenditure -elevated level in blood is one of the reasons of leptinresistance and obesity. In this study, the direct effect of resveratrol on leptin secretion from isolated adipocytes was investigated.

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“…In addition to the alleviation of metabolic diseases, such as cardiovascular disease (Sadruddin and Arora 2009), diabetes (Chi et al 2007) and fatty liver (Hou et al 2008), resveratrol may also improve brain function (Barber et al 2009;Bournival et al 2009). For the present study, the senescence-accelerated mouse P10 (SAMP10) was studied to determine how its aged-related metabolic functions are altered when treated with resveratrol, although SAMP10 has reportedly shown brain deterioration (Takeda 2009).…”

Section: Introductionmentioning

confidence: 99%

Closer association of mitochondria with lipid droplets in hepatocytes and activation of Kupffer cells in resveratrol-treated senescence-accelerated mice

Shiozaki

Hayakawa

Shibata

et al. 2011

Histochem Cell Biol

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Resveratrol has been extensively investigated because of its beneficial effects in delaying age-related diseases, thus extending the lifespan, possibly by mimicking calorie restriction. For this study, cell biological techniques were used to examine how resveratrol influenced hepatocytes in a senescence-accelerated mouse P10 (SAMP10), treated from 35 to 55 weeks of age, with special emphasis on the relationship between mitochondria and lipid droplets. Survival ratio, body weight and food intake of SAMP10 did not differ significantly between the control and resveratrol-treated groups. Compared with the control, the treated livers were altered significantly, as follows. Lipid droplets were reduced and mitochondria were increased in number in hepatocytes. Phosphorylation of acetyl-CoA carboxylase and the expression of both the mitochondrial ATP synthase β subunit and Mn superoxide dismutase (SOD2) were increased. Mitochondria, expressing more SOD2, were more tightly associated with lipid droplets, suggesting the enhancement of lipolysis through the activation of mitochondrial functions. Cathepsin D expression was less in hepatocytes but enhanced in Kupffer cells, which were increased in number and size with more numerous lysosome-related profiles. Together, resveratrol may activate mitochondria resulting in consuming lipids, and may also activate Kupffer cells by which a beneficial milieu for hepatocytes may be created. Both might be related to improvement in the functioning of the liver, which is the organ that is central to metabolic regulation.

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Phosphatidylinositol-3-kinase is involved in the antihyperglycemic effect induced by resveratrol in streptozotocin-induced diabetic rats

Cited by 139 publications

References 28 publications

Acute exercise reduces insulin resistance‐induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice

Acute exercise reduces insulin resistance‐induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice

The inhibitory effect of resveratrol on leptin secretion from rat adipocytes

Closer association of mitochondria with lipid droplets in hepatocytes and activation of Kupffer cells in resveratrol-treated senescence-accelerated mice

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