Abstract
Resveratrol, a non-flavonoid polyphenolic compound, is structurally and functionally similar to estrogen and has drawn great attention for its potentially beneficial effects on diabetes. However, it is not known whether it shares the same protective effect against diabetes as estrogen and the underlying mechanisms. The aim of the present study was to investigate the protective effects of phytoestrogen resveratrol and exogenous 17β-estradiol against streptozotocin (STZ)-induced type 1 diabetes. Female mice were ovariectomized (OVX) and chronically injected with different concentrations of resveratrol (0.1, 1 or 10 mg/kg) and 17β-estradiol (0.01, 0.1 or 1 mg/kg) subcutaneously for 4 weeks, and the levels of blood glucose, plasma insulin, plasma antioxidant capacity, the changes of pancreatic islet cells and the expressions of glucose transporter 4 (GLUT4), insulin receptor substrate 1 (IRS-1) and phosphorylation of extracellular signal-regulated kinase (p-ERK) were detected. Resveratrol and 17β-estradiol significantly inhibited the increase of the blood glucose level and the rise of plasma malondialdehyde in STZ-induced diabetic mice, improved the levels of plasma antioxidant capacity and plasma insulin, protected the pancreatic islet cells, and increased the expressions of GLUT4 and IRS-1, but decreased p-ERK expression in skeletal muscle and myocardial tissue. The results suggest that resveratrol or 17β-estradiol shows obvious protection against STZ-induced diabetes in OVX mice, the mechanisms probably involve their ameliorating antioxidant activities and islet function, promoting muscle glucose uptake and inhibiting the expression of p-ERK.
Highlights
The incidence of diabetes mellitus (DM) has been rising increasingly, in post-menopausal women [1, 2]
4] and ovariectomized female animals have a higher incidence of the disease than the respective sham-operated controls [5]. This indicates that reduced serum estrogen levels in post-menopause could induce insulin resistance (IR), which is causally associated with DM
For further understanding of mechanisms, we investigated the influences of resveratrol and 17β-estradiol on fasting weight, plasma total antioxidant capacity (T-AOC), malondialdehyde (MDA), and fasting plasma insulin levels (FPI) and on pancreatic islet cell morphology; we studied the expression of glucose transporter type 4 (GLUT4), insulin receptor substrate 1 (IRS-1), ERK and phosphorylation of extracellular signal-regulated kinase (p-ERK) in skeletal muscle and myocardial tissue
Summary
The incidence of diabetes mellitus (DM) has been rising increasingly, in post-menopausal women [1, 2]. 4] and ovariectomized female animals have a higher incidence of the disease than the respective sham-operated controls [5]. Together, this indicates that reduced serum estrogen levels in post-menopause could induce insulin resistance (IR), which is causally associated with DM. It is well established that estrogen can increase insulin sensitivity and improve glucose metabolism [5]. There are mixed views on the clinical potential for estrogen replacement therapy in treating DM, as long-term use increases the risk of breast and uterine cancer
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