Article
In this experiment, we used Western blot analysis and carbon monoxide assays of homogenized aorta and kidney tissues. CO levels are an indicator of total HO activity, and these were significantly lower in Diabetic rats without resveratrol than in lean control animals. This suggests that HO-1 is inactivated by obese/hyperglycemic conditions. In diabetic rats fed with resveratrol, however, CO levels increased to levels greater than those in the lean controls. This indicates that resveratrol was able to increase HO-1 activity.
In contrast, Glyclazide did not affect CO release.
This is an interesting finding because under normal physiological conditions, islets of
Langerhans produce CO and nitric oxide to regulate insulin release. While NO negatively modulates glucose-stimulated insulin
release, CO stimulates insulin secretion.
In addition, glucose stimulates pancreatic β-cells to produce CO, which in turn triggers insulin
release. This underlines the critical role of the HO system in insulin release and glucose metabolism.
This bar chart shows weights of subcutaneous fat on the left, and visceral fat on the right, harvested in diabetic rats.
Resveratrol-induced HO-1 induction significantly reduced weight gain in Diabetic rats treated with Resveratrol. After the Diabetic rats had been humanely killed, subcutaneous and visceral adipose tissue was dissected. Body weight, as well as SAT and VAT weights were significantly lower in the rats fed the resveratrol-enriched diet than in the diabetic rats without resveratrol. Most importantly, the reduction was particularly marked for visceral adipose tissue, which is known to be linked to insulin resistance, type 2 diabetes and inflammatory disease.