Zinc is an essential nutrient with a wide range of functions and closely involved in a variety of enzymatic processes of importance in
glucose,
protein and lipid metabolism.
Ghrelin is the endogenous
ligand of the
G protein coupled
growth hormone secretagogue receptor. The regulatory mechanism that explain the biosynthesis and secretion of
ghrelin in the gastrointestinal tract has not been clarified. This study was undertaken to examine the effect of
zinc supplementation on the
streptozotocin (STZ)-induced diabetic rats, which exhibits
ghrelin production and secretion, and lipid metabolism on the gastrointestinal tract. The animals were divided into four groups. Group I: Non-diabetic untreated animals. Group II:
Zinc-treated non-diabetic rats. Group III: STZ-induced diabetic untreated animals. Group IV:
Zinc-treated diabetic animals.
Zinc sulfate was given to some of the experimental animals by gavage at a dose of 100 mg/kg
body weight every day for 60 days. In the
zinc-treated diabetic group, the
blood glucose levels decreased and
body weight increased as compared to the diabetic untreated group.
Zinc supplementation to STZ-diabetic rats revealed the protective effect of
zinc on
lipids parameters such as total
lipid,
cholesterol, HDL-
cholesterol and atherogenic index. There is no statistically change in
ghrelin-immunoreactive cells in gastrointestinal tissue. But, it has found that
zinc supplementation caused a significant reduction in densities of
ghrelin-producing cells of fundic mucosa of
zinc-treated diabetic animals as compared to untreated, non-diabetic controls.
Zinc supplementation may contribute to prevent some complications of diabetic rats, biochemically.