Insulin secretion from the beta cells of the pancreas is under many regulatory influences, including neuropeptide Y (NPY). This 36 amino acid peptide is one of the most widespread peptide messengers in the body [1]. Among its many actions, an inhibition of insulin secretion by NPY has been found in mouse [2], pig [3] rat [4±6] and human [7]. In the islets, most NPY can be found in sympathetic nerves [8] and a role in the sympathetic regulation of insulin secretion has therefore been suggested. Recently, we have shown the presence of messenger RNA for NPY in islets from rats treated with 6-hydroxydopamine to remove sympathetic inervation [9]. This is supported by reports from others [10,11] and by work showing synthesis of NPY by clonal insulin-secreting cell lines [9,12]. These results suggest local production of NPY in the islet, and a paracrine or autocrine regulation of Diabetologia (1998) Summary Neuropeptide Y (NPY) has been shown to inhibit insulin secretion from the islets of Langerhans. We show that insulin secretion in the insulinoma cell line RIN 5AH is inhibited by NPY.

Our study observed further hypoadiponectinemia and IR in NAFLD with metabolic syndrome. The T45G and G276T of the adiponectin gene may not be the important determinants of NAFLD in Chinese people, but some of them still influence serum ALT, BMI, IR, lipid, glucose metabolism and plasma adiponectin concentration.