Aim: To investigate the acute and chronic effects of nateglinide versus acarbose on plasma asymmetric dimethylarginine (ADMA) levels and lipid profiles in patients with newly diagnosed type 2 diabetes. Methods: A crossover trial of nateglinide and acarbose was conducted on 16 drug-naïve patients with newly diagnosed type 2 diabetes during a total period of 9 weeks. Plasma glucose, serum insulin, free fatty acids (FFA), lipids and lipoproteins, and plasma ADMA were measured. Results: The efficiencies of a single dose of nateglinide (120 mg) and acarbose (50 mg) for lowering postprandial hyperglycemia were similar. Compared to acarbose, nateglinide significantly increased postprandial insulin release after a standard meal test in patients with type 2 diabetes. Nateglinide acutely decreased postprandial 120-min FFA concentrations and 240-min ADMA levels more significantly than acarbose. The fasting high-density lipoprotein cholesterol (HDL-C) level increased and the low-density lipoprotein cholesterol (LDL-C) level decreased significantly, but the fasting levels of triglycerides, total cholesterol, and ADMA were unchanged after 4 weeks of treatment with nateglinide. Acarbose did not affect fasting lipid profiles or the ADMA levels after 4 weeks of treatment. Conclusion: These results suggest that the reduction of postprandial FFA and ADMA concentrations induced by nateglinide may be associated with the partial restoration of early phase insulin secretion and may impart a cardiovascular advantage in comparison with acarbose.

The side population (SP) phenotype might represent a common molecular feature for a wide variety of stem cells. The aim of this study was to investigate whether monoclonal SP progenitor cells were established from human fetal pancreas. Islet-like cell clusters (ICCs) were isolated from human fetal pancreas. Monolayer epithelium-like cells were obtained from the ICCs and passaged thereafter. Single SP or non-SP cell were sorted from these cells at the sixth passage. The rate of clone formation was about 2.7% for the SP cells, whereas there was no clone formation for the non-SP cells. The SP cell clones were further expanded for more than 15 passages and induced for differentiation into cells with characteristics of pancreatic -cells. We show for the first time that the monoclonal SP progenitors are established from human fetal pancreas. Therefore, this study may offer a novel method to purify pancreatic progenitor cells from human tissues.