Earm, MD, PhD, Department of Physiology and Biophysics, Seoul National University, College of Medicine, 28 Yonkeun-Dong, Chongno-Ku,S eou111O -7 99, South Korea. Supported by the academic researchf imd (BM 97-39) of the Ministry of Education, South Korea. T1 - Evidence of enhancement of malate-aspartate shuttle activity in β cells of streptozotocin-induced non-insulin-dependent diabetic ratsįrom the Department of Physiology, Keimyung University School of Medicine, Taegu and Department of Physiology, College of Medicine, Seoul National University, Seoul, South Korea. These findings show that malate-aspartate shuttle activity is potentiated in pancreatic β cells of NIDDM rats, suggesting the development of a compensatory mechanism for the reduced activity of the glycerol- phosphate shuttle in NIDDM.", However, intracellularly applied aspartate in the inside-out mode did not inhibit K(ATP) channel activity. On the contrary, the increase of insulin secretion and the inhibition of K(ATP) channel activity induced by aspartate, which preferentially participates in the malate-aspartate shuttle, were significantly greater in NIDDM versus the control. The application of glyceraldehyde (10 mmol/L) in NIDDM or control islets elicited an increase in insulin secretion, but the difference between the 2 groups was indistinguishable. The increase of insulin secretion induced by 11.1 mmol/L glucose or 10 mmol/L dihydroxyacetone (DHA) was significantly reduced in NIDDM islets, suggesting an impaired glycerol-phosphate shuttle. The insulin secretory capacity of the islets and the K(ATP) channel activity in single β cells were measured in control and NIDDM rats injected with streptozotocin (STZ) during the neonatal period, using a radioimmunoassay and patch-clamp technique. This study was performed to clarify whether the malate-aspartate shuttle among the glucose metabolic pathways is intact in β cells of NIDDM rats. These findings show that malate-aspartate shuttle activity is potentiated in pancreatic β cells of NIDDM rats, suggesting the development of a compensatory mechanism for the reduced activity of the glycerol- phosphate shuttle in NIDDM.Ībstract = "Glucose-induced insulin secretion is selectively impaired in β cells from animals with non-insulin-dependent diabetes mellitus (NIDDM). Glucose-induced insulin secretion is selectively impaired in β cells from animals with non-insulin-dependent diabetes mellitus (NIDDM).
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