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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Blood Glucose, Calcium, Gene Expression Regulation, Ghrelin, Insulin, Islets of Langerhans, Male, Membrane Potentials, Potassium Channels, Inwardly Rectifying, RNA, Messenger, Rats, Rats, Wistar, Receptors, Ghrelin.
user
Does ghrelin inhibit insulin release by regulating the expression of inwardly rectifying potassium channel 6.2 in islets? Context: The objective is to investigate the influence of ghrelin administration on both the insulin secretion and the expression of ATP-sensitive K(+) channels in islet. Ghrelin and [D-Lys] growth hormone releasing peptide-6 were administered via intraperitoneal injection in Wistar rats at the doses 10 and 10 μmol/kg/d for 2 weeks, respectively. Then glucose tolerance tests were performed and plasma insulin concentrations were measured. Islets were isolated for insulin release experiments. Single β cells were isolated for electrophysiological experiments. Determination of the Kir6.2 and SUR1 mRNA and protein expression levels in islets was performed by polymerase chain reaction and western blotting. Intraperitoneal administration of exogenous ghrelin significantly (P < 0.05) increased blood glucose concentrations, attenuated insulin responses during glucose tolerance tests, reduced insulin release from the isolated islets induced by 11.1 and 16.7 mmol/L glucose, hyperpolarized the resting membrane potential and increased the Kir6.2 mRNA and protein expression levels. In contrast, counteraction of ghrelin by intraperitoneal injection of [D-Lys(3)] growth hormone releasing peptide-6 significantly (P < 0.05) attenuated the aforementioned changes. SUR1 expression levels were not altered in this study.
assistant
Ghrelin via pancreatic growth hormone secretagogue receptor up-regulates the Kir6.2 expression in islet by hyperpolarizing the resting membrane potential which results in the inhibition of insulin release. Final Decision: yes