title: Ghrelin inhibits insulin release by regulating the expression of inwardly rectifying potassium channel 6.2 in islets.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Surgery of Integrated Traditional and Western Medicine Department, Tianjin Medical University General Hospital, China.
authors.forename: Zhang
authors.initials: Z
authors.lastname: Peng
authors.forename: Zhou
authors.initials: Z
authors.lastname: Xiaolei
authors.forename: Hani
authors.initials: H
authors.lastname: Al-Sanaban
authors.forename: Xue
authors.initials: X
authors.lastname: Chengrui
authors.forename: You
authors.initials: Y
authors.lastname: Shengyi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002118:Calcium / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D054439:Ghrelin / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials; D024661:Potassium Channels, Inwardly Rectifying / Q000032:analysis / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D054440:Receptors, Ghrelin / Q000502:physiology; D000099161:Kcnj11 Channel
chemical_list: D001786:Blood Glucose; D002118:Calcium; D054439:Ghrelin; D007328:Insulin; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D054440:Receptors, Ghrelin; D000099161:Kcnj11 Channel