title: [Research on the effect of statins on insulin secretion from pancreatic islet in rats and its mechanisms].
abstract: OBJECTIVE
  To evaluate the inhibitory effect of statins on glucose-stimulated insulin secretion (GSIS) of pancreatic islet in rat and to explore its mechanisms.
  
  
  METHODS
  According to the average volume, freshly isolated or 24-hour cultured pancreatic islets were randomly divided into control group (incubated with Kreb-Ringer bicarbonate buffer), the atorvastatin group (incubated with 100 µmol/L atorvastatin), the fluvastatin group (incubated with 100 µmol/L fluvastatin) and the pravastatin group (incubated with 100 µmol/L pravastatin). Stimulated by 2.8, 5.5, 11.1, 16.7 mmol/L and 25.0 mmol/L glucose respectively, the effect of 100 µmol/L statins on ATP content and GSIS was compared in the four groups. GSIS was performed by the 37°C bath incubation method and ATP content was measured by chemiluminescence method.
  
  
  RESULTS
  Incubated with 100 µmol/L atorvastatin for 30 minutes, in the presence of 16.7 mmol/L glucose, the ATP content [(9.54 ± 1.64) pmol/islet vs (12.33 ± 1.89) pmol/islet] and GSIS (1.60 ± 0.21 vs 2.39 ± 0.30) were significantly reduced in comparison with the control group (P < 0.05). Cultured with 100 µmol/L fluvastatin for 24 hours, the ATP content [(10.24 ± 2.01) pmol/islet vs (12.31 ± 2.16) pmol/islet] and GSIS (3.12 ± 0.32 vs 4.17 ± 0.37) were all significantly decreased at the higher glucose concentration of 16.7 mmol/L (P < 0.05).
  
  
  CONCLUSIONS
  Atorvastatin and fluvastatin may inhibit GSIS by decreasing ATP content in pancreatic islet and the inhibitory effect is related to the strength of its lipophilicity.
authors.affiliation: Department of Nephropathy, Tianjin Medical University Metabolic Diseases Hospital, Tianjin 300070, China. changbc1970@126.com
authors.forename: Bao-cheng
authors.initials: BC
authors.lastname: Chang
authors.forename: Miao-yan
authors.initials: MY
authors.lastname: Zheng
authors.forename: Chun-yan
authors.initials: CY
authors.lastname: Shan
authors.forename: Ju-hong
authors.initials: JH
authors.lastname: Yang
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Hui-zhu
authors.initials: HZ
authors.lastname: Ren
authors.forename: Li-ming
authors.initials: LM
authors.lastname: Chen
authors.forename: Pei-hua
authors.initials: PH
authors.lastname: Fang
mesh_terms: D000818:Animals; D000069059:Atorvastatin; D002478:Cells, Cultured; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D000077340:Fluvastatin; D006538:Heptanoic Acids / Q000494:pharmacology; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007211:Indoles / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D007328:Insulin; D011758:Pyrroles; D000077340:Fluvastatin; D000069059:Atorvastatin