[A preliminary study on the mechanism of impaired beta cell function in monosodium glutamate obese rat with insulin resistance].
This study is to evaluate beta cell function and investigate the mechanism of impaired pancreatic islet beta cell function in monosodium glutamate (MSG) obese rat with insulin resistance, an animal model of metabolic syndrome. Insulin tolerance test was used to screen MSG obese rats with insulin resistance. Blood concentrations of glucose, triglyceride, total cholesterol and insulin were determined. Beta cell function was assessed with hyperglycemic clamp technique. The morphological alterations in pancreas and changes of islet beta cell mass were evaluated by hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining. Lipid, oxidative stress relevant factors, nitric oxide (NO) level and activity of ATPase in pancreas and pancreatic mitochondrial were tested. The MSG obese rats with insulin resistance could be validated as a typical metabolic syndrome animal model possessing increased fasting plasma triglycerides and insulin (P < 0. 001), markedly decreased weight indices of pancreas and impaired glucose-stimulated insulin secretion. Hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining showed increased adipocytes and fibroplasia deposition in pancreas and reduced beta cell mass. The increased contents of triglyceride and NO level, the decreased SOD levels and activities of total ATPase (P < 0.001), Na+-K+-ATPase (P < 0.001) and Ca2+-Mg2+-ATPase (P < 0.01) were observed in pancreas and its mitochondria versus normal rat. The study demonstrates that accumulation of lipids in pancreas could lead to increased systemic indicators of inflammation, such as NO, which may influence the activities of several kinds of ATPase in cell membranes and interfere the ion transport, substance metabolism and energy production in pancreas. Finally the MSG obese rats characterized with metabolic syndrome displayed an impairment of beta cell function.
Liu
Shuai-Nan
SN
Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Liu
Quan
Q
Shen
Zhu-Fang
ZF
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D024821:Metabolic Syndrome / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D008928:Mitochondria / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D009765:Obesity / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D009929:Organ Size; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D014280:Triglycerides; D009569:Nitric Oxide; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D000251:Adenosine Triphosphatases; D012970:Sodium Glutamate