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.