Diet-induced obesity and pancreatic islet blood flow in the rat: a preferential increase in islet blood perfusion persists after withdrawal of the diet and normalization of body weight.
The aim of the present study was to evaluate the effects of diet-induced obesity on pancreatic islet blood perfusion in normal Wistar rats. Furthermore, we investigated to what extent any obesity-associated changes in islet blood flow could be reversed after reversion to a normal diet with normalization of body weight. Young adult female Wistar rats were offered a palatable mixed high-caloric diet (cafeteria diet) in addition to standard pelleted chow. Age-matched control rats received standard pelleted chow only. After 4 weeks the diet-treated rats had a body weight of approximately 15% more than that of the controls. All diet-treated rats had decreased glucose tolerance and increased serum insulin concentrations, but basal blood glucose concentrations were similar in anesthetized diet-treated and control rats. Whole pancreatic and islet blood flow rates were measured with a microsphere technique. The islet blood flow as well as fractional islet blood flow were increased (P < 0.01) in rats fed the cafeteria diet, while blood perfusion of the whole pancreas was similar to that of the control rats. In a second experiment, rats received the cafeteria diet for 4 weeks and were then fed standard pelleted food alone for another 3 weeks, while controls received standard diet for 7 weeks. After this period total body weight, retroperitoneal fat pad weight and glucose tolerance were similar to those of the controls. Whole pancreatic blood flow was unchanged as compared with that of control rats. However, both islet blood flow (P < 0.01) and fractional blood flow (P < 0.01) were increased. We conclude that diet-induced obesity in rats is associated with decreased glucose tolerance, hyperinsulinemia and a specific increase in absolute and fractional islet blood perfusion. This increase persists for at least 3 weeks after the diet is withdrawn despite normalization of body weight and glucose tolerance.
Svensson
A M
AM
Department of Medical Cell Biology, Uppsala University, Sweden.
Hellerström
C
C
Jansson
L
L
D000818:Animals; D001835:Body Weight; D002149:Energy Intake / Q000502:physiology*; D005260:Female; D018149:Glucose Intolerance / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007515:Islets of Langerhans / Q000098:blood supply*; D009765:Obesity / Q000097:blood / Q000178:diet therapy / Q000503:physiopathology*; D010179:Pancreas / Q000098:blood supply; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology
D007328:Insulin