Gastric inhibitory polypeptide and the entero-insular axis in streptozotocin diabetic mice.
The function of the entero-insular axis and abnormalities of circulating gastric inhibitory polypeptide (GIP) were examined in mice for 40 days after induction of streptozotocin diabetes. Compared with untreated controls, streptozotocin diabetic mice exhibited marked hyperglycaemia and hypoinsulinaemia, with impaired body weight gain, lipoatrophy, hyperphagia, intestinal hypertrophy, polydipsia and renal hypertrophy. Plasma GIP concentrations were elevated in fed but not fasted streptozotocin diabetic mice, and oral fat evoked a greater GIP response than control mice. In spite of marked hyperglycaemia, fat-stimulated GIP release did not raise plasma insulin in streptozotocin diabetic mice. Neither oral nor intraperitoneal glucose produced a significant insulin response in streptozotocin diabetic mice, although oral glucose resulted in a smaller change in glycaemia. The results indicate that streptozotocin diabetes in mice is associated with ineffectiveness of the entero-insular axis, despite elevated GIP concentrations, which are probably mediated through hyperphagia and defective feedback inhibition by insulin on intestinal K cells.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D004041:Dietary Fats / Q000494:pharmacology; D005215:Fasting; D005749:Gastric Inhibitory Polypeptide / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008297:Male; D051379:Mice; D008820:Mice, Obese
D001786:Blood Glucose; D004041:Dietary Fats; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide