A DIET ENRICHED IN PROTEIN ACCELERATES DIABETES MANIFESTATION IN NOD MICE

Diet modifies the development of insulin-dependent diabetes mellitus i n animals and in humans. We examined female non-obese-diabetic (NOD) m ice, a diabetes-prone mouse strain with 70% spontaneous diabetes incid ence and metabolic abnormalities in non-overtly diabetic litters. They were fed a diet containing 55% (n=27) or 15% (n=26) protein, respecti vely, after weaning. At an age of 30 weeks, non-diabetic NOD mice were submitted to an intravenous glucose tolerance test (0.5 g/kg body wei ght; blood samples were taken after 2, 4, 8, 10, 15, 20 and 30 min) an d to perfusion of the pancreas (stimulation media were Krebs-Ringer-He pes buffer with 5 mmol/l glucose, 30 mmol/l glucose and 5 mmol/l gluco se plus 19 mmol/l arginine). Diabetic mice were removed from the exper iment. Serum glucose concentration and body weight were monitored week ly. Food ingestion was checked at an age of 11 weeks. On average, the onset of diabetes was diagnosed in mice on a high-protein diet (19.7+/ -1.3 weeks) 4 weeks earlier than in mice on a low-protein diet (23.5+/ -1.1 weeks; P<0.05). Non-diabetic NOD mice on a high-protein diet show ed significantly better glucose tolerance (as determined by the glucos e disappearance rate) and mean insulin secretion (at 30 mmol/l glucose ), No difference in the serum glucose concentration between non-diabet ic mice on the low-protein diet or high-protein diet could be proved. In non-diabetic mice on the high-protein diet the body weight and food ingestion exceeded those of mice on the low-protein diet (P<0.05). Hi gh insulin secretion and glucose tolerance in non-diabetic mice may re flect the capacity of beta-cells to adapt; however, beta-cells tend to be destroyed under such circumstances. Thus, a high-protein diet prom oted the onset of diabetes, but it did not increase significantly the incidence of the disease.