Diabetes predisposition is determined by pancreatic islet insulin secretion and insulin resistance. We studied female rat offspring exposed to low-protein maternal diet (50% control protein diet) in pregnancy and/or lactation at postnatal days 36, 110 and 450. Rats were fed either control 20% casein diet (C) or restricted diet (R – 10% casein) during pregnancy. After delivery, mothers received either C or R diet until weaning to provide four offspring groups: CC, RR, CR and RC (first letter denoting maternal pregnancy diet and the second lactation diet). Serum glucose, insulin and homeostatic model assessment (HOMA) were measured. Pancreatic islets were isolated and in vitro insulin secretion quantified in low glucose (5 mM) and high glucose (11 mM). Serum glucose, insulin and HOMA were similar in all groups at 36 and 110 postnatal days. HOMA was only higher in RR at 450 postnatal days. Only CC demonstrated differences in glucose sensitivity of β-cells to high and low doses at the three ages studied. At 36 days, RR, CR and RC and at 450 days RR and RC groups did not show glucose-stimulated insulin secretion differences between low and high glucose. Aging-associated glucose-stimulated insulin secretion loss was affected by maternal dietary history, indicating that developmental programming must be considered a major factor in aging-related development of predisposition to later-life dysfunctional insulin metabolism. Female offspring islets’ insulin secretion was higher than previously reported in males.

The objective of the present study was to investigate the changes in glucose and insulin metabolism in nutritionally stunted children that can be involved in the appearance of chronic diseases in adulthood. For this purpose, sixty-one children were selected, thirty-five boys and twenty-six girls, residents of slums in S˜o Paulo, Brazil. The children were classified according to the height-for-age as stunted (1·5 Z-score; n 21) or non-stunted (≥1·5 Z-score; n 40). The glucose and insulin plasma levels were determined and, from these values, the indexes that evaluate the pancreatic ·-cell function (homeostasis model assessment (HOMA-B)) and insulin sensitivity (HOMA-S) were assessed. Stunted children showed lower values of fasting insulin than those of the non-stunted group (boys: 29·7 (SD 14·9) v. 5=·4 (SD 29·2) pmol/l, P=·019; girls: 34·4 (SD 12·6) v. 62·3 (SD 28·7) pmol/l, P=·016) but the glucose levels were similar (boys: 4·6 (SD =·3) v. 4·5 (SD =·3) mmol/l; girls: 4·2 (SD =·3) v. 4·4 (SD =·3) mmol/l). Stunted children showed lower HOMA-B values (boys: 83 (SD 22) % v. 115 (SD 36) %, P=·011; girls: 107 (SD 23) % v. 144 (SD 46) %, P=·045) and higher HOMA-S values (boys: 196 (SD 92) % v. 120 (SD 62) %, P=·014; girls: 159 (SD 67) % v· 98 (SD 57) %, P=·016). The results show a decreased activity of μ-cell function and increased insulin sensitivity in stunted children. The decreased b-cell function of this group may strongly predict type 2 diabetes.