Experimental intrauterine growth retardation in the rat causes a reduction of pancreatic B-cell mass, which persists into adulthood

• <i>Background and Objectives:</i> The aim of this study was to investigate the possibility that intrauterine growth retardation (IUGR) causes alterations of glucose tolerance, insulin secretory response to glucose, and pancreatic B-cell growth, and if such changes may persist into adulthood. <i>Methods:</i> Pregnant rats were operated on day 16 of pregnancy ad modum Wigglesworth to induce IUGR. Operated rats gave birth to viable offspring but litter size was reduced. The mothers nursed their pups, which were subsequently weaned and reared to an age of 3 months in apparent good health. <i>Results:</i> At 1 day of age, IUGR pups were 10% lighter than control newborns whose mothers had been subjected to a sham operation. Pancreatic B-cell mass and insulin content were reduced by 35–40% in newborn IUGR offspring. Postnatal growth did not differ between IUGR and control animals of either sex and the difference in body weight at birth was not apparent from 1 week of age and onwards. Tests performed at 3 months of age could not demonstrate differences in glucose tolerance between IUGR and control animals. In females, but not in males, the peak insulin secretory response to glucose was lower in IUGR animals compared to controls. In the 3-month-old rats, B-cell mass was reduced by 40% in male and by 45% in female IUGR rats compared to controls, a reduction corresponding to a similar decrease in pancreatic insulin content (male reduction 48%, female reduction 45%). <i>Conclusions:</i> In the rat, IUGR causes a diminution of pancreatic B-cell mass which persists into adulthood. Normal glucose tolerance could be maintained but it is conceivable that increasing demands on insulin secretion may not be met by the reduced B-cell mass and that impaired glucose tolerance and even diabetes would hence develop.

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