Previous work in humans and rats has revealed a link between perinatal growth retardation and
glucose intolerance in adulthood. Both maternal semistarvation and severe diabetes are accompanied by perinatal growth retardation in rats. In this study, we compared the effect of these conditions on tissue
glucose uptake in their female offspring.
Glucose uptake was measured as
glucose metabolic index (GMI), using 2-deoxy-[1-3H]-
glucose, in the postabsorptive state and during euglycemic
hyperinsulinemia. The GMI was measured in
insulin-sensitive tissues (5 skeletal muscles, diaphragm and white adipose tissue) and in two noninsulin-sensitive tissues (duodenum and brain) of adult offspring of normal dams, dams rendered diabetic with
streptozotocin on d 11 of pregnancy, and dams fed half normal rations from d 11 of pregnancy. Whole-body
insulin resistance, measured by decreased
glucose infusion rate during
hyperinsulinemia, was milder in offspring of semistarved rats (O-SR) than in offspring of diabetic rats (O-DR). The basal GMI did not differ among the three groups in any tissue except tibialis anterior; during
hyperinsulinemia, GMI was significantly greater in the
insulin-sensitive tissues of all three groups. GMI of skeletal muscles and adipose tissue during
hyperinsulinemia did not differ between control rats and O-SR; in contrast, the GMI was 25-50% lower in skeletal muscles of O-DR during
hyperinsulinemia than in those of control rats or O-SR. Thus, maternal semistarvation and diabetes have dissimilar effects on peripheral
insulin sensitivity of the adult female offspring. Because both conditions are associated with perinatal growth retardation and fetal hypoinsulinemia, other mechanisms must be identified to explain impaired
glucose uptake by skeletal muscles in the offspring of diabetic rats.