Maternal Semistarvation and Streptozotocin-Diabetes in Rats Have Different Effects on the In Vivo Glucose Uptake by Peripheral Tissues in Their Female Adult Offspring

Abstract

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.

Adiposity in children born small for gestational age

“…16 Basically, similar observations have been made in sheep, although at different times postnatally, giving a strong support to the hypothesis that both low insulin secretion and insulin resistance contribute to impair glucose homeostasis after IUGR.…”

“…Intrauterine growth retardation (IUGR) can be induced in experimental animal models by energy restriction, 16 or by feeding an isoenergetic low-protein diet [17][18] during pregnancy. Decreased foetal nutritional delivery can also be induced by ligation of uterine arteries of pregnant rats.…”

Induction of diabetes by Streptozotocin in rats

“…The biochemical mechanism results in mammalian cell death. Streptozotocin prevents cellular reproduction with a much smaller dose than the dose needed for inhibiting the substrate connection to the DNA or inhibiting many of the enzymes involved in DNA synthesis (10). Although Streptozotocin prevents entry of cells into mitosis but no special phase of the cellular cycle is especially sensitive to its mortal effects.…”

“…If the environment of the rats is kept clean, there will be a change of color from white to pink. Otherwise, the change will be from white to gray (10). Pancreatic biopsy of normal and diabetic rats confirmed that the islet cells were Table.1 Shows data …”

Bone Marrow-Derived Mesenchymal Stem cells Infusion Ameliorates Hyperglycemia, Dyslipidemia, Liver and Kidney Functions in Diabetic Rats

“…This may be due to STZ impairs liver function, thus leading to leakage of these enzymes in the blood by STZ due to prevention of DNA synthesis in mammalian cells and prevents cellular reproduction by inhibiting the substrate binding to the DNA or inhibiting many of the enzymes involved in DNA synthesis [60]. Waer and Helmy [61] revealed that, diabetic hepatic injuries results from several agents and is not controllable only via inhibition of hyperglycemia.…”