title: 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.
authors.affiliation: Department of Obstetrics and Gynecology, Katholieke Universiteit Leuven, Leuven, Belgium.
authors.forename: K
authors.initials: K
authors.lastname: Holemans
authors.forename: R
authors.initials: R
authors.lastname: Van Bree
authors.forename: J
authors.initials: J
authors.lastname: Verhaeghe
authors.forename: K
authors.initials: K
authors.lastname: Meurrens
authors.forename: F A
authors.initials: FA
authors.lastname: Van Assche
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D004435:Eating / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism / Q000493:pharmacokinetics*; D015309:Glucose Clamp Technique; D006128:Growth / Q000502:physiology; D006946:Hyperinsulinism / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D008431:Maternal-Fetal Exchange; D018482:Muscle, Skeletal / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism* / Q000503:physiopathology; D011254:Pregnancy in Diabetics / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013217:Starvation / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D013311:Streptozocin; D015430:Weight Gain / Q000502:physiology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D013311:Streptozocin; D005947:Glucose