title: Maternal and fetal insulin-like growth factor system and embryonic survival during pregnancy in rats: interaction between dietary chromium and diabetes.
abstract: Chromium (Cr) depletion may exacerbate hyperglycemia and negative outcomes of pregnancy in the streptozotocin (STZ) diabetic pregnant rat model through the regulation of the insulin-like growth factor (IGF) system. To test this hypothesis, 40 female rats, all fed a low Cr diet (i.e., 70 microgram Cr/kg diet ) from 21 d of age, were randomly assigned one of four treatments, applied on Day 1 of pregnancy, in a 2 x 2 factorial design: 1) very low Cr diet (40 microgram Cr/kg diet) + citrate buffer injection, 2) very low Cr diet + STZ injection (30 mg STZ/kg body wt in citrate buffer), 3) adequate Cr diet (2 mg Cr [from added CrK(SO4)2]/kg diet) + citrate buffer injectionand 4) adequate Cr diet + STZ injection. Blood and tissues were collected on Day 20 of pregnancy. Chromium depletion increased (P < 0.05) urinary hydroxyproline excretion, 22-kDa IGF binding protein (IGFBP) concentration and litter size but decreased (P < 0. 05) placental wt, percentage of protein per fetus, and fetal IGF-I and -II concentrations. Chromium had no effect (P > 0.10) on maternal hormones, 32-kDa IGFBP, glucose, or placental and fetal hydroxyproline concentrations. Diabetes decreased (P < 0.05) maternal wt gain, embryonic survival, litter size, mean pup wt and maternal insulin concentrations, increased (P < 0.05) maternal blood glucose, IGF-I concentrations and maternal hydroxyproline excretion but did not affect fetal concentrations of hormones, IGFBP, glucose or hydroxyproline. Interaction between chromium and diabetes tended (P < 0.10) to affect maternal IGF-II concentrations, but had no effect on other maternal or fetal variables. In conclusion, maternal chromium depletion did not exacerbate hyperglycemia or pregnancy outcome in STZ-induced diabetic rats, but may negatively affect fetal protein content by decreasing fetal IGF-II concentrations. Diabetes may negatively affect fetal growth through its effect on maternal glucose, insulin and IGF-I.
authors.affiliation: Department of Nutritional Sciences, Oklahoma State University, Stillwater, OK 74078, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Spicer
authors.forename: B J
authors.initials: BJ
authors.lastname: Stoecker
authors.forename: T
authors.initials: T
authors.lastname: Chen
authors.forename: L J
authors.initials: LJ
authors.lastname: Spicer
mesh_terms: D000818:Animals; D002857:Chromium / Q000008:administration & dosage / Q000172:deficiency*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004032:Diet; D004305:Dose-Response Relationship, Drug; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D005260:Female; D005313:Fetal Death; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000187:drug effects* / Q000378:metabolism; D011247:Pregnancy; D011256:Pregnancy Outcome; D011257:Pregnancy Proteins / Q000378:metabolism; D011254:Pregnancy in Diabetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007328:Insulin; D011257:Pregnancy Proteins; D002857:Chromium; D007334:Insulin-Like Growth Factor I; D005947:Glucose