title: Maternal hypothyroidism during the first half of gestation compromises normal catabolic adaptations of late gestation in the rat.
abstract: Female rats were mated and thyroidectomized on the same day. Some animals were kept without treatment and killed on day 12 or 21 of gestation (T). Others were subsequently treated daily with 1.8 micrograms L-T4/100 g BW for either the first 12 days and then not treated from that time until day 21 [T+T4(I+0)] or else not treated for the first 12 days and then treated from days 12-21 [T+T4(0+II)]. A final group received treatment during the entire 21-day study [T+T4(I+II)] and was used as the control. The net maternal body weight increased until day 12 of gestation in T+T4(I+II) rats, but not in T animals. On day 21 net maternal body weight was significantly lower in T and T+T4(0+II) than in T+T4(I+II) rats. Lipoprotein lipase activity in the lumbar fat pads increased from days 0 to 12 of gestation and decreased on day 21, whereas in the heart the change was in the opposite direction, and these changes were greater in T+T4(I+II) rats than in T rats. Incorporation of [U-14C]glucose administered in vivo into liver [14C]fatty acids or [14C]glycogen was significantly lower in T rats than in T+T4(I+II) on either the 12th or 21st day of gestation. The response of plasma triglyceride, glycerol, or beta-hydroxybutyrate levels to 24 h of starvation was similar in 12-day pregnant rats regardless of whether they were treated with T4, whereas on day 21 the change was greater in T+T4(I+II) or T+T4(I+0) animals than in T or T+T4(0+II) animals. Results show that maternal hypothyroidism during the first half of gestation impaired the anabolic events occurring during this phase and compromised the normal catabolic response during late gestation even when T4 treatment was restored. However, once maternal metabolic stores were built up normally during the first half of gestation, maternal hypothyroidism during late gestation did not affect the mother's normal metabolic adaptation, including the accelerated response to starvation.
authors.affiliation: Departamento de Investigación, Hospital Universitario Ramón y Cajal, Universidad de Alcalá de Henares, Madrid, Spain.
authors.forename: B
authors.initials: B
authors.lastname: Bonet
authors.forename: E
authors.initials: E
authors.lastname: Herrera
mesh_terms: D000273:Adipose Tissue / Q000201:enzymology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D007037:Hypothyroidism / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008071:Lipoprotein Lipase / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology; D011247:Pregnancy; D011248:Pregnancy Complications; D051381:Rats; D011919:Rats, Inbred Strains; D013217:Starvation / Q000378:metabolism; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D013997:Time Factors; D015430:Weight Gain
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin; D013972:Thyrotropin; D006003:Glycogen; D008071:Lipoprotein Lipase; D005947:Glucose; D013974:Thyroxine