Estradiol may limit lipid oxidation via Cpt 1 expression and hormonal mechanisms.
OBJECTIVE
Evidence indicates that estrogen depresses hepatic lipid oxidation. We tested the hypothesis that estradiol (E(2)) treatment depresses transcription of carnitine palmitoyltransferase-1 (Cpt 1) mRNA and increases adiposity.


METHODS
Six ovariectomized female rats were given a subcutaneous pellet of E(2) (5 mg/d), and six were given placebo. Rats were pair-fed by group for 18 days. Body composition was assessed chemically: mRNA for liver Cpt 1, adipose tissue uncoupling protein-2 (Ucp 2), and quadriceps Ucp 3 by Northern analysis; serum glucose, triglycerides (TGs), and free fatty acids by standard techniques; and serum insulin and glucagon by radioimmunoassay.


RESULTS
E(2)-treated rats lost more weight than placebo-treated rats (37.3 +/- 6.0 vs. 16.2 +/- 2.6 g, p < 0.01), but did not differ in final carcass composition (adjusted for eviscerated body mass). E(2)-treated rats had lower liver Cpt 1 (p < 0.001) and skeletal muscle Ucp 3 (p < 0.05) mRNA and lower concentrations of glucose, glucagon, and free fatty acids (p < 0.05). E(2)-treated rats tended to have higher insulin (p = -0.067) and TG (p = 0.097). TG tended to be correlated with Cpt 1 mRNA (r = -0.56 and p = 0.07).


CONCLUSIONS
These results suggest that, although E(2) is likely to suppress lipid oxidation and promote TG synthesis, these effects are not manifested in a relative increase in carcass adiposity after 18 days of treatment, at least under conditions of negative energy balance. The possible role of E(2)-mediated changes in insulin and glucagon secretion on hepatic substrate metabolism warrants further study.
Gower
Barbara A
BA
Department of Nutrition Sciences and Physiology, University of Alabama at Birmingham and the Clinical Nutrition Research Center, Birmingham, Alabama 35294-3360, USA. bgower@uab.edu
Nagy
Tim R
TR
Blaylock
Matthew L
ML
Wang
Chenxi
C
Nyman
Lara
L
D000818:Animals; D015152:Blotting, Northern; D001823:Body Composition / Q000502:physiology; D002334:Carnitine O-Palmitoyltransferase / Q000096:biosynthesis* / Q000235:genetics; D002352:Carrier Proteins / Q000097:blood; D004435:Eating / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005934:Glucagon / Q000097:blood*; D007328:Insulin / Q000097:blood*; D007473:Ion Channels; D050356:Lipid Metabolism; D008565:Membrane Proteins / Q000097:blood; D024101:Mitochondrial Proteins; D010084:Oxidation-Reduction; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood; D000071256:Uncoupling Protein 1
D002352:Carrier Proteins; D007328:Insulin; D007473:Ion Channels; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D014280:Triglycerides; D000071256:Uncoupling Protein 1; D004958:Estradiol; D005934:Glucagon; D002334:Carnitine O-Palmitoyltransferase