Estradiol may limit lipid oxidation via Cpt 1 expression and hormonal mechanisms.
Estradiol may limit lipid oxidation via Cpt 1 expression and hormonal mechanisms.
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DOI：
10.1038/oby.2002.26
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发表时间：
2002-03
期刊：
影响因子：
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通讯作者：
B. Gower;T. Nagy;Matthew L Blaylock;Chenxi Wang;Lara R Nyman
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文献类型：
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作者：
B. Gower;T. Nagy;Matthew L Blaylock;Chenxi Wang;Lara R Nyman
Objective:Evidence indicates that estrogen depresses hepatic lipid oxidation. We tested the hypothesis that estradiol (E2) treatment depresses transcription of carnitine palmitoyltransferase‐1 (Cpt 1) mRNA and increases adiposity.Research Methods and Procedures:Six ovariectomized female rats were given a subcutaneous pellet of E2(5 mg/d), and six were given placebo. Rats were pair‐fed by group for 18 days. Body composition was assessed chemically: mRNA for liverCpt 1, adipose tissue uncoupling protein‐2 (Ucp 2), and quadricepsUcp 3by Northern analysis; serum glucose, triglycerides (TGs), and free fatty acids by standard techniques; and serum insulin and glucagon by radioimmunoassay.Results:E2‐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). E2‐treated rats had lower liverCpt 1(p< 0.001) and skeletal muscleUcp 3(p< 0.05) mRNA and lower concentrations of glucose, glucagon, and free fatty acids (p< 0.05). E2‐treated rats tended to have higher insulin (p= −0.067) and TG (p= 0.097). TG tended to be correlated withCpt 1mRNA (r= −0.56 andp= 0.07).Discussion:These results suggest that, although E2is 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 E2‐mediated changes in insulin and glucagon secretion on hepatic substrate metabolism warrants further study.
