Sex Steroid Modulation of Fatty Acid Utilization and Fatty Acid Binding Protein Concentration in Rat Liver

Ockner, Robert K.; Lysenko, N.; Manning, Joan A.; Monroe, Scott M.; Burnett, David

doi:10.1172/jci109753

Cited by 118 publications

(36 citation statements)

References 37 publications

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“…This proposal is supported by in vitro studies showing that pharmacological concentrations of estrogen reduce ketogenesis (a product of fatty acid oxidation) and increase fatty acid incorporation into triglycerides (29,30). These in vitro findings are in accordance with clinical observations that oral but not transdermal estrogen therapy stimulates hepatic triglyceride synthesis and increases triglyceride levels (31).…”

Section: Discussionsupporting

confidence: 78%

The route of estrogen replacement therapy confers divergent effects on substrate oxidation and body composition in postmenopausal women.

O’Sullivan¹,

Crampton²,

Freund³

et al. 1998

J. Clin. Invest.

197

140

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The route of estrogen replacement therapy has a major impact on the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis. Estrogen administration by the oral, but not the transdermal route, reduces IGF-I and increases GH levels in postmenopausal women. To investigate whether these perturbations have metabolic consequences, we compared the effects of 24 wk each of oral (Premarin 1.25 mg) and transdermal (Estraderm 100TTS) estrogen on energy metabolism and body composition in 18 postmenopausal women in an open-label randomized crossover study. Energy expenditure, lipid oxidation (lipid ox ), and carbohydrate oxidation (CHO ox ) were measured by indirect calorimetry in the fasted and fed state before and after 2 and 6 mon treatment. Lean body mass, fat mass, and total body bone mineral density were measured by dual X-ray absorptiometry before and after 6 mon treatment.Mean ( Ϯ SE) Luteinizing hormone levels fell to comparable levels during oral and transdermal estrogen, and bone mineral density was significantly increased by both treatments. Mean IGF-I was significantly lower during oral estrogen (77 Ϯ 7 versus 97 Ϯ 7 g/liter, P Ͻ 0.05) treatment.

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Section: Discussionsupporting

confidence: 78%

The route of estrogen replacement therapy confers divergent effects on substrate oxidation and body composition in postmenopausal women.

O’Sullivan¹,

Crampton²,

Freund³

et al. 1998

J. Clin. Invest.

197

140

View full text Add to dashboard Cite

show abstract

“…Oral estrogen treatment has been demonstrated to decrease lipid oxidation in a dose-dependent manner in humans (22), and has been shown to reduce ketogenesis (a by-product of hepatic lipid oxidation) in cell culture studies (23). E 2 action in the liver therefore likely involves channeling FFAs from oxidative to nonoxidative pathways (primarily VLDL-TG production).…”

Section: Discussionmentioning

confidence: 99%

Acute estrogen exposure does not affect basal very low-density lipoprotein–triglyceride production or oxidation in postmenopausal women

Gormsen¹,

Høst²,

Hjerrild³

et al. 2010

European Journal of Endocrinology

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Context: Long-term hormone replacement therapy (HRT) with estradiol (E 2 ) is associated with an altered lipid profile including unfavorable increases in triglyceride (TG) concentrations and augmented hepatic very low-density lipoprotein (VLDL)-TG production. There are indications that this effect of estrogens may be immediate. Objective: To study the in vivo effect of a single dose of E 2 on VLDL-TG kinetics and oxidation in humans. Methods: Eight healthy, postmenopausal women were given a single dose of either placebo or E 2 (4 mg) orally. VLDL-TG kinetics was assessed by a 240-min primed-continuous infusion of ex vivo labeled [1-14 C]triolein-labeled VLDL. Fractional and absolute VLDL-TG oxidation was determined by hyamin trapping of exhaled 14 C label. Indirect calorimetry provided measurements of lipid oxidation. Results: Administration of 4 mg of E 2 orally rapidly increased plasma E 2 concentrations from below detection threshold to premenopausal levels. Free fatty acids (FFA) and TG concentrations were unaltered. No immediate effect was observed on either VLDL-TG production (placebo versus E 2 ): 20.0G12.4 vs 24.1G10.7 mmol/min, PZ0.33; VLDL-TG oxidation: 12.3G10.9 vs 12.6 G5.6 mmol/min, PZ0.93); or VLDL-TG clearance rates: 51.4G16.8 vs 64.9G28.8 ml/min, PZ0.34). Conclusions: Short-term E 2 elevation does not affect VLDL-TG production, oxidation, or clearance in humans. We therefore propose that HRT-associated dyslipidemia has a gradual rather than immediate onset.

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“…The gender infl uence on FABP1 corresponds to the effects of sex steroid hormones. Testosterone decreases, whereas estrogen increases, FABP1 levels in rats ( 32 ). The higher level of FABP1 in female rats, as well as the increased FABP1 content in male animals treated by clofi brate, is not related to differences in the turnover rate of FABP1, but appears to be correlated with an increased content of tissue FABP1 mRNA ( 33 ).…”

mentioning

confidence: 99%

Recent insights into the biological functions of liver fatty acid binding protein 1

Wang

Bonkovsky

Lemos

et al. 2015

Journal of Lipid Research

194

175

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Sex Steroid Modulation of Fatty Acid Utilization and Fatty Acid Binding Protein Concentration in Rat Liver

Abstract: A B S T R A C T The mechanism by which sex steroids influence very low density hepatic lipoprotein triglyceride production has not been fully elucidated. In previous studies we showed that ['4C]

Cited by 118 publications

References 37 publications

The route of estrogen replacement therapy confers divergent effects on substrate oxidation and body composition in postmenopausal women.

The route of estrogen replacement therapy confers divergent effects on substrate oxidation and body composition in postmenopausal women.

Acute estrogen exposure does not affect basal very low-density lipoprotein–triglyceride production or oxidation in postmenopausal women

Recent insights into the biological functions of liver fatty acid binding protein 1

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