Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015:2015:294278.
doi: 10.1155/2015/294278. Epub 2015 Sep 27.

Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis

Minqian Shen  1 , Haifei Shi  1
Affiliations
Review

Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis

Minqian Shen et al. Int J Endocrinol. 2015.

Abstract

The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver. In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism. In males, testosterone works via androgen receptors to increase insulin receptor expression and glycogen synthesis, decrease glucose uptake and lipogenesis, and promote cholesterol storage in the liver. These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Action of estrogens and androgens via estrogen receptors (ERs) and androgen receptors (ARs) in the liver cells. (a) Genomic effects of estrogens and androgens via nuclear ERs and ARs. (b) Nongenomic effects of estrogens and androgens via membrane-associated ERs and ARs.
Figure 2
Figure 2
Metabolic effects of estrogens and androgens on regulation of lipid, glucose, and cholesterol in the liver.
See this image and copyright information in PMC

References

    1. Martensson U. E. A., Salehi S. A., Windahl S., et al. Deletion of the G protein-coupled receptor 30 impairs glucose tolerance, reduces bone growth, increases blood pressure, and eliminates estradiol-stimulated insulin release in female mice. Endocrinology. 2009;150(2):687–698. doi: 10.1210/en.2008-0623. - DOI - PubMed
    1. Alberti K. G. M. M., Zimmet P., Shaw J. Metabolic syndrome—a new world-wide definition. A consensus statement from the International Diabetes Federation. Diabetic Medicine. 2006;23(5):469–480. doi: 10.1111/j.1464-5491.2006.01858.x. - DOI - PubMed
    1. Home P. D., Pacini G. Hepatic dysfunction and insulin insensitivity in type 2 diabetes mellitus: a critical target for insulin-sensitizing agents. Diabetes, Obesity and Metabolism. 2008;10(9):699–718. doi: 10.1111/j.1463-1326.2007.00761.x. - DOI - PubMed
    1. Perry R. J., Samuel V. T., Petersen K. F., Shulman G. I. The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes. Nature. 2014;510(7503):84–91. doi: 10.1038/nature13478. - DOI - PMC - PubMed
    1. Carr M. C. The emergence of the metabolic syndrome with menopause. Journal of Clinical Endocrinology and Metabolism. 2003;88(6):2404–2411. doi: 10.1210/jc.2003-030242. - DOI - PubMed