Year: 2007
Type: article
Abstract: Chronic ethanol consumption induces hepatic steatosis and represents an independent risk factor for type 2 diabetes, associated with the disruption of lipid and glucose homeostasis.Adipose tissue acts as a regulator for maintaining whole-body lipid and glucose homeostasis; therefore, it was hypothesized that lipid and glucose homeostasis in adipose tissue might be vulnerable to chronic ethanol exposure.Increases in lipolysis, and the resulting release of free fatty acids into the circulation, have been associated with the development of insulin resistance and liver injury in other model systems.Therefore, the effects of chronic ethanol feeding on regulation of triglyceride metabolism in adipose tissue were first investigated.The current study has demonstrated that chronic ethanol feeding to rats increased the turnover rate of triglycerides in epididymal adipose tissue; the rate of triglyceride synthesis was increased 1.9-fold and the rate of triglyceride degradation was increased 3.1-fold over pair-fed controls.Triglyceride degradation is stimulated by β-adrenergic receptor activation and inhibited by insulin.Since chronic ethanol increased the rate of triglyceride degradation, it was first hypothesized that the lipolytic responses of adipocytes to β-adrenergic receptors was increased by chronic ethanol.However, chronic ethanol feeding actually xvi
Author: Li Kang
Institution: Case Western Reserve University
Language: English
Subfield: Biochemistry
Domain: Life Sciences
Open Access status: green
Funder: National Institutes of Health
OpenAlex ID: W2223604495