Masters Theses

Date of Award

8-2000

Degree Type

Thesis

Degree Name

Master of Science

Major

Nutrition

Major Professor

Naima Moustaid Moussa

Committee Members

Jay Whelan, James Bailey

Abstract

Adipose tissue functions as a secretory organ. Adipocyte-derived All and prostaglandins are involved in promotion of adipocyte hyperplasia through enhancement of preadipocyte differentiation as well as adipocyte hypertrophy. All was proposed to regulate adipocyte differentiation in part via prostacyclin. The peptide hormone leptin encoded by the ob gene is produced primarily by adipocytes and is believed to be the signal indicating the level of adiposity. We have previously demonstrated that All increases ob gene transcription in adipocytes. In this study, we have examined mechanisms of All effect on leptin secretion in adipocytes. All at physiological concentrations significantly increased leptin secretion in human adipose tissue and 3T3-Ll adipocytes in a dose and time response manner. Consistently, 6-keto PGF1a (a stable degradation product of PGI2) and PGE2 secretions were also significantly stimulated by physiological doses of AII. Inhibitors of prostaglandin biosynthesis, namely indomethacin and aspirin significantly blocked basal as well as All-induced prostaglandin synthesis. However, inhibition of prostaglandin synthesis by these inhibitors did not modify All-induced leptin secretion. Consequently, these findings demonstrate that All regulation of leptin secretion from adipocytes is independent of prostaglandin.

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