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Updated: May 4, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive
Cleto Alvarez-Aguilar1, Alfonso Rafael Alvarez-Paredes2, Bengt Lindholm3
1Hospital General Regional N°1, Instituto Mexicano del Seguro Social (IMSS), Morelia, México ; Facultad de Ciencias Médicas y Biológicas "Dr. Ignacio Chávez" Universidad Michoacana de San Nicolás de Hidalgo (UMSNH), Morelia, Michoacán, México ; División de Estudios Superiores, Universidad Nacional Autónoma de México (UNAM), México DF, México.
Background:
A reduction of dopaminergic (DAergic) activity with increased prolactin levels has been found in obese and hypertensive patients, suggesting its involvement as a pathophysiological mechanism promoting hypertension. Similarly, leptin action increasing sympathetic activity has been proposed to be involved in mechanisms of hypertension. The aim of this study was to analyze the effects of DA, norepinephrine (NE), and prolactin on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients.
Methods:
Leptin release and OB gene expression were analyzed in cultured adipocytes from 16 obese and hypertensive patients treated with DA (0.001, 0.01, 0.1, and 1.0 μmol/L), NE (1.0 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L), and from five nonobese and normotensive controls treated with DA (1 μmol/L), NE (1 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L).
Results:
A dose-related reduction of leptin release and OB gene messenger ribonucleic acid expression under different doses of DA was observed in adipocytes from obese hypertensive patients. Whereas prolactin treatment elicited a significant increase of both leptin release and OB gene expression, NE reduced these parameters. Although similar effects of DA and NE were observed in adipocytes from controls, baseline values in controls were reduced to 20% of the value in adipocytes from obese hypertensive patients.
Conclusion:
These results suggest that DAergic deficiency contributes to metabolic disorders linked to hyperleptinemia in obese and hypertensive patients.
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