Room 309 Crowe Research Building
(901) 448-6009
FAX (901) 448-7300
sbahouth@utmem.edu

Education:

American University of Beirut, Lebanon. B.S. in Pharmacy 1975 with distinction.
New York University, New York, NY Ph.D. 1985, Pharmacology
SUNY at Stony Brook, Stony Brook, NY Post-doctoral training, 1984, Pharmacology & Molecular Biology.

Research Interests:

1. Genomics and proteomics of G protein-coupled receptors (GPCR).
The GPCR is one of the most numerous protein motifs in the mammalian genome. This superfamily is characterized by a seven transmembranal loop motif, and is involved in linking the inside of the cell to the outside environment. Our research group has been involved in elucidating the mechanisms of genetic regulation of the GPCR family using the ß1-adrenergic receptor gene as the model. The ß1-adrenergic receptor mediates the effects of catecholamines on heart rate and on the force of myocardial contractions. By fusing different promoter elements of the rat ß1-adrenergic receptor gene to luciferase, we determined that the core promoter of the ß1-adrenergic receptor is a relatively strong promoter. However, since the expression of ß1-adrenergic receptor mRNA is very low, suppressor sequences that lie 5’ and 3’ to the transcriptional start site inhibit the expression of the ß1-adrenergic receptor gene. Future studies aim to identify the inhibitory sequences and their mechanisms of suppression.
2. Mechanisms of human obesity:
Obesity is the leading cause of metabolic diseases in the U.S., and roughly one third of the U.S. population is obese. Leptin is a 19,000 Mr protein that is secreted by white adipocytes. A lack of functional leptin is a molecular defect that results in obesity and diabetes. The factors involved in regulating the secretion of leptin from morbidly-obese human adipose tissue are unknown. The roles of the immune system, prostaglandins and the cyclooxygenase-2 enzyme are under active investigation.

Selected publications:

Bahouth, S.W., X. Cui, M.J. Beauchamp, H. Shimomura, S.T. George, and E.A. Park. Promoter analysis of the rat _1-adrenergic receptor gene identifies sequences involved in basal expression. Mol. Pharmacol., 51:620-629, 1997.

Bahouth, S.W., M.J. Beauchamp, and E.A. Park. Identification of a retinoic acid response domain involved in the activation of the _1-adrenergic receptor gene by retinoic acid in F9 teratocarcinoma cells. Biochem. Pharmacol. 55:215-255, 1998.

Fain, J.N., and S.W. Bahouth. Effect of tri-iodothyronine on leptin release and leptin mRNA accumulation in rat adipose tissue. Biochem. J., 332: 361-366,1998.

Fain, J.N., Ihle, J.H., and S.W. Bahouth. Stimulation of lipolysis but not leptin release by growth hormone is abolished in adipose tissue from STAT5a/b-/- Knockout mice. Biochem. Biophys. Res. Comm. 263:201-205, 1999.

Fain, J.N., and S.W. Bahouth.Regulation of leptin biosynthesis in mammalian adipose tissue. Biochem. Biophys. Res. Comm. 274, 571-575, 2000.