Syed A. Latif, Ph.D.

Associate Director of Chemistry, Lifespan AMC
Associate Professor (Clinical) of Pathology
slatif@lifespan.org
T: 401 793-4272
F: 401 274-5152

The Miriam Hospital
Dept of Pathology and Lab Medicine
164 Summit Ave.
Providence, RI 02906

Graduate education:

M.Sc. in Biochemistry, University of Karachi, Pakistan - 1966
M.S. in Biochemistry, University of Connecticut - 1969
Ph.D. in Biochemistry, University of Rhode Island - l976
Biochemistry, Microbiology, Metabolism, Endocrinology and Clinical Chemistry

Board certification:

Clinical Chemist (National Registry in Clinical Chemistry)

Research interests:

Collaborators: Drs. David J. Morris and Mathew P. Hardy
Regulation of Steroid Hormones and their Metabolites and their mechanism of actions; of particular interest related to Androgens, Progestogens, Glucocorticoids and Mineralocorticoids

Our main interest is in the study of regulation of metabolism of adrenal steroids in salt balance and hypertension. We are studying adrenal steroids and their metobolites on the hypertensinogenic effects and their antinatriuretic and/or kaliuretic renal effects in rats.

We have also shown the presence of endogenous substances in human urine which inhibit 11b-hydroxysteroid dehydrogenase and steroid 5b-reductase and may be involved in salt balance and hypertension. In an on-going program we have isolated and we are in a process of chemically characterizing these endogenous substances present in Low-Renin/High-Renin Hypertension in human urine and in other pathalogical conditions.

Recently, we have been studying the expanded role of endogenous inhibitors of 11ß-HSD1 in the regulation of Androgen synthetic pathway in Rat leydig cell. The goal of this project is to study the mechanism of glucocorticoids in the supression of androgen synthesis. In collaboration with Dr. Mathew Hardy ( Population Council, New York), we have recently shown that rat leydig cell do express and synthesize 11ß-hydroxylase. We have also demonstrated that 11ß-hydroxlated- and 11keto-metabolites of progesterone and testosterone are potent inhibitors of 11ß-HSD1 for dehydrogenase and oxidoreductase activities, respectively. Thus, rat leydig cell would be a good model to study the role of glucocorticoid and 11ß-HSD1 in the regulation of androgen levels.

Current approved research grants:

Sub-contract (collaboration) of a NIH Grant.

Most recent significant publications:

Wang, G.-M, GE, R-S, Latif, S.A, Morris, D.J, and Hardy, M.P. 2002. Expression 11ß-hydroxylase in Rat Leydig cells. Endocrinol. 143, 621-626.

Latif, S.A., Sheff, M.F., Ribeiro, C.E., and Morris, D.J. 1997. Selective inhibition of sheep kidney 11ß-hydroxysteroid dehydrogenase isoform 2 activity by 5a-reduced (but not 5ß-) derivatives of adrenocorticosteroids. Steroids 62:230-237.