Farid F. Chehab, PhD
UCSF
Laboratory Medicine, Box 0134
185 Berry Street, Suite 290
San Francisco, CA 94143
United States
- Diabetes and Endocrinology Research Center (DERC)
- Institute of Human Genetics
My research activities are aimed at understanding novel signaling pathways in preadipocytes and adipocytes using cell culture and mouse models. More specifically, we are interested in the roles of the FoxO family of forkhead transcription factors in lipid metabolism and how they impact on triacylglycerols accumulation. Other activities include the characterization of the mechanisms that allow transgenic mice overexpressing leptin to transition from a fatless to fat accumulating state as a result of aging or a high fat diet. Clinical research is aimed at the continuous development and implementation of novel molecular diagnostics assays and monitoring their impact on patient care and prognosis.
- Chehab, F.F. Lim, M.E. and Lu, R. Correction of the sterility defect in homozygous obese female mice by treatment with the recombinant human leptin. Nature Genetics 12:318-320, 1996.
- Chehab, F.F., Mounzih, K., Lu, R., Lim, M.E. Early onset of reproductive function in normal female mice treated with leptin. Science 275: 88-90, 1997.
- Qiu, J., Ogus, S., Lu, R., Chehab, F.F. Transgenic mice overexpressing leptin accumulate adipose mass at an older but not younger age. Endocrinology 142:348-358, 2001
- Ogus, S, Ke, Y, Qiu ,J, Wang, B., Chehab, F.F. Hyperleptinemia precipitates diet induced obesity in transgenic mice overexpressing leptin. Endocrinology 44:2865-2869, 2003.
- Han, X.D, Powell, B.R, Phalin, J.L, Chehab, F.F. Mosaicism for a full mutation, premutation, and deletion of the CGG repeats results in 22% FMRP and elevated FMR1 mRNA levels in a high-functioning fragile X male. Am. J. Med. Genet. 140:1463-71, 2006