Desai M, Li T, Han G, Ross MG. (2014). Programmed hyperphagia secondary to increased hypothalamic SIRT1. Brain Res, 1589, 26-36.
Mina Desai, PhD
Investigator, The Lundquist Institute
Associate Professor of Obstetrics & Gynecology, David-Geffen School of Medicine at UCLA
Developmental origins of adult obesity
Research DescriptionDr. Desai, alongside fellow Lundquist researcher, Michael G. Ross, MD, MPH, investigates the mechanisms of developmental origins of obesity using rodent models of maternal under- and over-nutrition as well as exposure to environmental chemical endocrine disruptors (e.g., bispheol A) during pregnancy and/or lactation. They study the offspring using multiple approaches that include stem cells, epigenetics, gene expression, cellular signaling, physiology and transgenic mice. Their two main areas of research include:
1) Role of appetite in programmed obesity – investigating the properties of neural stem cells that populate and develop arcuate nucleus center (appetite regulatory site) and the underlying contributory mechanism.
2) Role of adipogenesis in programmed obesity - investigating the properties of adipocyte stem cells and the mechanisms which predispose to increased fat storage.
- BSc (Honors), 1987, Maharaja Sayajirao University, Baroda, India
- MSc (Honors), 1989, Maharaja Sayajirao University, Baroda, India
- PhD, 1996, University of Cambridge, Cambridge, UK
Recent and/or Significant Publications
Desai M, Jellyman JK, Han G, Lane RH, Ross MG. (2015) Programmed regulation of rat offspring adipogenic transcription factor (PPARγ) by maternal nutrition. J Dev Orig Health Dis 6:530-8.
Desai M, Han G, Ross MG. (2016) Programmed Hyperphagia in Offspring of Obese Dams: Altered Expression of Hypothalamic Nutrient Sensors, Neurogenic Factors and Epigenetic Modulators. Appetite 99:193-199.
Desai M, Ferrini MG, Han G, Jellyman JK, Ross MG. (2018) In vivo maternal and in vitro BPA exposure effects on hypothalamic neurogenesis and appetite regulators. Environ Res. Jul;164:45-52.