Developmental origins of adult obesity
Research DescriptionDr. Ross, alongside fellow LA BioMed researcher, Mina Desai, PhD, 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.
- BS, 1974, Massachusetts Institute of Technology, Cambridge, MA
- MD, 1978, Harvard Medical School, Cambridge, MA
- MPH, 1978, Harvard School of Public Health, Cambridge, MA
Recent and/or Significant Publications
- Desai M, Li T, Han G, Ross MG. (2014). Programmed hyperphagia secondary to increased hypothalamic SIRT1. Brain Res, 1589, 26-36.
- 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.