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RESEARCH

Dr. Prashant Rajbhandari's laboratory uses molecular biology, biochemistry, and genomic science to study lipid metabolism. Dr. Rajbhandari completed his doctoral studies at the University of Wisconsin-Madison, where he elucidated how structural changes in the unstructured region of Estrogen Receptor-alpha increase its ligand-independent transcriptional function to promote drug resistance in breast cancer. An intriguing relationship between metabolism and cancer led him to pursue postdoctoral studies in the Lab of Dr. Peter Tontonoz, MD, PhD in the Howard Hughes Medical Institute (HHMI) at the University of California-Los Angeles (UCLA). At UCLA, his interests broadly focused on understanding lipid metabolism, particularly in adipose tissues, and how it affects adipocytes and hepatic and cardiovascular function. He discovered immune-adipocyte crosstalk in the adipose microenvironment that limits mitochondrial respiration, energy expenditure, and lipid mobilization and blocks the adipose tissue's thermogenic transcriptional program. He pioneered using snRNA-seq to study mature adipocyte heterogeneity and mammary duct and adipocyte crosstalk. His works are published in Nature,  Cell, Nature Medicine, Nature Metabolism, Journal of Clinical Investigation, eLIFE, Cell Metabolism, and Nature Chemical Biology. The NIH has recognized his work as meritorious: he received an NRSA F32 individual postdoctoral training grant and a prestigious K99/R00 Transition to Independence Award and R01 grants recently to support his work from NIDDK. His lab in DOMI at Mt. Sinai will focus on identifying and studying novel factors that control lipid metabolism using a combination of genetics, cell biology, biochemistry, and Next-Gen sequencing.

White adipose tissue (WAT) stores energy as triglycerides and releases free fatty acids in times of metabolic requirement. WAT dysfunction contributes to metabolic disorders such as type 2 diabetes and insulin resistance. At molecular level, there are cascades of biochemical and transcriptional events that orchestrate the formation of WAT, a process known as adipogenesis. We are interested in learning about the transcriptional basis of adipogenesis utilizing Next Generation Sequencing and Data analysis techniques

Brown adipose tissue (BAT) dissipates stored chemical energy in the form of heat through the induction of thermogenic genes such as Ucp1. BAT mass inversely correlates with body mass index and has been ascribed an anti-obesity function. Recent studies have revealed the ability of WAT to activate a subpopulation of cells in inguinal WAT (iWAT) known as “beige” cells express UCP1 and carries out thermogenesis. Our research interest is focused on how this process occurs and how local and systemic factors affect this process.

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B3-AR agonist

Control

scRNA-Seq on ADIPOSE IMMUNE CELLS

The immune system plays a vital role in metabolic homeostasis. Immune cells are in constant talk with its host tissue to maintain balance in metabolism. Using the power of single cell RNA-Sequencing, we are interested in understanding perturbations in the gene program and cell types of peripheral tissue adaptive and innate immune system under dietary and metabolic stress. 

Liver plays a key role in lipid metabolism. It is a hub for glucose, triglyceride, cholesterol, and fatty acid metabolism. We are interested in identifying new factors in regulating lipid metabolism in the liver

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