International webinar on Autophagy and regulation of metabolism

Event Details

Autophagy is a cellular recycling program that maintains quality control by degrading unwanted cytoplasmic contents in acidic organelles called lysosomes. Autophagy occurs at basal levels in all cells and is induced during starvation and stress. Autophagy requires greater than ~30 ATG proteins to orchestrate the de novo formation of a double-walled limiting membrane that sequesters cargo destined for degradation and seals upon itself to form an autophagosome. The delivery of the engulfed cargo to lysosomes by autophagosome-lysosome fusion results in cargo degradation. 

The Focus of Dr. Singh’s laboratory is to examine the organ-specific roles of autophagy in the integrative regulation of lipid and energy metabolism using complementary approaches in mouse models. Our interests lie in understanding how autophagy controls energy, glucose, and lipid metabolism in a time‑, diet‑, and age-dependent manner. The Second Focus of the laboratory is to examine the consequences of aging-associated reduction of autophagy on the development of the metabolic syndrome. 

Dr. Singh’s lab is interested in understanding how autophagy decreases with age, and whether restoration of autophagy prevents the metabolic syndrome of aging. To that end, Dr. Singh has recently established an Isocaloric twice-a-day (ITAD) feeding intervention in mice that stimulates autophagy and prevents the metabolic syndrome of aging. Major benefits of ITAD feeding are — improved glucose tolerance, lower lipids levels, and increased muscle mass. Using different mice that lacked autophagy in POMC neurons or liver or fat tissue or myogenic progenitors, we have found that autophagy in different tissues contributes to distinct benefits of ITAD feeding. Given the positive outcomes of ITAD feeding in mice, Dr. Singh’s lab is currently collaborating with Dr. Jill Crandall (Division Chief, Endocrinology) to determine whether ITAD feeding will prevent the metabolic syndrome of aging by stimulating autophagy in human subjects.

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