Abstract Adipose tissue is a critical endocrine mediator of metabolic health that is functionally altered during aging and obesity. Our data demonstrate that dietary protein restriction (DPR) increases whole body glucose homeostasis and energy expenditure and protects against age-related metabolic decline, and that these metabolic effects are associated with a remodeling of white adipose tissue that includes increased thermogenic markers and adiponectin secretion. This project tests the hypothesis that the remodeling of adipose tissue during dietary protein restriction directly improves metabolic health during aging. This model will be tested by assessing the transcriptional and cell signaling pathways in adipose tissue that contribute to glucose homeostasis and insulin sensitivity and determining which of these are altered during DPR in an age- dependent fashion. Lastly, we will test whether increases in adiponectin contribute to whole body improvements in glucose homeostasis during protein restriction, and whether using adipose tissue grafts from protein restricted mice combats age-related insulin resistance in an adiponectin-dependent manner.

Project Narrative Adipose tissue is a critical endocrine mediator of metabolic health that is functionally altered during aging and obesity. Our preliminary data demonstrate that dietary protein restriction (DPR) improves metabolic health and remodels adipose tissue. This application tests the hypothesis that the remodeling of adipose tissue during dietary protein restriction directly improves metabolic health during aging.