Project Grant R01DK146220

The National Institute of Diabetes and Digestive and Kidney Diseases awarded the University of California, Berkeley $782,184 on August 5, 2026, under the Diabetes, Digestive, and Kidney Diseases Extramural Research program (CFDA 93.847) to investigate the metabolic role of FAM3D protein in brown adipose tissue thermogenesis and whole-body metabolism.

The research addresses obesity and diabetes as global health crises by examining how FAM3D functions as a negative regulator of brown adipose tissue thermogenesis and mitochondrial function. Human genetic studies identify FAM3D as a putatively causal protein for type 2 diabetes. The research team will define FAM3D's physiological role through three specific aims: characterizing FAM3D's role in brown adipose tissue thermogenesis and mitochondrial function using mouse and human brown adipocytes; dissecting how FAM3D-FPR2 signaling suppresses beta-adrenergic activation and induces mitochondrial stress responses; and determining the physiological and metabolic roles of brown adipose tissue-specific FAM3D knockdown. Preliminary data show that brown adipose tissue-specific FAM3D knockdown enhances cold tolerance, energy expenditure, insulin sensitivity, and glucose homeostasis, while FAM3D overexpression produces opposite effects. The research proposes that FAM3D acts through formyl peptide receptor 2, a G-protein-coupled receptor linked to inhibitory signaling.

Performance occurs at Berkeley, California, with a period of performance through May 31, 2030.