Sona Kang
University of California-Berkeley, CA·Physiology
Fat tissue is far more than passive storage. It burns or stores energy and sends chemical signals that control how the whole body handles sugar.
- Fields
Physiology
Biology
Genetics
- Topics
brown adipose tissue
thermogenesis
white adipose tissue
- Grants
- 3 known grants, through May 2030
What they work on
- Define how FAM3D, a protein genetically linked to type 2 diabetes, suppresses heat production and mitochondrial function in mouse and human brown fat cells.
- Dissect how FAM3D signaling through the receptor FPR2 blocks β-adrenergic activation and triggers mitochondrial stress, and measure the whole-body effects on temperature control and metabolism in mice with brown-fat-specific changes in FAM3D.
- Determine how the fat-derived hormone NRN1 controls fat-tissue biology and insulin sensitivity, using mice in which NRN1 is added or removed only in fat cells, and test FGFR1-dependent effects on fat-cell maturation, fat breakdown and inflammation.
- Test whether giving NRN1 throughout the body, by AAV gene delivery or as recombinant protein, reduces insulin resistance and glucose intolerance in mice made obese by diet.
- Establish how the DNA-demethylating enzyme TET3 drives new fat-cell formation, using Tet3 conditional knockout and lineage-tracing mice targeted to fat precursor cells.
- Identify the genes that TET3 regulates, including extracellular-matrix genes, using transcriptomic and DNA-methylation profiling and targeted epigenetic editing, and determine the metabolic effects of losing TET3 in mice on a high-fat diet.
More about the research
When fat tissue malfunctions, the result can be obesity, insulin resistance (in which cells stop responding properly to insulin) and type 2 diabetes. The lab's projects ask how fat tissue is built and controlled. One project studies a protein that slows heat production in brown fat. A second studies a hormone released by fat that improves insulin sensitivity. A third studies an enzyme that edits chemical marks on DNA to control the growth of white fat.
Why it matters
Obesity and type 2 diabetes affect people worldwide and are driven by insulin resistance and disrupted energy balance. Blocking FAM3D–FPR2 signaling could boost calorie burning by brown fat. Restoring the fat-derived hormone NRN1 might ease insulin resistance. TET3 targets could help prevent unhealthy fat growth on high-calorie diets. Each could become a new therapeutic target for metabolic disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Trayambak Pathak
Louisiana State University Health Sciences Center-New Orleans, LA·Physiology·Early-career
Test whether calcium entry through Orai3 channels drives mitochondrial heat production in brown adipose tissue to limit fat buildup, by measuring mitochondrial metabolism in Orai3 knockout mice.
Diana Elizondo
University of Maryland-Baltimore County, MD·Physiology·Early-career
Determine how TGases in myeloid cells, including macrophages, drive adipose tissue inflammation and unhealthy fat expansion in obesity, using conditional knockout mice.
Jonathan Campbell
Duke University, NC·Physiology
Test whether pericytes, cells lining blood vessels, are the main GIP receptor (GIPR)-expressing cells in fat tissue, using mouse models that mark and lineage-trace GIPR-positive cells over time.
The school
University of California-Berkeley: 46 labs on PI Pages, $1.1B a year on research, 825 research doctorates a year.
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