Matthew Brady, Ph.D.


  • Chair, Committee on Molecular Metabolism and Nutrition
  • Associate Professor; Department of Medicine- Section of Endocrinology, Diabetes and Metabolism; Committee on Molecular Medicine/MPMM; Committee on Cell Physiology


Ph.D., The University of Chicago, 1994


The University of Chicago
KCBD 8124
900 East 57th Street
Chicago, IL  60637

Phone: (773) 702-2346

Website (Department of Medicine)


The Brady lab in the Kovler Diabetes Center has a long standing interest in studying adipocyte (fat cell) biology and insulin sensitivity.  The lab is primarily focused on two collaborative transdisciplinary projects: 1) determining the impact of altered sleep quality and circadian behavior on cellular and systemic insulin sensitivity in humans; 2) elucidation the role of chronic social isolation on mammary adipose tissue biology and the progression of triple negative breast cancer in mice.

Sleep and human adipocyte function.  We have a standing collaboration with Drs. Eve Van Cauter and researchers in the Sleep Metabolism and Health Center at the University of Chicago.   We previously reported that 4 nights of partial sleep restriction (4.5 hr in bed/night) in young healthy lean control subjects resulted in a 30% reduction in insulin sensitivity in adipocytes isolated by peri-umbilical fat biopsy.  This is the equivalent of metabolically aging the participants by nearly two decades.  We have recently initiated a study to examine the impact of central circadian alignment in obese subjects scheduled to undergo bariatric surgery.  Half of the randomized participants will be enrolled in a week of fixed lights on/off and meal schedules to determine if this intervention improves circadian gene expression and insulin sensitivity in adipose biopsies.  Additionally, the impact of bariatric surgery on circadian behavior and insulin action in fat cells will also be examined.  In addition to increased exercise and decreased energy consumption, these findings may elucidate novel roles for adequate sleep and daily rhythms of behavior to combat the obesity and type 2 diabetes epidemic.

Chronic social isolation and breast cancer progression.  We have a second ongoing collaboration with Drs. Suzanne Conzen (Hematology/Oncology) and Martha McClintock (Institute for Mind and Biology) to elucidate the impact of a constant stressor on mammary adipocyte biology and triple negative breast cancer proliferation in mice.  Transgenic mice expressing the Tag protein were used, as all the female mice will develop triple negative breast cancer in a predictable timed fashion.  We found that social isolation (housing one female mouse per cage) increased the rate of breast cancer progression, and importantly, altered the glucose metabolism in only the mammary adipose tissue (no other fat depot was affected) and not in the breast epithelial cells from which the tumors will arise.  These findings suggested that the impact of chronic social isolation on breast cancer development was not direct but rather mediated through alterations in mammary adipose tissue metabolism and secretion of specific endocrine hormones and metabolites.  We have initially identified one lipid species whose expression is increased upon social isolation and can promote breast cancer cell proliferation.  Work is ongoing to identify other factors secreted from mammary adipose tissue that can support breast cancer cell proliferation and the pathways underlying these responses in an attempt to identify novel therapeutic sites for intervention in triple negative breast cancer.

Research Papers in PubMed