Document Type


Publication Date




MeSH Headings

Diabetes Mellitus, Diabetes Mellitus


Accumulation of excess fat in white adipose tissue is associated with an increase in risk for type 2 diabetes. Within white fat tissue resides a population of “beige” adipocytes that are activated by cold exposure and expend energy contained in fats, which is released as heat. Increasing energy expenditure through beige adipocyte activation has been shown to reduce diabetic symptoms in rodent models of obesity. However, activation of beige adipocytes through exposure of humans to cold temperatures is uncomfortable and likely not a realistic strategy to control body weight. In addition to its fat burning potential, secreted factors derived from activated beige adipocytes may enter the circulation and reduce diabetic symptoms such as insulin resistance in other tissues. The mechanisms by which these secreted factors act on distant tissues may in part be due to their transport inside extracellular vesicles, known as exosomes. Exosomes carry a diverse array of signaling molecules, including microRNAs that are transported and released into recipient cells and tissues. The goal of this project was to determine if beige adipocytes grown in cell culture secrete exosomes that contain microRNAs that may harbor anti-diabetic properties. Unexpectedly, we found that during the activation of beige adipocytes, secreted exosomes contain elevated expression of a number of microRNAs known to be negative regulators of beige adipocyte activation, including mir27. This suggests that exosome secretion may be a way to increase beige adipocyte activation by decreasing the expression of specific microRNAs. Future testing of these microRNA candidates may translate to improved therapies for obese patients that develop diabetes.


Lambrew Research Retreat

Acknowledgements: This work was supported by NIH COBRE award P20GM121301 (A. Brown, L. Liaw, and C.J. Rosen). The project utilized services of the Molecular Phenotyping and Progenitor Cell Analysis Core Facility funded by the NIH COBRE award P20GM106391 (R. Friesel, PI).



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