One out of every 10 Americans has diabetes, increasing their risk of death by 50% and more than doubling their health care costs. Delineating how the brain regulates metabolism, including feeding behavior and glucose homeostasis, may shed light on how those processes are altered in disease. The medial amygdalar nucleus (MeA) regulates the intersection of stress, social behavior, and metabolism. Fos expression in the MeA of mice is altered by changes in energy availability - fasting/re-feeding and hyper-/hypoglycemia - suggesting this nucleus may regulate feeding behavior and blood glucose levels in response to internal cues. The primary downstream targets of the MeA are the principle nucleus of the bed nucleus of the stria terminalis (prBNST) and ventromedial hypothalamus (VMH), regions previously shown to regulate metabolism. Cfos immunohistochemistry and retrograde labeling show that MeA neurons that project to the VMH (MeA-->VMH) are preferentially activated by a 36h fast, compared to ad libitum feeding and a 1h refeed. Selectively activating MeA-->VMH neurons using chemogenetics induces hyperglycemia independent of changes to circulating insulin and changes in feeding. Ongoing fos, axonal tracing, and behavioral studies aim to delineate the contributions of different MeA cell types to glucose homeostasis in the context of other competing behaviors including social interaction and stress.


K. Devarakonda: None. K. Conner: None. D. Garibay: None. S. Stanley: None.


American Diabetes Association/Pathway to Stop Diabetes (1-17-ACE-31 to S.S.); American Heart Association (18PRE33960254)

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at