Education

1984
Bachelor of Science, Zoology
Birmingham University-United Kingdom

1988
Doctorate in Neuroscience
Cambridge University-United Kingdom

1988-1993
Postdoctoral Fellow
Department of Neurobiology, Pharmacology & Physiology
University of Chicago-Chicago, IL

1993-1998
Postdoctoral Fellow
DFepartment of Pharmacology
Yale University-New Haven, CT

1998-2002
Postdoctoral Fellow
Department of Pharmacology
University College London-United Kingdom

Publications

M.D. Whim (2025). Mouse adrenal macrophages are associated with pre- and post-synaptic neuronal elements and respond to multiple neuromodulators. eNeuro 0153-24.2025.

Gupta R, Wang M, Ma Y, Offermanns S and * M.D. Whim (2022). The β-hydroxybutyrate-GPR109A receptor regulates fasting-induced plasticity in the mouse adrenal medulla. Endocrinology. 163: bqac077.

Ma Y, Wang Q, Joe D, Wang M and * M.D. Whim (2018). Recurrent hypoglycemia inhibits the counterregulatory response by suppressing adrenal activity. J. Clin. Invest. 128: 3866-3871.

Gupta R, Ma Y, Wang M, * M.D. Whim (2017). AgRP-expressing adrenal chromaffin cells are involved in the sympathetic response to fasting. Endocrinology. 158: 2572-2584.

Wang M, Wang Q, * M.D. Whim (2016). Fasting induces a form of autonomic synaptic plasticity that prevents hypoglycemia. Proc Natl Acad Sci USA. 113: E3029-38.

Research

Control of blood glucose by the autonomic nervous system.

We are interested in the neuronal mechanisms that regulate the levels of blood glucose. Ensuring that enough energy-rich molecules, including glucose and fatty acids, are present in the plasma is essential for life. If the levels drop too low, hypoglycemia and coma can ensue. If the levels are too high this increases the risk of obesity and diabetes. It is clear that the nervous system plays a central role in this homeostatic process. Our particular interest is in determining how the autonomic nervous system controls the response to hypoglycemia. When the level of blood glucose falls below a threshold value the neuroendocrine chromaffin cells in the adrenal medulla become progressively activated and as a result epinephrine secretion is increased. This hormone acts on the liver to increase glucose production and on the pancreas to inhibit insulin secretion: both actions help to restore euglycemia.

My lab is investigating the signaling mechanisms that underlie this release of epinephrine. In this work we use a variety of experimental approaches including slice electrophysiology, optogenetics and in vivo measurements of circulating hormones and metabolites. We would like to understand how the adrenal response to hypoglycemia is initiated, how it is regulated and why it sometimes fails. The importance of the adrenal contribution to metabolic regulation is exemplified by the clinical problems experienced by type I and II diabetics in whom the response is markedly deficient.