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Dr. Matthew Merrins is a faculty member in the Division of Endocrinology, Diabetes and Metabolism within the Department of Medicine. He is jointly appointed in the Department of Biomolecular Chemistry, and the William S. Middleton Memorial Veterans Hospital. Dr. Merrins is a trainer on the Molecular Biophysics Training Grant (NIGMS T32), the Molecular and Applied Nutritional Training Program (NIGMS T32), and the Biology of Aging and Aging-Related Diseases Training Program (NIA T32). In addition to mentoring graduate students, postdocs and scientists, he teaches endocrinology and metabolism to undergraduate, graduate and medical students.
Dr. Merrins also directs the University of Wisconsin Optical Imaging Core, the flagship microscopy core of the University of Wisconsin School of Medicine and Public Health, which serves 150 laboratories across multiple schools.
Dr. Merrins has received numerous research awards in addition to NIH R01 awards from NIDDK and NIA, including a Ruth L. Kirschstein National Research Service Award (NIDDK F32), a Research Scientist Development Award from (NIDDK K01), the American Diabetes Association Innovative Basic Science Award, an Exploratory/Developmental Research Grant Award from the NIA, and the Wisconsin Partnership New Investigator Award.
View Dr. Matthew Merrins' publications on NCBI My Bibliography
Research in the Merrins laboratory applies state of the art imaging, electrophysiological, biochemical, and genetic technologies to understand metabolic signaling and hormone secretion in pancreatic islet cells.
A major focus of the lab is the use of fluorescence microscopy to study cellular metabolism in real time, using imaging modalities including widefield, confocal, spinning disk, TIRF, STED, multi-photon and lightsheet microscopy. Using these tools, the Merrins lab has uncovered the pivotal roles of pyruvate kinase and the PEP cycle in β-cell nutrient sensing and localized ATP signaling. It has also discovered a novel paradigm in which plasma-membrane associated pyruvate kinase controls ATP-sensitive K+ (KATP) channel closure and insulin secretion, and the ability of the PKm1 and PKm2 isoforms to tune the amino acid sensitivity of KATP closure via the phosphoenolpyruvate (PEP) cycle.
The Merrins lab has provided a quantitative description of the mechanisms that encode nutrient stimuli into the metabolic and electrical oscillations that drive pulsatile insulin secretion, and a clearer understanding of the external cues arising from the gut incretin hormones and neighboring α-cells that act via β-cell GPCRs. Efforts are ongoing to understand how these processes are disrupted in aging, obesity, and type 2 diabetes.