Eric Klett, MD
Assistant Professor of Medicine and Nutrition
Specialty Areas: General endocrinology, thyroid disease, lipid disorders, and transgender medicine.
Chronology: MD: Medical University of South Carolina, 1999; Intern and Resident Internal Medicine: Medical University of South Carolina, 1999-2002; Endocrinology, Diabetes and Metabolism Fellowship: Medical University of South Carolina, 2002-2005; Lexington Medical Specialists, 2005-2008; Instructor of Medicine: University of North Carolina, 2008-2010; Assistant Professor of Medicine: University of North Carolina 2010-present; Assistant Professor of Nutrition: University of North Carolina 2015-present.
Dr. Klett practices General Endocrinology with clinical interests in thyroid disease, lipid disorders and transgender medicine. He is interested in teaching Endocrinology and serves as the Associate Endocrinology Fellowship Director.
Dr. Klett’s research interest is in the role of dietary fatty acid and intra-pancreatic beta-cell fatty acid metabolism on glucose-stimulated insulin secretion (GSIS). Insulin secretion is a complex process initiated by nutrient secretagogues, including glucose and fatty acids. GSIS is augmented by saturated long-chain fatty acids, but is impaired by ω-6 polyunsaturated fatty acids (PUFA). Glucose and fatty acids are essential to GSIS, though the exact molecular mechanism by which specific fatty acids alter GSIS remains unclear.
Dr. Klett has examined the role of one of the rate-limiting enzymes in glycerolipid synthesis on beta-cell function, acyl-CoA synthetase (ACSL). Specifically, exposing beta-cells to ω-6 PUFAs (arachidonate or linoleate) not only impairs GSIS, but also reduces ACSL isoform-4 (ACSL4) mRNA and protein expression. Further, reducing ACSL4 specific activity decreases GSIS. The reduction in insulin secretion is due to the accumulation of unesterified epoxyeicosatrienoic acids (EETs). The hypothesis that ACSL4 plays a key role in eicosanoid metabolism has significant implications in all disease processes that involve eicosanoid metabolism, including diabetes, cardiovascular disease, and cancer.
Klett EL, Chen S, Edin ML, Li LO, Ilkayeva O, Zeldin DC, Newgard CB, Coleman RA. (2013) Diminished acyl-CoA synthetase isoform 4 activity in INS 832/13 cells reduces cellular epoxyeicosatrienoic acid levels and results in impaired glucose-stimulated insulin secretion. J Biol Chem 288(30): 21618-21629. PMID: 23766516.
Grevengoed T, Klett EL, Coleman RA (2014) Acyl-CoA metabolism and partitioning. Ann Rev Nutr 34: 2.1-2.30. PMID 24819326.
Cooper DE, Young PA, Klett EL, Coleman RA. (2015) Physiological Consequences of Compartmentalized Acyl-CoA Metabolism. J Biol Chem. 290(33): 20023-31. PMID: 26124277.