Yuri Sautin, PhD
Yuri Sautin, PhD, DSc
Division of Nephrology, Hypertension & Renal Transplantation
Associate Professor of Medicine
1600 SW Archer Road
Room CG-95, Communicore Building
PO Box 100224
Gainesville, FL 32610-0224
|MS||Chernivtsy State University, Ukraine||Biochemistry|
|PhD||Academy of Sciences of Ukrainian SSR||Physiology|
|Research Associate||Academy of Sciences of Ukrainian SSR||Physiology of Aquatic Organisms|
|DSc||Academy of Medical Sciences of Ukraine||Endocrinology and Signal Transduction|
|Postdoctoral Associate||University of Florida||Signal transduction|
Dr. Sautin’s academic interests include the receptor-mediated and receptor-independent mechanisms of the signal transduction with the emphasis on the metabolic diseases, oxidative stress, inflammation, and pro-survival mechanisms.
One of the specific topics is the signaling mechanisms mediating effects of glucose metabolism in the renal tubular epithelial cells on the trafficking, assembly, and functional activity of the vacuolar H+-ATPase. This enzyme represents a unique ATP-driven proton pump, a molecule of tremendous complexity, which consists of thirteen different subunits dynamically interacting with each other and other proteins. These studies demonstrated that V-ATPase is activated by the PI3K/Akt-dependent signaling mechanism, which controls trafficking and assembly of the functional proton pump on the apical membrane of the proximal tubular cells.
Another topic of research of Dr. Sautin is related to the prodiabetic and proinflammatory effects of fructose and uric acid, the product of the fructose overload, and the underlying signaling mechanisms responsible for these effects. According to many epidemiological studies, hyperuricemia is always associated, and in many cases, predicts obesity, predominantly its visceral form, and the metabolic syndrome. Moreover, increased consumption of fructose, which is ubiquitous in modern Western diet and may induce hyperuricemia, may play an important role in the development of the current epidemic of obesity and the metabolic syndrome, in addition to lack of exercise, overnutrition, and genetic predisposition. Cells with the high rate of fructose metabolism are the most affected by the detrimental effects of fructose overload followed by the production of uric acid. These cell types include the renal proximal tubular cells, hepatocytes and adipocytes. These studies showed that fructose metabolism followed by purine degradation to uric acid induce prodiabetic phenotype, which is characterized by oxidative stress mediated by activation of NADPH oxidase, proinflammatory redox-dependent signaling via p38 MAP kinase followed by an increase in the expression of the proinflammatory mediator MCP-1. Currently, these mechanisms are investigated in the animal models of the metabolic syndrome.
Read about his research HERE
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