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Internal Medicine - Endocrinology

INTERNAL MEDICINE

Endocrinology

CONTACT

Lisa Tannock, M.D.

Academic Title Associate Professor
Chief, Division of Endocrinology and Molecular Medicine
Photo of Dr. Lisa Tannock
Departmental Affiliation Internal Medicine
Mailing Address UK Medical Center
MN524
Lexington, KY
40536-0298

Office/Lab Wethington Building, room 567
Telephone (859) 323-5821
Fax (859) 323-5707
E-mail Lisa.Tannock@uky.edu

Clinical Interests

Dr. Lisa Tannock has special interests in hyperlipidemia, diabetic dyslipidemia, metabolic syndrome, and lipodystrophy. She received her medical degree and completed a residency at the University of Toronto, Ontario, Canada. Dr. Tannock completed a fellowship at the University of Washington, Seattle, Washington.

Internal Medicine

She is board certified in internal medicine and endocrinology and is a Fellow of the American Heart Association. To refer a patient to Dr. Tannock, call UK·MDs at (800) 888-5533 or in Lexington, call (859) 231-9922.

Research/Clinical Interests

Cardiovascular disease remains the primary cause of morbidity and mortality in developed countries. Although cardiovascular death rates have declined in recent years, likely due to increased prevention and improved medical care, the death rates have not dropped as dramatically in men with diabetes, and have actually increased in women with diabetes. Thus, therapies which reduce atherosclerosis, particularly in the diabetic population, are urgently needed.

Proteoglycans have been shown to play a critical role in the initiation of atherosclerosis due to their ability to bind atherogenic lipoproteins leading to retention in the artery wall, as outlined in the "response to retention hypothesis".

The goal of this laboratory is to identify modifications of proteoglycans that may be atheroprotective. A major focus of the lab is to identify the underlying mechanisms leading to the reduced proteoglycan-lipoprotein interactions, and to understand the regulation of proteoglycan synthesis.

Diabetic nephropathy occurs in 30% of individuals with type 1, and 10% of individuals with type 2 diabetes. Diabetic nephropathy is characterized by mesangial cell injury and progressive accumulation of mesangial matrix and proteoglycans. Lipids and lipoproteins have been shown to accumulate in the glomerulus and are thought to play a role in the pathogenesis of renal injury. Proteoglycans, which play a key role in the development of atherosclerosis due to their ability to bind and retain lipoproteins in the artery wall, may also contribute to lipoprotein retention in the glomerulus.

An additional focus of this laboratory is to test the hypothesis that lipoprotein retention is a key step in the pathogenesis of nephropathy. Thus, we are interested in comparing the effects of factors shown to modify lipoprotein retention by vascular proteoglycans with their effects on lipoprotein retention by mesangial proteoglycans. Mouse models are used to evaluate the relative contributions of hyperglycemia and hyperlipidemia on the development of diabetic atherosclerosis and glomerulosclerosis in vivo.

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Page last updated Tuesday, October 27, 2009