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June 6, 2019 | 12:30 p.m. - 1:30 p.m.
Category: Seminar
Location: Scott Hall #5364 | Map
540 E. Canfield
Detroit, MI 48201
Cost: Free
Audience: Current Graduate Students, Faculty

The Campus Community is invited to a research seminar  

Fructose-induced hypertension: The pathway to an epidemic is paved with good intentions

hosted by

Departments of Pathology, Physiology and

Ophthalmology, Visual and Anatomical Sciences


The Office of the Vice President for Research

with guest speaker, Jeffrey L. Garvin, Ph.D.

Professor of Physiology & Biophysics

Case Western Reserve University

June 6, 2019

12:30 p.m. to 1:30 p.m. - an informal lunch will follow Dr. Garvin's presentation

Scott Hall, Room 5364

The Wayne State University community is invited to attend a research  presentation with guest speaker, Jeffrey Garvin, Ph.D., professor of physiology & biophysics, Case Western Reserve University.

The presentation will be held on June 6, 2019 at 12:30 p.m. in 5364 Scott Hall. The seminar is free and open to the entire university community. 

Dr. Garvin will present, "Fructose-induced hypertension: The pathway to an epidemic is paved with good intentions."

Dr. Garvin earned his B.S. degree in biology and chemistry at University of Miami and a Ph.D. in physiology from Duke University. 


Dietary fructose consumption has increased from less than 2 pounds/person/year in the early 70’s to more than 40 pounds/person/year currently. 16 million Americans consume >20% of their calories as fructose, and half the population consumes >11% of their calories as fructose. Dietary fructose causes hypertension and cardiovascular disease. These effects are mimicked in model organisms. Rats consuming 20% of their calories as fructose, but not glucose, develop salt-sensitive hypertension. Fructose-induced hypertension can be blunted by angiotensin II receptor antagonists. Angiotensin II is a key regulator of blood pressure primarily through actions on the kidney, including the proximal tubule, the only segment of the nephron that metabolizes fructose to an appreciable extent. The proximal nephron reabsorbs ~70% of the filtered Na via Na/H exchanger type 3 (NHE3). However, the mechanisms by which fructose causes salt-sensitive hypertension, and the role of the proximal nephron are unknown. Our data show that dietary fructose activates protein kinase C and enables low concentrations of angiotensin II, such as would be found when rats are on a high-salt diet, to stimulate proximal tubule transport. This effect is unique to angiotensin II. Part of the enhanced actions of angiotensin II are likely mediated by increases in intracellular Ca and reactive oxygen species. Our more recent data show that the effects of dietary fructose on the proximal nephron cause it to release proteases that enter the forming urine. There they flow downstream to the collecting duct where they likely cleave and activate Na reabsorption. Additionally we have found that dietary fructose alters genes associated with the normal circadian rhythm of Na reabsorption by the kidney. Our data support the hypothesis that dietary fructose has concerted actions on renal function which together contribute to salt-sensitive hypertension that are initiated by metabolism in the proximal nephron.

We hope you can join us for this interesting seminar! 

For more information about this event, please contact Julie O'Connor at 7-5600 or