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Sudesh Vasdev

Researcher at Memorial University of Newfoundland

Publications -  87
Citations -  2936

Sudesh Vasdev is an academic researcher from Memorial University of Newfoundland. The author has contributed to research in topics: Blood pressure & Insulin resistance. The author has an hindex of 31, co-authored 87 publications receiving 2773 citations. Previous affiliations of Sudesh Vasdev include St. John's University.

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Food addiction: its prevalence and significant association with obesity in the general population.

TL;DR: It is demonstrated that ‘food addiction’ contributes to severity of obesity and body composition measurements from normal weight to obese individuals in the general population with higher rate in women as compared to men.
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Altered Calcium Homeostasis Is Correlated With Abnormalities of Fasting Serum Glucose, Insulin Resistance, and β-Cell Function in the Newfoundland Population

TL;DR: The results suggest that alteration of serum calcium homeostasis is significantly correlated with the abnormality of glucose level, insulin resistance, and beta-cell function.
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Serum visfatin concentrations are positively correlated with serum triacylglycerols and down-regulated by overfeeding in healthy young men

TL;DR: Under physiologic conditions, visfatin does not appear to control glucose metabolism but may play a regulatory role in lipid metabolism and be down-regulated by overfeeding.
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Plasma methylglyoxal and glyoxal are elevated and related to early membrane alteration in young, complication-free patients with Type 1 diabetes

TL;DR: In complication-free patients, increased plasma methylglyoxal, plasma gly oxal, and erythrocyte Na+/K+ ATPase activity may foretell future diabetic complications, and emphasize a need for aggressive management.
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Plasma protein advanced glycation end products, carboxymethyl cysteine, and carboxyethyl cysteine, are elevated and related to nephropathy in patients with diabetes.

TL;DR: CMC or CEC in combination with HbA1C were better predictors of nephropathy than any one of these variables alone, suggesting that glucose, glyoxal, and methylglyoxal may all be involved in the etiology of diabetic nephtropathy.