ABSTRACT:

Glycine is a nutritionally non-essential amino acid and has significantly lower plasma concentration in individuals with obesity. However, the glycine metabolic pathway that is dysregulated in obesity is unknown. Plasma glycine concentration also correlates inversely with insulin resistance. Still, it remains unclear whether altered glycine metabolism in obesity is a cause or consequence of insulin resistance and whether correcting glycine “deficiency” improves insulin resistance. To better understand glycine metabolism in obesity, I compared the glycine kinetic parameters between individuals with morbid obesity to controls with healthy weight using stable-isotope tracer methods. I also examined the relationship between altered glycine metabolism with insulin resistance by measuring the changes in glycine kinetics in patients with morbid obesity undergoing bariatric surgery. Another group of individuals with morbid obesity received dietary glycine supplementation for two weeks to explore the therapeutic potential of correcting glycine deficiency. I found significantly impaired glycine de novo synthesis in individuals with morbid obesity, and dysregulated glycine metabolism in obesity is most likely secondary to insulin resistance. Thus, in obesity, glycine should be regarded as a conditionally essential amino acid. Dietary glycine supplementation corrected glycine deficiency but did not reduce insulin resistance. Nonetheless, glycine supplementation may promote hepatic fatty acid oxidation.

THESIS ADVISOR:  
Prof. Tai E Shyong

VENUE: 
Duke-NUS, Level 2, Amphitheatre