Allen, Sierra; Meyer-Ficca, Mirella; Wandersee, Miles (Utah State University)
Faculty Advisor: Meyer-Ficca, Mirella (College of Agriculture and Applied Sciences; Animal, Dairy, and Veterinary Sciences Department)
Niacin, a component of vitamin B3, is necessary for the synthesis of nicotinamide adenine dinucleotide (NAD+). NAD+ is an essential coenzyme in several metabolic processes, including those that regulate glucose and fat homeostasis in the body. Niacin is available to humans in its dietary form through foods such as meat, various legumes, nuts and vegetables. Niacin deficiency has been linked to health problems including age-related decline of cognitive abilities, as seen in Alzheimer's disease, and impaired dermal repair. In cases of extreme niacin deficiency, individuals may even develop pellagra, a disease characterized by dermatitis, diarrhea and dementia. Recent studies in niacin deficient mice indicate that niacin deficiency impairs proper glucose metabolism. Compared to mice with adequate niacin levels, niacin deficient mice experience a significant loss of total body weight and body fat and have impaired glucose regulation in response to insulin. We hypothesize that these metabolic defects result from inadequate levels of NAD+ preventing the conversion of lactate to pyruvate in the gluconeogenesis pathway, which in turn results in decreased blood glucose levels. Another potential explanation is that niacin deficiency results in decreased glycogen stores in the liver, also impeding glucose production. To test these hypotheses, we are studying the relationship between dietary niacin and glucose metabolism in a transgenic mouse model with acquired niacin dependency that accurately represents human niacin metabolism. Results of this study will contribute to better understanding of niacin's role in proper glucose metabolism, with important implications for diabetes and other glucose-related diseases, particularly in populations with limited access to quality food.