Class
Article
College
S.J. & Jessie E. Quinney College of Natural Resources
Department
Wildland Resources Department
Faculty Mentor
Mirella Meyer-Ficca
Presentation Type
Poster Presentation
Abstract
Niacin, a component of vitamin B3, is necessary for the synthesis of nicotinamide adenine dinucleotide (NAD). NAD is an essential coenzyme in many biologic functions, including a number of metabolic processes that regulate glucose and fat homeostasis. Humans obtain niacin in its dietary form, common in meats, nuts, legumes and some leafy vegetables. While severe niacin deficiency, or pellagra, has been drastically reduced in the United States, some populations remain vulnerable to deficiency, particularly pregnant women, cancer patients, the elderly and alcoholics. Age-related NAD deficiency is emerging as being positively correlated with cognitive decline and impaired dermal repair.. At the same time, the rates of metabolism-related diseases such as diabetes and metabolic syndrome are rising in the United States, yet niacin deficiency’s role in these diseases have not been widely studied. The purpose of this study was to explore several possible mechanisms that cause such metabolic dysregulation. In order to more accurately replicate human metabolism, we used an Acquired Niacin-Deficiency (ANDY) mouse model. Previous studies using ANDY mice showed 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, lower energy levels, and impaired glucose response. In the present study, mice were put either on a control diet (CD1) with adequate dietary niacin or a diet that completely lacked dietary niacin (ND1). To test our hypothesis that inadequate levels of niacin prevent the conversion of lactate to pyruvate in the gluconeogenesis pathway, we measured blood lactate and blood glucose levels following a pyruvate challenge. The results showed that the ND1 mice had significantly lower glucose levels (p=0.0003) and higher lactate levels (P0.0177) than the control group. Additionally, we measured hepatic glycogen levels post-mortem. There was no significant difference between treatment groups. We conclude that impaired gluconeogenesis rather than low glycogen liver stores contribute to the defective glucose homeostasis in NAD-deficient mice.Presentation Time: Thursday, 10-11 a.m.Zoom link: https://usu-edu.zoom.us/j/87913811390?pwd=RTR2dEJjaEJ1akJVYTdFMmZIcDNrQT09
Location
Logan, UT
Start Date
4-13-2021 12:00 AM
Possible Mechanisms Behind Impaired Glucose Metabolism in Niacin-Deficient Mice
Logan, UT
Niacin, a component of vitamin B3, is necessary for the synthesis of nicotinamide adenine dinucleotide (NAD). NAD is an essential coenzyme in many biologic functions, including a number of metabolic processes that regulate glucose and fat homeostasis. Humans obtain niacin in its dietary form, common in meats, nuts, legumes and some leafy vegetables. While severe niacin deficiency, or pellagra, has been drastically reduced in the United States, some populations remain vulnerable to deficiency, particularly pregnant women, cancer patients, the elderly and alcoholics. Age-related NAD deficiency is emerging as being positively correlated with cognitive decline and impaired dermal repair.. At the same time, the rates of metabolism-related diseases such as diabetes and metabolic syndrome are rising in the United States, yet niacin deficiency’s role in these diseases have not been widely studied. The purpose of this study was to explore several possible mechanisms that cause such metabolic dysregulation. In order to more accurately replicate human metabolism, we used an Acquired Niacin-Deficiency (ANDY) mouse model. Previous studies using ANDY mice showed 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, lower energy levels, and impaired glucose response. In the present study, mice were put either on a control diet (CD1) with adequate dietary niacin or a diet that completely lacked dietary niacin (ND1). To test our hypothesis that inadequate levels of niacin prevent the conversion of lactate to pyruvate in the gluconeogenesis pathway, we measured blood lactate and blood glucose levels following a pyruvate challenge. The results showed that the ND1 mice had significantly lower glucose levels (p=0.0003) and higher lactate levels (P0.0177) than the control group. Additionally, we measured hepatic glycogen levels post-mortem. There was no significant difference between treatment groups. We conclude that impaired gluconeogenesis rather than low glycogen liver stores contribute to the defective glucose homeostasis in NAD-deficient mice.Presentation Time: Thursday, 10-11 a.m.Zoom link: https://usu-edu.zoom.us/j/87913811390?pwd=RTR2dEJjaEJ1akJVYTdFMmZIcDNrQT09