Effects of Nicotinamide Riboside on Endocrine Pancreatic Function and Incretin Hormones in Nondiabetic Men With Obesity

Blood Glucose Male Niacinamide Pyridinium Compounds Gastric Inhibitory Polypeptide METABOLISM INSULIN-SECRETION Islets of Langerhans 03 medical and health sciences IMPAIRED GLUCOSE-TOLERANCE SIRT1 BETA-CELL FUNCTION Double-Blind Method Glucagon-Like Peptide 1 Humans Insulin GLUCAGON Obesity FATTY LIVER-DISEASE ORAL GLUCOSE 2. Zero hunger 0303 health sciences C-Peptide Glucose Tolerance Test Middle Aged Glucagon 3. Good health MONONUCLEOTIDE RESISTANCE
DOI: 10.1210/jc.2019-01081 Publication Date: 2019-08-07T09:04:53Z
ABSTRACT
Abstract Objective Augmenting nicotinamide adenine dinucleotide (NAD+) metabolism through dietary provision of NAD+ precursor vitamins translates to improved glucose handling in rodent models of obesity and diabetes. Preclinical evidence suggests that the NAD+/SIRT1 axis may be implicated in modulating important gut-related aspects of glucose regulation. We sought to test whether NAD+ precursor supplementation with nicotinamide riboside (NR) affects β-cell function, α-cell function, and incretin hormone secretion as well as circulating bile acid levels in humans. Design A 12-week randomized, double-blind, placebo-controlled, parallel-group trial in 40 males with obesity and insulin resistance allocated to NR at 1000 mg twice daily (n = 20) or placebo (n = 20). Two-hour 75-g oral glucose tolerance tests were performed before and after the intervention, and plasma concentrations of glucose, insulin, C-peptide, glucagon, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) were determined. β-Cell function indices were calculated based on glucose, insulin, and C-peptide measurements. Fasting plasma concentrations of bile acids were determined. Results NR supplementation during 12 weeks did not affect fasting or postglucose challenge concentrations of glucose, insulin, C-peptide, glucagon, GLP-1, or GIP, and β-cell function did not respond to the intervention. Additionally, no changes in circulating adipsin or bile acids were observed following NR supplementation. Conclusion The current study does not provide evidence to support that dietary supplementation with the NAD+ precursor NR serves to impact glucose tolerance, β-cell secretory capacity, α-cell function, and incretin hormone secretion in nondiabetic males with obesity. Moreover, bile acid levels in plasma did not change in response to NR supplementation.
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