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
AUTHORS (9)
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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