Metabolic dysfunction-associated steatotic liver disease (MASLD) (aka non-alcoholic fatty liver disease), commonly occurring in individuals with obesity and type 2 diabetes can lead to liver inflammation/ fibrosis. MASLD results from fat being disproportionately deposited in the liver.
The goal of this mechanistic study is to investigate metabolic response in patients aged 20 to 80 years with non-alcoholic fatty liver disease, after niacin (vitamin B3) treatment.
The main questions it aims to answer are:
* Does Niacin lower the fat deposition in the liver? * Does Niacin raise White Adipose Tissue storage of dietary fatty acids?
Researchers will compare Niacin to a placebo (a look-alike substance that contains no drug) to compare the metabolic response.
Duration of study per participant: Up to 28 weeks
aged 20 to 80 years;
diagnosed with MASLD, defined as the presence of liver steatosis + abdominal obesity (as defined by the International Diabetes Federation country/ethnic group-specific criteria;
None
Crossover
Niacin (250mg)
DrugNiacin will be orally taken once daily with the largest meal. There will be a 3-week escalation period from 250 mg to 750 mg: * Week 1: 250mg * Week 2: 500mg * Week 3 to Week 12: 750mg (3 x 250mg caplets)
Placebo Oral Tablet
DrugPlacebo will be orally taken once daily with the largest meal. There will be a 3-week escalation period from 250 mg to 750 mg: * Week 1: 250mg * Week 2: 500mg * Week 3 to Week 12: 750mg (3 x 250mg caplets)
Prolonged small-dose niacin treatment does not lead to desensitization of the niacin-induced reduction in hepatic total fatty acids flux.
Total 6 h integrated uptake of circulating NEFAs, DFAs, and all FAs in liver: represents the sum of the rate of NEFA uptake integrated over 360 min for the entire organ and the rate of DFA uptake integrated over 360 min for the entire organ.
Change in White Adipose Tissue (WAT) and lean tissue Dietary Fatty Acid (DFA) uptake
Determined from the same static (whole-body) acquisition image using oral administration of \[18F\]-Fluoro-6-Thia-Heptadecanoic Acid (FTHA)
Change in total hepatic fatty acid flux
represents the sum of the rate of NEFA uptake and DFA uptake (PET scan using \[18F\]-FTHA and \[11C\]-palmitate
Change in hepatic Non-Esterified-Fatty-Acid (NEFA) uptake oxidation, esterification and secretion into very low-density lipoprotein (VLDL)
\[11C\]-Palmitate PET. Calculated from the same multicompartmental equation using liver \[11C\]-palmitate kinetics
Change in Endogenous Glucose production and meal glucose systemic flux
i.v. and oral stable isotope tracer
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Université de Sherbrooke
Lead sponsor
CHU de Quebec-Universite Laval
Collaborator
Centre de recherche du Centre hospitalier universitaire de Sherbrooke
Collaborator
