AIM: Ezetimibe selectively blocks intestinal cholesterol absorption by 
inhibiting Niemann-Pick C1-like 1 (NPC1L1) and reducing LDL cholesterol (LDL-C). 
In animals, ezetimibe reversed diet-induced obesity, liver steatosis, and 
insulin resistance. In humans, its potential effects on liver steatosis and 
insulin resistance have been suggested. We investigated the effects of ezetimibe 
on postprandial hyperlipidaemia and hyperglycaemia in obese subjects with 
dyslipidaemia in a double-blind randomized crossover trial.
METHODS: Twenty obese men with hypertriglyceridaemia were assigned randomly to 
an ezetimibe- or a placebo-precedence-treated group. Subjects in the ezetimibe 
group were treated with ezetimibe (10 mg/day) for the first 4 weeks, followed by 
a 4-week interval and then treated with placebo for another 4 weeks. The placebo 
group received these treatments in reverse order. Subjects were requested to 
fast for at least 12 hours and then received a standard meal. Blood samples were 
collected at 0, 30, 60, 120, 240, 360 and 480 minutes after the meal on Days 0, 
28, 56 and 84 and were used to measure the lipid and glucose metabolism markers.
RESULTS: Ezetimibe significantly decreased the postprandial serum triglyceride 
excursion (p=0.01) and fasting serum LDL-C, remnant-like particles(RLP) and 
ApoB48 levels (p<0.05). Postprandial glucose excursion, serum insulin levels, 
serum glucose-dependent insulinotropic polypeptide (GIP) and active 
glucagon-like peptide-1 (GLP-1) were not significantly affected by ezetimibe 
treatment.
CONCLUSION: Ezetimibe restored the postprandial dysregulation of lipid but did 
not affect glucose metabolism in a double-blind randomized crossover trial.