Altered postprandial lipemia and fatty acid handling in obese vs. Normal-weight men is rectified by reducing dietary fat load: A dose-response trial

Abstract

International audienceBackground Postprandial hyperlipemia and altered dietary lipid beta-oxidation are now recognized as metabolic risk factors in obesity that are directly associated with dietary fat intake. The amount and size of chylomicrons are known to impact their clearance and thus possibly modulate the final partitioning of dietary fatty acids (FA) between β-oxidation and storage, which is altered in obesity. However, the detailed impact of ingested fat amount on postprandial lipemia and dietary FA fate in obese subjects remains to be elucidated. Methods In a randomized crossover study, eighteen healthy normal-weight (NW) and obese men ingested meals containing 10g or 40g of fat (typical breakfast fat contents) labeled with a mix of 13C-triglyceride tracers. Chylomicron triglyceride content and size were measured during 8h of digestion. Plasma concentrations of 13C-palmitate and 13C-oleate were also measured during 8h in parallel with their fecal loss (72h-stool collection). 13CO2 breath-test coupled to indirect calorimetry measures during 8h allowed to calculate exogenous lipid fate. Results Chylomicron triglycerides increased in all subjects according to ingested fat amount (P<0.01). After 40g of fat, obese men had delayed postprandial lipemia compared to NW men (PtimexBMI<0.0001) especially at 5–8h post-breakfast (P<0.01), with different variations in chylomicron size (PtimexBMI<0.01). This was associated with a lower appearance of tracers in plasma in obese men (P<0.01 for AUC 0–5h vs. NW), and a tendency to higher fecal excretion of 13C-oleate (P=0.1 vs. NW) after 40g of fat. However after 10g of fat, chylomicron TG and size, and tracer kinetics and fecal loss, were similar regardless of BMI. Finally, the impact of fat amount on exogenous lipid β-oxidation was different according to BMI (PdosexBMI<0.01): 39.6% of ingested lipids were β-oxidized after 40g of fat in obese (vs. 45.1% in NW) but this was increased to 53.1% in obese for 10g of fat (vs. 49.7% in NW subjects; P<0.001 vs. 40g). Conclusions Postprandial lipemia profile after a realistic high-fat load is altered in obese subjects. Although the reduction of ingested fat amount seems to normalize the postprandial fate of dietary lipids in obese men, further research is needed to understand mechanisms of altered postprandial lipid metabolism in obesity