A low-fat, high-complex carbohydrate diet supplemented with long-chain (n-3) fatty acids alters the postprandial lipoprotein profile in patients with metabolic syndrome.
Study Goal
The researchers aimed to determine how different types and quantities of dietary fat (high-SFA, high-MUFA, and low-fat high-complex carbohydrate diets) affect postprandial lipoprotein metabolism in patients with metabolic syndrome (MetS).
Results Summary
The study found that high-MUFA diets improved postprandial triglyceride clearance, while low-fat high-complex carbohydrate diets with omega-3 supplementation reduced postprandial triglyceride levels. Long-term low-fat diets without omega-3 supplementation worsened postprandial lipid metabolism.
Population
Patients with metabolic syndrome (MetS).
Effective Dosage
1.24 g/d of long-chain (n-3) PUFA or placebo (1.24 g/d of high-oleic sunflower-seed oil).
Duration
12 weeks per diet.
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA] diet | increase | postprandial TG clearance | MetS patients | - | began earlier and was faster | #1 |
high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA] diet | increase | large TRL-TG clearance | MetS patients | - | began earlier and was faster | #2 |
LFHCC (n-3) diet | decrease | postprandial TG concentration | MetS patients | - | had a lower | #3 |
LFHCC diet | increase | TG area under the curve | MetS patients | - | increased | #4 |
LFHCC diet | increase | large TRL-TG area under the curve | MetS patients | - | increased | #5 |
LFHCC diet | increase | TRL-cholesterol area under the curve | MetS patients | - | increased | #6 |
LFHCC diet | increase | TRL-retinyl palmitate area under the curve | MetS patients | - | increased | #7 |
LFHCC diet | increase | TRL-apo B area under the curve | MetS patients | - | increased | #8 |
LFHCC (n-3) diet | no change | postprandial TG metabolism | MetS patients | - | did not augment | #9 |
LFHCC (n-3) diet | no change | TRL metabolism | MetS patients | - | did not augment | #10 |
LFHCC (n-3) diet | decrease | postprandial abnormalities associated with MetS | MetS patients | - | attenuated | #11 |
HMUFA diet | decrease | postprandial abnormalities associated with MetS | MetS patients | - | attenuated | #12 |
concomitant LC (n-3) PUFA supplementation | decrease | adverse postprandial TG-raising effects of long-term LFHCC diets | weight-stable MetS patients | - | may be avoided | #13 |
Dietary fat intake plays a critical role in the development of metabolic syndrome (MetS). This study addressed the hypothesis that dietary fat quantity and quality may differentially modulate postprandial lipoprotein metabolism in MetS patients. A multi-center, parallel, randomized, controlled trial conducted within the LIPGENE study randomly assigned MetS patients to 1 of 4 diets: high-SFA [HSFA; 38% energy (E) from fat, 16% E as SFA], high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA], and 2 low-fat, high-complex carbohydrate [LFHCC; 28% E from fat] diets supplemented with 1.24 g/d of long-chain (LC) (n-3) PUFA (ratio 1.4 eicosapentaenoic acid:1 docosahexaenoic acid) or placebo (1.24 g/d of high-oleic sunflower-seed oil) for 12 wk each. A fat challenge with the same fat composition as the diets was conducted pre- and postintervention. Postprandial total cholesterol, triglycerides (TG), apolipoprotein (apo) B, apo B-48, apo A-I, LDL-cholesterol, HDL-cholesterol and cholesterol, TG, retinyl palmitate, and apo B in TG-rich lipoproteins (TRL; large and small) were determined pre- and postintervention. Postintervention, postprandial TG (P < 0.001) and large TRL-TG (P = 0.009) clearance began earlier and was faster in the HMUFA group compared with the HSFA and LFHCC groups. The LFHCC (n-3) group had a lower postprandial TG concentration (P < 0.001) than the other diet groups. Consuming the LFHCC diet increased the TG (P = 0.04), large TRL-TG (P = 0.01), TRL-cholesterol (P < 0.001), TRL-retinyl palmitate (P = 0.001), and TRL-apo B (P = 0.002) area under the curve compared with preintervention values. In contrast, long-term ingestion of the LFHCC (n-3) diet did not augment postprandial TG and TRL metabolism. In conclusion, postprandial abnormalities associated with MetS can be attenuated with LFHCC (n-3) and HMUFA diets. The adverse postprandial TG-raising effects of long-term LFHCC diets may be avoided by concomitant LC (n-3) PUFA supplementation to weight-stable MetS patients.