Mixed meals containing slowly digestible carbohydrate that induces low glycemic and insulinemic responses reduce the postprandial accumulation of both hepatically and intestinally derived triacylglycerol-rich lipoproteins in obese subjects with insulin resistance.

The role of postprandial insulin in the regulation of postprandial lipid metabolism is still poorly understood. The roles of hyperinsulinemia and insulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, we submitted healthy men to acute hyperinsulinemia in two different ways. In the first study, we compared in 10 men the effects of four isolipidic test meals that induce different degrees of hyperinsulinemia on postprandial lipid metabolism. Three different carbohydrate sources were compared according to their glycemic indexes (GIs; 35, 75, and 100 for white kidney bean, spaghetti, and white bread test meals, respectively); the fourth test meal did not contain any carbohydrates. Postprandial plasma insulin levels were proportional to the GIs (maximal plasma insulin concentrations: 113 ± 16 to 266 ± 36 pmol/l). We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r 2 = 0.70; P = 0.0001). In a second study, 5 of the 10 subjects again ingested the carbohydrate-free meal, but during a 3-h hyperinsulinemic-(550 ± 145 pmol/l plasma insulin) euglycemic (5.5 ± 0.8 mmol/l plasma glucose) clamp. A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome. Diabetes 50:462-469, 2001

The goal of the present study was to compare the plasma lipid responses of massively obese and lean women to a fat load and a carbohydrate load. For this purpose, 11 lean [body mass index (BMI), 21.6 +/- 2 kg/m(2)] and 8 obese (BMI, 50.8 +/- 7 kg/m(2)) normolipidemic women were given, in random order, either a dietary carbohydrate load (3.43 MJ, 166 g carbohydrates, 38 g proteins) or a dietary fat load (3.35 MJ, 70 g fat, 36 g proteins). Blood samples were collected hourly for 9 h after the test meal for measurements of triglyceride-rich lipoprotein (TRL)-lipid, apolipoprotein (apo)B-48 and apoB-100. Triglycerides (P < 0.0001), TRL triglycerides (P < 0.0001), TRL cholesterol (P < 0.04) and apoB-48 (P < 0.0001) peaked 3 h after the fat meal and returned progressively to baseline values in both obese women and lean controls. These lipid and apolipoprotein changes did not differ between the two groups. In contrast, after the carbohydrate load, the plasma triglyceride (P < 0.0001) and TRL triglyceride (P < 0.0001) increments were significantly greater in obese women than in lean controls. This carbohydrate-induced TRL triglyceride increment was half of that following the isocaloric fat load. The carbohydrate load did not affect apoB-100 and apoB-48 levels. These findings suggest that postprandial triglyceride metabolism is impaired after a carbohydrate load in normolipidemic massively obese women.

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Ingestion of fat is characterized by plasma accumulation of chylomicrons and very low density lipoprotein, which represent the triglyceride-rich lipoprotein (TRL). TRL accumulation depends on endovascular lipolysis by lipoprotein lipase and hepatic lipase and lipoprotein receptor-mediated uptake by the liver. The low density lipoprotein (LDL) receptor (LDL-R) and LDL R-related protein could be the major candidates implicated in this process. More recently, it was suggested that the lipolysis-stimulated receptor (LSR) could also play a role in the TRL uptake. As defect of TRL clearance generates the formation of atherogenic remnants, postprandial hypertriglyceridemia eventually leads in the long term to the development of arteriosclerosis. This study aimed to evaluate if the postprandial triglyceride response induced by saturated fatty acid or monounsaturated fatty acids is related to hepatic LDL-R and LSR activities. MATERIALS AND METHODSRabbits (28 NZW) were fed during 2 or 4 wk, with either a control diet (2.7% vegetable fat) or 10%-fat diet providing either saturated fatty acid (SFA) (coconut oil) or monounsaturated fatty acid (MUFA) (olive oil).Rabbits had a fat test-meal containing either SFA or MUFA and [t4C]triglycerides. Control rabbits ingested the SFA and the MUFA test-meal. Chronically coconut oil-fed rabbits for 2 or 4 wk were given a SFA-rich meal at the end of the dietary experiment. Following the same protocol, olive oil-fed rabbits were given a MUFA-rich meal. Hasma triglyceride and radiolabeled dietary triglyceride concentrations were assayed. Postheparin plasma lipoprotein lipase and hepatic lipase were checked. Lipoprotein binding to low density lipoprotein (LDL) receptor (LDL-R) and lipolysis-stimulated receptor (LSR) in control and fat-fed rabbits was measured. Hepatocyte plasmic membranes were isolated with a sucrose-gradient method.Then, i25I-LDL were incubated with hepatocyte plasmic membrane in two conditions: (i) with CaC12 (binding to LDL-R calcium-dependent) and (ii) with EDTA (prevent the binding to LDL-R) and oleate (LSR activated by free fatty acids). RESULTSAs compared to control rabbits, postprandial triglyceridemia as well as plasma dietary [14C]triglyceride accumulation was slightly altered in olive oil-fed rabbits. On the contrary, postprandial plasma triglyceride and [14C]triglyceride concentrations were significantly higher in rabbits fed the coconut oilrich diet for 4 wk, as compared to control and olive oil-fed rabbits.Chronic ingestion of the MUFA diet did not alter hepatic lipase activity, while the SFA diet decreased it after 2 wk and increased it after 4 wk. The two experimental diets did not modify lipoprotein lipase activity as compared to the control diet.Binding of lipoprotein to the LDL-R and to the LSR is expressed as ~amol I25I-LDL/mg plasma membrane protein. As compared to control rabbits, the SFA diet decreased lipoprotein binding to LDL-R, while the MUFA diet significantly increased lipoprotein binding to LDL-R. As compared to control rabbits, the MUFA diet in...

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Energy restriction had no effect on the liver fatty acid profile. In contrast, high-fat energy restricted diets (groups C and D) induced important modifications to the profile. By comparing groups C and D with group A, the