Why Do Low-Fat High-Carbohydrate Diets Accentuate Postprandial Lipemia in Patients With NIDDM?

Abstract

OBJECTIVE To understand why low-fat high-carbohydrate (CHO) diets lead to higher fasting and postprandial concentrations of triglyceride (TG)-rich lipoproteins in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS Patients with NIDDM were placed randomly on diets containing either 55% CHO, 30% fat, and 15% protein or 40% CHO, 45% fat, and 15% protein for 6 weeks, followed by crossover to the other diet. Test meals at the end of each diet period were consumed at 8:00 A.M. and 12:00 P.M. (noon) and contained 20 and 40% of daily calories, respectively. Vitamin A was also given at noon, and TG-rich lipoproteins of intestinal origin were identified by the presence of vitamin A esters. Frequent measurements were made throughout the 24-h study period of plasma glucose, insulin, and TG concentrations. Plasma samples obtained from 12:00 P.M. (noon) until 12 A.M. (midnight) were subjected to ultracentrifugation, and measurements were made of TG and vitamin A ester concentrations in plasma and in both the Svedberg flotation constant (Sf) >400 (chylomicron) and Sf 20-400 (chylomicron remnant) lipoprotein fractions. In addition, very-low-density lipoprotein (VLDL)-TG turnover rate was estimated by following the decay of [3H]VLDL-TG. Finally, postheparin lipoprotein lipase and hepatic lipase activities were measured at the end of each dietary period. RESULTS Mean ± SE hourly concentrations of glucose (8.0 ± 0.8 vs. 7.5 ± 0.7 mmol/1), insulin (184 ± 26 vs. 158 ± 19 pmol/1), and TG (2.8 ± 0.2 vs. 2.1 ± 0.2 mmol/1) were higher (P < 0.05-0.001) after the 55% CHO diet. The 55% CHO diet also led to an increase (P < 0.05-0.01) in the mean ± SE hourly concentrations of vitamin A esters in plasma (2.3 ± 0.3 vs. 1.6 ±0.1 μmol/l) and in both the chylomicron (2.0 ± 0.3 vs. 1.4 ±0.1 μmol/l) and chylomicron remnant fractions (0.36 ± 0.04 vs. 0.14 ± 0.03 μmol;/l). In addition, the VLDL-TG production rate was higher (17.2 ± 1.4 vs. 12.8 ± 1.0 mg · kg−1 · h−1, P < 0.003) and the VLDL-TG fractional catabolic rate lower (0.22 ± 0.02 to 0.28 ± 0.02 l/h, P < 0.005) after the 55% CHO diet. Finally, there was an increase in lipoprotein lipase activity (7.0 ± 0.8 to 8.1 ± 0.7 μmol free fatty acids released · ml−1 · h−1, P < 0.02) in response to the CHO-enriched diet. CONCLUSIONS A low-fat high-CHO diet in patients with NIDDM led to 1) higher day-long plasma glucose, insulin, and TG concentrations; 2) postprandial accumulation of TG-rich lipoproteins of intestinal origin; 3) increased production of VLDL-TG; and 4) increased postheparin lipoprotein lipase activity. These data provide a mechanism for the hypertriglycer-idemic effect of CHO-enriched diets in patients with NIDDM and demonstrate that multiple risk factors for coronary heart disease are accentuated when these individuals consume diets recommended to reduce this risk.