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Original Articles

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

  1. Y-D Ida Chen,
  2. Ann M Coulston, MS,
  3. Ming-Yue Zhou, MD,
  4. Clarie B Hollenbeck, PHD and
  5. Gerald M Reaven, MD
  1. Department of Medicine, Stanford University School of Medicine and Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, Palo Alto, California
  1. Address correspondence and reprint requests to Gerald M. Reaven, MD, GRECC (182-B), VA Medical Center, 3801 Miranda Ave., Palo Alto, CA 94304.
Diabetes Care 1995 Jan; 18(1): 10-16. https://doi.org/10.2337/diacare.18.1.10
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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.

  • Received March 21, 1994.
  • Revision received August 18, 1994.
  • Accepted August 18, 1994.
  • Copyright © 1995 by the American Diabetes Association
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Why Do Low-Fat High-Carbohydrate Diets Accentuate Postprandial Lipemia in Patients With NIDDM?
Y-D Ida Chen, Ann M Coulston, Ming-Yue Zhou, Clarie B Hollenbeck, Gerald M Reaven
Diabetes Care Jan 1995, 18 (1) 10-16; DOI: 10.2337/diacare.18.1.10

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Why Do Low-Fat High-Carbohydrate Diets Accentuate Postprandial Lipemia in Patients With NIDDM?
Y-D Ida Chen, Ann M Coulston, Ming-Yue Zhou, Clarie B Hollenbeck, Gerald M Reaven
Diabetes Care Jan 1995, 18 (1) 10-16; DOI: 10.2337/diacare.18.1.10
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