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,
N. M. O'MEARA,
P. A. SOLTYS,
J. D. BLACKMAN,
P. H. IVERIUS
,
W. L. PUGH,
G. S. GETZ and
K. S. POLONSKY
Departments of Medicine and Pathology, University of Chicago, Pritzker School of Medicine Chicago, Illinois 60637; and the Department of Internal Medicine, University of Utah School of Medicine, Veterans Administration Medical Center (P.H.I.) Salt Lake City, Utah 84148
Address all correspondence and requests for reprints to: Kenneth S. Polonsky, Department of Medicine, University of Chicago, Box 435, 5841 South Maryland Avenue, Chicago, Illinois 60637.
Supported by the Pew National Nutrition Program.
Supported by the V.A. and NIH Grant HL-39595.
Postprandial lipoprotein metabolism may be important in atherogenesis and has not been studied in detail in noninsulin-dependent diabetes mellitus (NIDDM). We used the vitamin A fat-loading test to label triglyceride-rich lipoprotein particles of intestinal origin after ingestion of a high fat mixed meal containing 60 g fat/m2 and 60,000 U vitamin A/m2 in 12 untreated NIDDM subjects with normotriglyceridemia (NTG; triglycerides, <1.7 mmol/L), 7 untreated NIDDM subjects with moderate hypertriglyceridemia (HTG; triglycerides, 1.7–4.7 mmol/L), and 8 age- and weight-matched normotriglyceridemic nondiabetic controls.
The postprandial triglyceride increment was greater in NIDDM with HTG (P = 0.0001) and correlated strongly in all groups with the fasting triglyceride concentration (r = 0.83; P = 0.0001). Retinyl palmitate measured in whole plasma, an Sf greater than 1000 chylomicron fraction, and an Sf less than 1000 nonchylomicron fraction was also significantly greater in NIDDM with HTG, but did not differ significantly between NIDDM with NTG and controls. In NIDDM with HTG, chylomicrons appeared to be cleared at a slower rate, as evidenced by the significantly later intersection of the chylomicron and nonchylomicron retinyl palmitate response curves (13.7 h in HTG NIDDM vs. 8.5 h in NTG NIDDM vs. 7.3 h in controls; P < 0.01).
Although fasting FFA levels were similar in all three groups, the HTG diabetic subjects had a late postprandial surge in FFAs that lasted for up to 14 h. The postprandial FFA elevation in all groups correlated with the fasting triglyceride concentration (r = 0.57; P < 0.002) and postprandial triglyceride increment (r = 0.80; P = 0.0001).
The fasting core triglyceride content of the HDL particles in NIDDM with HTG was significantly elevated compared to those in NIDDM with NTG and controls (21.0% vs. 14.0% vs. 14.1% respectively; P < 0.05), and this increased proportionately in all groups after the meal at the expense of cholesteryl ester, the increase correlating with total plasma postprandial triglyceride increment (r = 0.51; P < 0.01).
We conclude that moderate fasting hypertriglyceridemia in NIDDM is predictive of a constellation of postprandial changes in lipids and lipoproteins that may potentiate the already unfavorable atherogenic fasting lipid profile in these subjects. (J Clin Endocrinol Metab 72: 934–944, 1991)
* This work was supported by NIH Grants DK-31842, DK-13941, DK-20595 (Diabetes Research and Training Center), HL-15062-18 (SCOR in Atherosclerosis), DK-26678 (Clinical Nutrition Research Unit), and RR-00055 (Clinical Research Center), and a Research Grant from the American Diabetes Association. This paper was presented in part (in abstract form) at the 48th Annual Scientific Sessions of the American Diabetes Association, Detroit, MI, June 1989.
Received June 7, 1990.
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