Fasting Hypertriglyceridemia in Non insulin-Dependent Diabetes Mellitus Is an Important Predictor of Postprandial Lipid and Lipoprotein Abnormalities*

Abstract

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, less than 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 less than 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 less than 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 less than 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 less than 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.

Exacerbation of insulin resistance and postprandial triglyceride response in newly diagnosed hypertensive patients with hypertriglyceridaemia

“…Fasting TG has been repeatedly reported in literature 11,12,13,27 as well as in this study (Table 2) to be highly correlated with postprandial TG response. Karamanos et al 28 have challenged the relation in a recent study involved normotriglyceridaemic healthy participants with a 4-h meal test.…”

“…The fasting TG level can be regarded as a measure of the VLDL pool. 13 The higher the fasting TG is, the larger the VLDL pool, the more difficult for chylomicrons to compete with VLDL for the removal, and the higher response the postprandial TG.…”

“…The MMT was carried out by a protocol reported before. 13,19 In brief, the patients received the MMT in the morning after an overnight fast of 12 h. After the collection of the baseline blood samples, the patients were subjected to a 1000 kcal mixed meal consisting of 73 g (65.9% of calories) fat, 47 g (18.9%) carbohydrates and 38 g (15.2%) protein. The meal included scrambled eggs, bread, hot dog and whole milk added with sugar.…”

“…10 Exaggerated postprandial TG levels have been reported in persons with fasting hypertriglyceridaemia, 11 visceral obesity, 12 and type 2 DM. 13 However, there was little study on postprandial TG response in patients with hypertension. 14 Multiple risk factors tend to increase CVD risk synergistically.…”

Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM

“…However, the link between a high plasma triglyceride concentration and CHD is far from obvious. For example, patients with NIDDM and/or hypertriglyceridaemia have been shown to have increases in plasminogen activator inhibitor-1 [35,36], smaller, denser LDL particles [37,38], and increased postprandial lipaemia [2,39]; changes which have been proposed as increasing the risk of CHD in non-diabetic subjects [3][4][5][6][7][8][9]. It seems reasonable to speculate that a similar relationship between these changes and CHD would also exist in patients with NIDDM.…”