OBJECTIVETo search for a better dietary approach to treat postprandial lipid abnormalities and improve glucose control in type 2 diabetic patients.RESEARCH DESIGN AND METHODSAccording to a randomized crossover design, 18 type 2 diabetic patients (aged 59 ± 5 years; BMI 27 ± 3 kg/m2) (means ± SD) in satisfactory blood glucose control on diet or diet plus metformin followed a diet relatively rich in carbohydrates (52% total energy), rich in fiber (28g/1,000 kcal), and with a low glycemic index (58%) (high-carbohydrate/high-fiber diet) or a diet relatively low in carbohydrate (45%) and rich in monounsaturated fat (23%) (low-carbohydrate/high–monounsaturated fat diet) for 4 weeks. Thereafter, they shifted to the other diet for 4 more weeks. At the end of each period, plasma glucose, insulin, lipids, and lipoprotein fractions (separated by discontinuous density gradient ultracentrifugation) were determined on blood samples taken at fasting and over 6 h after a test meal having a similar composition as the corresponding diet.RESULTSIn addition to a significant decrease in postprandial plasma glucose, insulin responses, and glycemic variability, the high-carbohydrate/high-fiber diet also significantly improved the primary end point, since it reduced the postprandial incremental areas under the curve (IAUCs) of triglyceride-rich lipoproteins, in particular, chylomicrons (cholesterol IAUC: 0.05 ± 0.01 vs. 0.08 ± 0.02 mmol/l per 6 h; triglycerides IAUC: 0.71 ± 0.35 vs. 1.03 ± 0.58 mmol/l per 6 h, P < 0.05).CONCLUSIONSA diet rich in carbohydrate and fiber, essentially based on legumes, vegetables, fruits, and whole cereals, may be particularly useful for treating diabetic patients because of its multiple effects on different cardiovascular risk factors, including postprandial lipids abnormalities.
The trial was funded by European Community's Seventh Framework Programme FP7/2009-2012 under grant agreement FP7-KBBE-222639, Etherpaths Project and 'Ministero Istruzione Università e Ricerca' PRIN 2010-2011 - 2010JCWWKM.
The aim of this study was to evaluate exogenous and endogenous lipoprotein responses to a standard fat-rich meal in type 2 diabetic patients with optimal fasting triglyceridemia and optimal blood glucose control. Seven type 2 diabetic patients and five nondiabetic controls (age, 49 +/- 7 and 48 +/- 4 yr; body mass index, 28.3 +/- 3.6 and 25.1 +/- 3.6 kg/m(2); mean +/- SD) were given, after at least 12 h of fasting, a standard fat-rich meal. Before and over the 6 h after the meal, serial blood samples were taken for determination of glucose, insulin, lipids, lipoproteins, apolipoprotein B-48 (apo B-48), apo B-100, free fatty acids, and lipoprotein lipase activity. The main abnormality in the postprandial lipid response of diabetic patients involved large very low density lipoproteins. In these particles, apo B-48, apo B-100, cholesterol, and triglyceride incremental areas were, in fact, significantly higher in diabetics compared with controls [7.08 +/- 2.65 vs. 1.17 +/- 0.88 mg/liter.h, 65.5 +/- 11.5 vs. 12.4 +/- 1.77 mg/liter.h, 29.7 +/- 3.9 vs. 13.1 +/- 3.1 mg/dl.h (0.77 +/- 0.10 vs. 0.34 +/- 0.08 mmol/liter.h), 170 +/- 31 vs. 94 +/- 22 mg/dl.h (1.93 +/- 0.35 vs. 1.06 +/- 0.25 mmol/liter.h)] (all P < 0.05; mean +/- SEM). Postprandial preheparin lipoprotein lipase plasma activity was, if anything, higher in diabetic patients. In conclusion, even with fasting normotriglyceridemia and optimal blood glucose control, type 2 diabetic patients are characterized, in the postprandial period, by a significant increase in large very low density lipoproteins of both endogenous and exogenous origins.
Animal studies have already shown the possibility to modulate insulin action by changing not only the amount of total fat, but also the type of fat. In these studies, saturated fat significantly increased insulin resistance, long‐ and short‐chain ω3 fatty acids significantly improved it, whereas the effects of monounsaturated and ω6 polyunsaturated fatty acids ranged somewhere in between the two. A recent multicenter study (the Kanwu study) on humans has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improved insulin sensitivity in healthy people, while a moderate ω3 supplementation did not affect it; this second finding confirms previous results in type 2 diabetic patients with hypertriglyceridemia. There are also other aspects of the metabolic syndrome that can be influenced by the different type of dietary fat, particularly blood pressure and lipid metabolism. With respect to blood pressure, the majority of studies show that ω3 fatty acids are able to reduce blood pressure in hypertensive patients, but not in normotensive individuals; this result has been confirmed also by the Kanwu study, where no changes in blood pressure were seen after ω3 supplementation in healthy people. On the other hand, in this study, the change from saturated to monounsaturated fatty acids was able to significantly reduce diastolic blood pressure. As to the lipid abnormalities more frequently present in the metabolic syndrome (i.e., hypertriglyceridemia and low HDL cholesterol), the main effects are related to ω3 fatty acids, which surely reduce triglyceride levels, but at the same time increase LDL cholesterol. In conclusion, there is so far sound evidence in humans that the quality of dietary fat is able to influence insulin resistance and some of the related metabolic abnormalities.
Objective-To evaluate the role of insulin resistance in development of postprandial dyslipidemia in type 2 diabetic patients in an experimental setting in which these patients were compared with nondiabetic subjects at similar glucose and insulin blood levels. Methods and Results-Eight type 2 diabetic patients in optimal blood glucose control and 7 control subjects (aged 50.0Ϯ2.6 and 48.1Ϯ1.3 years; body mass index 28.3Ϯ1.2 and 25.6Ϯ1.1 kg/m 2 ; fasting plasma triglycerides 1.12Ϯ0.13 and 0.87Ϯ0.08 mmol/L, respectively; meanϮSEM; NS) consumed a mixed meal during an 8-hour hyperinsulinemic glycemic clamp. Mean blood glucose during clamp was Ϸ7.8 mmol/L, and plasma insulin during the preprandial steady state was Ϸ480 pmol/L in both groups, that differed for insulin sensitivity (M/I value lower in diabetic subjects [1.65Ϯ0.30 and 3.42Ϯ0.60; PϽ0.05]). Subjects with diabetes had higher postprandial levels of lipids and apolipoprotein B (apoB) in large very low-density lipoprotein (incremental area for triglycerides 1814Ϯ421 versus 549Ϯ153 mol/ Lϫ6 hours; PϽ0.05; cholesterol 694Ϯ167 versus 226Ϯ41 mol/Lϫ6 hours; PϽ0.05; apoB-48 6.3Ϯ1.0 versus 2.6Ϯ0.7 mg/Lϫ6 hours; PϽ0.05; apoB-100 56.5Ϯ14.9 versus 26.2Ϯ11.0 mg/Lϫ6 hours; NS). Basal lipoprotein lipase (LPL) activity before and after meal was higher in diabetic subjects, whereas postheparin LPL activity 6 hours after the meal was similar. Key Words: postprandial lipemia Ⅲ large VLDL Ⅲ insulin resistance Ⅲ type 2 diabetes Ⅲ lipoprotein lipase P atients with type 2 diabetes mellitus show abnormalities of the plasma lipoprotein profile in the postprandial state, mainly concerning triglyceride-rich lipoproteins. 1 Because postprandial lipoprotein abnormalities have been consistently associated with an increased risk of coronary heart disease, 2 they could be a major factor explaining the higher rate of cardiovascular diseases observed in these patients. The magnitude of postprandial lipemia is related to the fasting level of plasma triglycerides, 3 and fasting hypertriglyceridemia is a main feature of diabetic dyslipidemia. 4 However, we have shown recently in a group of patients with type 2 diabetes in very good blood glucose control that even with normal fasting triglyceridemia, these patients had higher postprandial levels of large very low-density lipoprotein (VLDL) particles of exogenous and endogenous origin. 5 The factors responsible for these abnormalities, and the mechanisms through which they may influence postprandial lipid response in type 2 diabetic patients, are presently very much debated. 4 Insulin resistance, or the compensatory hyperinsulinemia, as well as hyperglycemia (conditions characterizing type 2 diabetes) have been suggested as major determinants of postprandial lipemia. A possible role for insulin resistance was suggested by Jeppesen et al, 6 who showed in healthy nondiabetic individuals that resistance to insulin-mediated glucose disposal, determined by a modification of the insulin suppression test, was the only independent factor associated with ...
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