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Dietary polyphenols and long chain n-3 polyunsaturated fatty acids (LCn3) are associated with lower cardiovascular risk. This may relate to their influence on glucose metabolism and diabetes risk. We evaluated the effects of diets naturally rich in polyphenols and/or LCn3 of marine origin on glucose metabolism in people at high cardiometabolic risk. According to a 2 × 2 factorial design, individuals with high waist circumference and at least one more component of the metabolic syndrome were recruited at the obesity outpatient clinic. Eighty-six participants were randomly assigned by MINIM software to an isoenergetic diet: (1) control, low in LCn3 and polyphenol (analysed n = 20); (2) rich in LCn3 (n = 19); (3) rich in polyphenols (n = 19); or (4) rich in LCn3 and polyphenols (n = 19). The assigned diets were known for the participants and blinded for people doing measurements. Before and after the 8 week intervention, participants underwent a 3 h OGTT and a test meal with a similar composition as the assigned diet for the evaluation of plasma glucose, insulin and glucagon-like peptide 1 (GLP-1) concentrations, and indices of insulin sensitivity and beta cell function. During OGTT, polyphenols significantly reduced plasma glucose total AUC (p = 0.038) and increased early insulin secretion (p = 0.048), while LCn3 significantly reduced beta cell function (p = 0.031) (two-factor ANOVA). Moreover, polyphenols improved post-challenge oral glucose insulin sensitivity (OGIS; p = 0.05 vs control diet by post hoc ANOVA). At test meal, LCn3 significantly reduced GLP-1 total postprandial AUC (p

Eur J Clin Invest 2010; 41 (1): 39–44 Abstract Background Fatty liver is commonly associated with insulin-resistant conditions, often related to increased abdominal visceral fat. Our objective was to elucidate the specific roles of obesity, type 2 diabetes mellitus, insulin-resistance and abdominal fat distribution. Materials and methods The study population comprised 13 diabetic obese (DO), 10 nondiabetic obese (NDO), and nine normal-weight control (C) men aged 28–65 years, with normal plasma triglyceride levels. DO were in good glycaemic control (HbA1c = 6·8 ± 0·8%) (M ± SD) with diet (n = 8) or diet + metformin (n = 5). Liver fat content was measured by 1H-magnetic resonance spectroscopy, abdominal fat distribution by magnetic resonance imaging and insulin sensitivity by hyperinsulinaemic euglycaemic clamp. Results DO and NDO subjects had similar whole-body insulin resistance, BMI and waist circumference, higher than those of C subjects (P

OBJECTIVE To search for a better dietary approach to treat postprandial lipid abnormalities and improve glucose control in type 2 diabetic patients. RESEARCH DESIGN AND METHODS According 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. RESULTS In 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). CONCLUSIONS A 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.

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 omega(3) fatty acids significantly improved it, whereas the effects of monounsaturated and omega(6) 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 omega(3) 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 omega(3) 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 omega(3) 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 omega(3) 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.

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 P0.05; 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.

Objective: To assess whether a diet containing foods enriched with beta-glucans (3.6 g/d), folic acid (1600 mu g/d), long-chain (800 mg/d) and short-Chain (400 mg/d) n-3 fatty acids, and tocopherols (120 mg/d) is able to modulate positively the cardiovascular risk profile in people at slightly increased cardiovascular risk. Methods: Sixteen subjects with mild plasma lipid abnormalities were studied according to a randomized crossover design. After a 2-week run-in period, they followed a diet containing baked products enriched with active nutrients (active diet) or a diet containing the same products but without active nutrients (control diet) for 1 month and then crossed over to the other diet. At the end of each period, a test meal of the same composition as the corresponding diet was administered, and plasma samples were obtained before and for 6 hours after the meal. Hunger and satiety were evaluated by the visual analog scale at fasting and after the meal. Results: Fasting plasma triglycerides were significantly lower after the active versus the control diet (1.56 +/- 0.18 vs 1.74 +/- 0.16 mmol/l, p < 0.05), as was the postprandial level of chylomicron triglycerides and the insulin peak (p < 0.05). The active diet also reduced fasting homocysteine (8 +/- 0.6 vs 10 +/- 0.8 mu mol/l, p < 0.05) and the feeling of hunger at the fifth and sixth hour (p < 0.05). Conclusions: Baked functional products enriched with n-3 fatty acids, folates, beta-glucans, and tocopherols within the context of a balanced diet lower fasting and postprandial plasma triglycerides, fasting homocysteinemia, and the postprandial insulin peak. They induce a greater feeling of satiety with possible beneficial implications on energy intake.

To improve the quality of diabetes care, a project of integrated diabetes management (PIDM) involving some general practitioner (GPs) has been recently undertaken. The purpose of this study is to compare features and treatment of patients followed by diabetic outpatient clinics (DOCs) with those cared for by GPs trained to the PIDM. Twenty-one DOCs and eleven GPs participated in the study. Patients followed by DOCs (n. = 1110) showed longer duration of diabetes, higher prevalence of metabolic syndrome than patients followed by GPs (n. = 305). More patients followed in DOCs performed insulin therapy, while a lower number received ACE /angiotensin blockers, antiplatelet, lipid lowering drugs and multifactorial intervention than patients followed by GPs. The proportion of patients in good control for glucose, pressure and lipid levels was similar in the two groups. Conversely, a higher number of patients attending DOCs were in poor glycemic, pressure, and lipid control compared with patients followed by GPs. In conclusions, PIDM provides satisfactory results in terms of overall glucose, pressure and lipid control, thus encouraging implementation of PIDM to meet the increasing demand for diabetes care.

We investigated postprandial plasma and adipose tissue (AT) adiponectin changes in relation to obesity and type 2 diabetes mellitus. Fasting and 6 hours after a standard fat-rich meal blood samples (adiponectin, glucose, insulin, lipids) and needle biopsies of abdominal subcutaneous AT (adiponectin messenger RNA, lipoprotein lipase activity) were taken in 10 obese diabetic (OD), 11 obese nondiabetic (OND), and 11 normal-weight control (C) men. The OD and OND subjects had similar adiposity (body mass index, waist circumference) and insulin resistance (hyperinsulinemic euglycemic clamp). Fasting plasma adiponectin and AT gene expression were not significantly different between groups. After meal, plasma adiponectin decreased in OD but significantly increased in OND and C, the changes being significantly different between groups (analysis of variance, P = .01); adiponectin messenger RNA decreased in OD (-0.27 +/- 0.25 AU, P = .01) but was unchanged in OND (P = .59) and C (P = .45). After meal, plasma adiponectin correlated inversely with triglyceride and cholesterol concentrations in chylomicrons and large very low-density lipoprotein, and directly with AT lipoprotein lipase activity (P < .05 for all). Type 2 diabetes mellitus is associated with lower postprandial plasma levels and AT gene expression of adiponectin independently of degree of adiposity and whole-body insulin sensitivity. In patients with diabetes, this may exacerbate postprandial abnormalities of lipoprotein metabolism.

BACKGROUND AND AIMS: Postprandial lipoprotein abnormalities in type 2 diabetes are associated with insulin resistance. The role of other diabetes-related factors is still not clear. The aim of this study is to differentiate the effects of whole-body insulin resistance, obesity, and type 2 diabetes on postprandial dyslipidaemia and lipoprotein lipase (LPL) in adipose tissue. METHODS AND RESULTS: Ten subjects with obesity and diabetes (OD), 11 with obesity alone (O), and 11 normal-weight controls (C) - males, aged 26-59 years, with fasting normo-triglyceridaemia underwent measurements of cholesterol, triglycerides, apo B-48 and apo B-100 concentrations in plasma lipoproteins separated by density gradient ultracentrifugation before and after a fat-rich meal. Fasting and postprandial (6h) LPL activity was determined in abdominal subcutaneous adipose tissue biopsy samples. Insulin sensitivity was measured by hyperinsulinaemic euglycaemic clamp. OD and O subjects had similar degrees of adiposity (BMI, waist circumference, fat mass) and insulin resistance (insulin stimulated glucose disposal and M/I). They also showed a similarly higher postprandial increase in large VLDL lipids (triglyceride incremental AUC 188+/-28 and 135+/-22 mg/dl.6h) than C (87+/-13 mg/dl.6h, M+/-SEM, p

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 50.0±2.6 and 48.1±1.3 years; body mass index 28.3±1.2 and 25.6±1.1 kg/m 2 ; fasting plasma triglycerides 1.12±0.13 and 0.87±0.08 mmol/L, respectively; mean±SEM; NS) consumed a mixed meal during an 8-hour hyperinsulinemic glycemic clamp. Mean blood glucose during clamp was ≈7.8 mmol/L, and plasma insulin during the preprandial steady state was ≈480 pmol/L in both groups, that differed for insulin sensitivity (M/I value lower in diabetic subjects [1.65±0.30 and 3.42±0.60; P P P P Conclusions— Insulin resistance is also associated with postprandial lipoprotein abnormalities in type 2 diabetes after acute correction for hyperglycemia and hyperinsulinemia.