Acute differential effects of dietary protein quality on postprandial lipemia in obese non-diabetic subjects.

Non-fasting triglyceridemia is much closer associated to cardiovascular risk compared to fasting triglyceridemia. We hypothesized that there would be acute differential effects of four common dietary proteins (cod protein, whey isolate, gluten, and casein) on postprandial lipemia in obese non-diabetic subjects. To test the hypothesis we conducted a randomized, acute clinical intervention study with crossover design. We supplemented a fat rich mixed meal with one of four dietary proteins i.e. cod protein, whey protein, gluten or casein. Eleven obese non-diabetic subjects (age: 40-68, body mass index: 30.3-42.0 kg/m(2)) participated and blood samples were drawn in the 8-h postprandial period. Supplementation of a fat rich mixed meal with whey protein caused lower postprandial lipemia (P = .048) compared to supplementation with cod protein and gluten. This was primarily due to lower triglyceride concentration in the chylomicron rich fraction (P = .0293). Thus, we have demonstrated acute differential effects on postprandial metabolism of four dietary proteins supplemented to a fat rich mixed meal in obese non-diabetic subjects. Supplementation with whey protein caused lower postprandial lipemia compared to supplementation with cod and gluten. As postprandial lipemia is closely correlated to cardiovascular disease, long-term dietary supplementation with whey protein may prove beneficial in preventing cardiovascular disease in obese non-diabetic subjects.

Effects of different protein sources on plasminogen inhibitor-1 and factor VII coagulant activity added to a fat-rich meal in type 2 diabetes.

BACKGROUND: Exaggerated postprandial triglyceride concentration is believed to be atherogenic, and to influence the risk of thrombosis. Both elevated plasminogen inhibitor 1 (PAI-1) and increased factor VII coagulant activity (FVIIc) are potential important contributors to the increased risk of cardiovascular disease in type 2 diabetes. AIM: We aimed to investigate the effect of adding four different protein types (i.e. casein, whey, cod, and gluten) to a fat-rich meal on postprandial responses of PAI-1 and FVIIc in type 2 diabetic patients. METHODS: Twelve type 2 diabetic patients ingested four isocaloric test meals in random order. The test meals contained 100 g of butter and 45 g of carbohydrate in combination with 45 g of casein (Cas-meal), whey (Whe-meal), cod (Cod-meal), or gluten (Glu-meal), respectively. Plasma concentrations of PAI-1 and FVIIc were measured before meal, and at regular intervals for 8-h postprandially. RESULTS: The postprandial PAI-1 concentration decreased significantly by 49% to 56% in response to the four test meals. There were no significant differences between the outcomes from the four test-meals. The FVIIc levels decreased by 8% to 11% after the meals. Again, we observed no significant differences in outcomes between the four protein-enriched meals. CONCLUSIONS: The four proteins casein, whey, cod, and gluten, added to a fat-rich meal, all decreased the PAI-1 and FVIIc concentrations postprandially in type 2 diabetic subjects. However, postprandial levels of PAI-1 and FVIIc were not acutely influenced by the protein source.

Differential effects of protein quality on postprandial lipemia in response to a fat-rich meal in type 2 diabetes: comparison of whey, casein, gluten, and cod protein.

BACKGROUND: Enhanced and prolonged postprandial triglyceride responses involve increased cardiovascular disease risk in type 2 diabetes. Dietary fat and carbohydrates profoundly influence postprandial hypertriglyceridemia, whereas little information exists on the effect of proteins. OBJECTIVE: The objective was to compare the effects of the proteins casein, whey, cod, and gluten on postprandial lipid and incretin responses to a high-fat meal in persons with type 2 diabetes. DESIGN: A crossover study was conducted in 12 patients with type 2 diabetes. Blood samples were collected over 8 h after ingestion of a test meal containing 100 g butter and 45 g carbohydrate in combination with 45 g casein (Cas-meal), whey (Whe-meal), cod (Cod-meal), or gluten (Glu-meal). We measured plasma concentrations of triglycerides, retinyl palmitate (RP), free fatty acids, insulin, glucose, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide. RESULTS: The incremental area under the curve for triglyceride was significantly lower after the Whe-meal than after the other meals. The RP response was lower after the Whe-meal than after the Cas-meal and Cod-meal in the chylomicron-rich fraction and higher after the Whe-meal than after Cod- and Glu-meals in the chylomicron-poor fraction. Free fatty acids were most pronouncedly suppressed after the Whe-meal. The glucose response was lower after the Whe-meal than after the other meals, whereas no significant differences were found in insulin, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide responses. CONCLUSION: The data suggest that as a supplement to a fat-rich meal in patients with type 2 diabetes, whey protein seems to outperform other proteins in terms of postprandial lipemia improvement, possibly because of the formation of fewer chylomicrons or increased clearance of chylomicrons. The trial was registered at ClinicalTrials.gov as NCT00817973.

Effects of one single bout of low-intensity exercise on postprandial lipaemia in type 2 diabetic men.

Fighting type 2 diabetes and its high risk of CVD, lifestyle intervention with diet and exercise is of uttermost importance. Epidemiological studies strongly suggest an inverse association between increased physical activity, moderate alcohol drinking and the incidence of both type 2 diabetes and CVD. However, alcohol is known to increase postprandial lipaemia, a risk marker of CVD, and exercise to reduce postprandial lipaemia in healthy individuals. The aim of the present study was to investigate how type 2 diabetic men respond, in the postprandial period, to a single exercise session feasible to perform on a daily basis for type 2 diabetic men. The twelve participants ingested a test meal containing 100 g butter, 50 g carbohydrate, together with 40 g alcohol, at each meal test, imitating a social meal situation. Two protocols included exercise sessions with 40 min at 40% VO2max, one where they exercised 3.5 h after, and another the afternoon before the test meal. One protocol was without any exercise. No significant effect of low-intensity exercise on postprandial lipaemia following a fat-rich meal with alcohol was seen in the middle-aged type 2 diabetic men.

Ethanol with a mixed meal decreases the incretin levels early postprandially and increases postprandial lipemia in type 2 diabetic patients.

Increased postprandial lipemia is a risk marker of cardiovascular disease (CVD). While moderate alcohol drinking is associated with a reduced risk of CVD in nondiabetic and type 2 diabetic patients, it is also known that alcohol increases postprandial triacylglycerol levels. The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are important hormones from the gut that enhance nutrient-stimulated insulin secretion. Their responses to a moderate alcohol dose in type 2 diabetes have not previously been studied. We sought to determine how alcohol influences postprandial lipid and incretin levels in patients with type 2 diabetes when taken in combination with a fat-rich mixed meal. Eleven patients with type 2 diabetes ingested on 3 separate days in random order 3 different meals containing: 100 g butter alone or 100 g butter in combination with 40 g alcohol and 50 g carbohydrate, or 100 g butter and 120 g carbohydrate. The meal with alcohol and 50 g carbohydrate was isocaloric to that of 120 g carbohydrate. Triacylglycerol levels were measured after separation by ultracentrifugation into a chylomicron-rich fraction with Svedberg flotation unit values (Sf) > 1,000, and a chylomicron-poor fraction with Sf < 1,000. Supplementation of a fat-rich mixed meal with alcohol in type 2 diabetic subjects suppressed GLP-1 early in the postprandial phase and increased the late triacylglycerol responses compared with the 2 other meals. In the chylomicron-rich fraction, both triacylglycerol and cholesterol were increased by alcohol. No significant differences in high-density lipoprotein (HDL)-cholesterol levels were seen. Isocaloric amounts of carbohydrate and alcohol suppressed equally the postprandial free fatty acid levels, but carbohydrate increased the postprandial glucose, GIP, and insulin levels the most. Early in the postprandial phase, alcohol suppresses the incretin responses and increases the late postprandial triacylglycerol levels in type 2 diabetic patients. Whether this reflects an alcohol-induced suppression of the incretin response, which adds to the alcohol-induced impairment of triacylglycerol clearance in type 2 diabetic patients, remains to be elucidated.

Differential postprandial lipoprotein responses in type 2 diabetic men with and without clinical evidence of a former myocardial infarction.

Postprandial lipemia plays an important role in the development of coronary heart disease through an elevation of triglyceride-rich lipoproteins. In type 2 diabetic male subjects, our aim was to compare postprandial lipemia in a high-risk population with former myocardial infarction (MI) with that of a lower risk population free of clinically detectable heart disease. 32 male type 2 diabetic subjects were included in the study. We matched 17 cases with a verified history of MI with 15 controls according to age, BMI, HbA1c, diabetes duration, smoking, and treatment of diabetes. Ongoing metformin, insulin, or lipid lowering pharmacological treatment were exclusion criteria. After a maximal exercise tolerance test and echocardiography, the subjects underwent a hyperinsulinemic, euglycemic clamp and a vitamin A fat loading test. Plasma triglyceride levels in the case group were significantly higher after 360 minutes (4.6 +/- 3.1 vs. 2.8 +/- 1.8 mmol/l, p = 0.04) and 480 minutes (3.6 +/- 2.2 vs. 2.4 +/- 2.4 mmol/l, p = 0.03), as was the incremental Area Under the Curve (iAUC) for the whole period (560 +/- 452 vs. 297 +/- 214 mmol x 480 min./l; p = 0.048). In addition, the retinyl palmitate responses in the chylomicron-fraction from the case group were significantly higher (iAUC 311,502 +/- 194,933 vs. 187,004 +/- 102,928 ng x 480 min./ml; p = 0.035). Type 2 diabetic males with prior MI had higher postprandial triglyceride-rich lipoprotein responses than those without MI, indicating that high responses may be a marker for a high-risk population.

Incremental area under response curve more accurately describes the triglyceride response to an oral fat load in both healthy and type 2 diabetic subjects.

Elevation of postprandial triacylglycerol (TG)-rich plasma lipoproteins is considered potentially atherogenic. Type 2 diabetic patients have exaggerated postprandial TG compared with healthy subjects. Postprandial TG responses to oral fat loads are usually studied as the area under the TG curve. No consensus exists regarding the method of choice when calculating the TG response area. We evaluated the correlation between fasting TG and postprandial TG responses calculated by the trapezoid rule as total area under the curve (AUC) and incremental area under the curve (iAUC). Furthermore, we compared the AUC and iAUC to a 3-point calculation method. Ten healthy subjects and 47 type 2 diabetic patients ingested test meals consisting of an energy-free soup plus 80 g fat and 50 g carbohydrate. TG responses were measured in total plasma, in a chylomicron (CM)-rich fraction and in a CM-poor fraction. In healthy subjects the AUC, but not iAUC, correlated positively to fasting TG. In type 2 diabetic patients a strong correlation was found between fasting TG and AUC, whereas weak associations were found to the iAUCs. The iAUC was strongly correlated to the postprandial TG rise in both groups. The 3-point areas differed significantly from the trapezoid measurements in both healthy and type 2 diabetic subjects. In conclusion, in both healthy and type 2 diabetic subjects total AUC is highly correlated to fasting TG, whereas iAUC more accurately describes the TG response to an oral fat load. The 3-point test seems less suitable for the determination of postprandial response in both healthy and type 2 diabetic subjects.

Differential effects of saturated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes.

BACKGROUND: Postprandial lipemia is important in the development of coronary artery disease because of elevated postprandial triacylglycerol-rich plasma lipoproteins and suppressed HDL-cholesterol concentrations. We showed in healthy subjects a possible association between postprandial lipid metabolism and the responses of the duodenal incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide after meals rich in saturated and monounsaturated fatty acids (oleic acid), respectively. OBJECTIVE: The objective was to compare the postprandial responses (8 h) of glucose, insulin, fatty acids, triacylglycerol, gastric inhibitory polypeptide, and GLP-1 to saturated- and monounsaturated-rich test meals. DESIGN: Twelve overweight patients with type 2 diabetes ingested 3 meals randomly: an energy-free soup with 50 g carbohydrate (control meal), the control meal plus 100 g butter, and the control meal plus 80 g olive oil. Triacylglycerol responses were measured in total plasma and in a chylomicron-rich and a chylomicron-poor fraction. RESULTS: No significant differences in the glucose, insulin, or fatty acid responses to the 2 fat-rich meals were seen. The plasma triacylglycerol and chylomicron triacylglycerol responses were highest after the butter meal. HDL-cholesterol concentrations decreased significantly after the butter meal but did not change significantly after the olive oil meal. GLP-1 responses were highest after the olive oil meal. CONCLUSIONS: Olive oil induced lower triacylglycerol concentrations and higher HDL-cholesterol concentrations than did butter, without eliciting significant changes in glucose, insulin, or fatty acids. Furthermore, olive oil induced higher concentrations of GLP-1, which may indicate a relation between fatty acid composition, incretin responses, and triacylglycerol metabolism postprandially in patients with type 2 diabetes.

Carvedilol does not alter the insulin sensitivity in patients with congestive heart failure.

BACKGROUND: Congestive heart failure (CHF) has previously been shown to be associated with insulin resistance and hyperinsulinemia. A beneficial effect of the non-selective beta-blocker carvedilol has been demonstrated in patients with CHF. However, whether the drug affects the insulin sensitivity (S(i)) is unknown. AIMS: To investigate whether treatment with carvedilol alters the S(i) in patients with CHF during a prospective, double-blinded, placebo-controlled study. METHODS AND RESULTS: The patients were randomized to receive either carvedilol (n=29) or matched placebo (n=17). Insulin and glucose responses were measured during a 0.3 g/kg intravenous glucose tolerance test, and S(i) was calculated according to Bergman's Minimal Model. Baseline S(i) values correlated significantly with body mass index (r=-0.42, P=0.002), plasma urate (r=-0.42, P=0.002), plasma HDL-cholesterol (r=0.39, P=0.003), maximal oxygen uptake (r=0.35, P=0.009), plasma triglycerides (r=-0.34, P=0.01) and weight (r=-0.29, P=0.03). During the study the insulin sensitivity was unchanged in the carvedilol group compared with placebo (2.63+/-1.45 to 2.38+/-1.64 vs. 2.81+/-2.36 to 2.48+/-1.84x10(-4) min(-1)/mUl(-1), P=0.83). CONCLUSION: Additional treatment with carvedilol is neutral with regard to influence the insulin sensitivity in patients with mild to moderate CHF.