Postprandial Free Fatty Acid Concentrations Research Articles

Effects of potato resistant starch intake on insulin sensitivity, related metabolic markers and appetite ratings in men and women at risk for type 2 diabetes: a pilot cross-over randomised controlled trial.

BackgroundThe intake of certain types of resistant starch (RS) has been associated in some studies with increased whole‐body insulin sensitivity. This randomised, cross‐over pilot trial evaluated the effect of consuming cooked, then chilled potatoes, a source of RS, compared to isoenergetic, carbohydrate (CHO)‐containing control foods, on insulin sensitivity and related markers.MethodsNineteen adults with body mass index 27.0‐39.9 kg m−2 consumed 300 g day−1 RS‐enriched potatoes (approximately two potatoes; ~18 g RS) or CHO‐based control foods, as part of lunch, evening and snack meals, over a 24‐h period. After an overnight fast, insulin sensitivity, CHO metabolism markers, free fatty acids, breath hydrogen levels and appetite were assessed for up to 5 h after the intake of a standard breakfast. The primary endpoint was insulin sensitivity, assessed with the Matsuda index. P < 0.05 (one‐sided) was considered statistically significant.ResultsInsulin sensitivity was not significantly different between the potato and control conditions. The potato intervention resulted in higher postprandial breath hydrogen (P = 0.037), lower postprandial free fatty acid concentrations (P = 0.039) and lower fasting plasma glucose (P = 0.043) compared to the control condition. Fullness ratings were significantly lower after potato versus control (P = 0.002). No other significant effects were observed; however, there was a trend toward lower fasting insulin (P = 0.077) in the potato versus the control condition.ConclusionsThe results of this pilot study suggest RS‐enriched potatoes may have a favourable impact on carbohydrate metabolism and support the view that additional research in a larger study sample is warranted.

An acute intake of theobromine does not change postprandial lipid metabolism, whereas a high-fat meal lowers chylomicron particle number

Postprandial responses predict cardiovascular disease risk. However, only a few studies have compared acute postprandial effects of a low-fat, high-carbohydrate (LF) meal with a high-fat, low-carbohydrate (HF) meal. Furthermore, theobromine has favorably affected fasting lipids, but postprandial effects are unknown. Because both fat and theobromine have been reported to increase fasting apolipoprotein A-I (apoA-I) concentrations, the main hypothesis of this randomized, double-blind crossover study was that acute consumption of an HF meal and a theobromine meal increased postprandial apoA-I concentrations, when compared with an LF meal. Theobromine was added to the LF meal. Nine healthy men completed the study. After meal intake, blood was sampled frequently for 4hours. Postprandial apoA-I concentrations were comparable after intake of the 3 meals. Apolipoprotein B48 curves, however, were significantly lower and those of triacylglycerol were significantly higher after HF as compared with LF consumption. Postprandial free fatty acid concentrations decreased less, and glucose and insulin concentrations increased less after HF meal consumption. Except for an increase in the incremental area under the curve for insulin, theobromine did not modify responses of the LF meal. These data show that acute HF and theobromine consumption does not change postprandial apoA-I concentrations. Furthermore, acute HF consumption had divergent effects on postprandial apolipoprotein B48 and triacylglycerol responses, suggesting the formation of less, but larger chylomicrons after HF intake. Finally, except for an increase in the incremental area under the curve for insulin, acute theobromine consumption did not modify the postprandial responses of the LF meal.

Thiazolidinedione Response in Familial Lipodystrophy Patients with LMNA Mutations: A Case Series

Type 2 familial partial lipodystrophy (FPLD2) patients show impaired glucose and lipid metabolism resulting from lipodystrophic 'lipid pressure' and an intrinsic defect in skeletal muscle metabolism. Since mutated lamin A may interfere with peroxisome proliferator activator gamma (PPARγ) expression, we hypothesized that PPARγ stimulation improves fat distribution and metabolic abnormalities in these patients. 5 nondiabetic FPLD2 patients were treated with rosiglitazone over 12 months. We assessed body composition, body fat distribution, and skinfold thickness/subcutaneous tissue thickness. We also determined venous glucose, insulin, and free fatty acid (FFA) concentrations, and respiratory quotient (RQ) before and during oral glucose tolerance testing. Adipose tissue and muscle fasting and postprandial metabolism were studied by microdialysis. Within 12 months treatment, hip circumference increased from 93.6±2.78 cm to 96.2±2.3 cm (p<0.05). Rosiglitazone reduced fasting glucose levels and liver transaminases. Baseline and postprandial FFA concentrations were significantly lower after 12 months treatment. RQ and muscle interstitial pyruvate and lactate did not respond to treatment. We conclude that PPARγ stimulation with rosiglitazone modestly improves glucose metabolism in FPLD2 patients presumably through proximal adipose tissue expansion. The intrinsic muscular metabolic defect does not respond to rosiglitazone.

Orally Disintegrating and Oral Standard Olanzapine Tablets Similarly Elevate the Homeostasis Model Assessment of Insulin Resistance Index and Plasma Triglyceride Levels in 12 Healthy Men

Treatment with olanzapine is associated with obesity, diabetes mellitus, and dyslipidemia. Reports have indicated that orally disintegrating tablets (ODT) cause less weight gain than oral standard tablets (OST). The aim of this study was to compare the effect of short-term treatment with these 2 distinct olanzapine formulations on glucose and lipid metabolism in healthy men. Twelve healthy men (mean ± SEM age: 25.1 ± 5.5 years) received olanzapine ODT (10 mg od, 8 days), olanzapine OST (10 mg od, 8 days), or no intervention in a randomized crossover design. At breakfast and dinner, glucose, insulin, free fatty acids (FFA), and triglyceride concentrations were measured at 10-minute intervals from 30 minutes prior to 2 hours after ingestion of standard meals. Leptin and adiponectin concentrations were measured at 20- and 30-minute intervals, respectively, between 0000h-1200h. Physical activity was assessed with an accelerometer. Fuel oxidation was measured in fasting condition by indirect calorimetry. The study was conducted from April 2006 through September 2006. Treatment with olanzapine ODT and OST equally elevated the homeostasis model assessment of insulin resistance (HOMA-IR) (P = .005). At breakfast, both formulations equally increased fasting and postprandial triglyceride concentrations (P = .013 and P = .005, respectively) while decreasing fasting and postprandial FFA concentrations (P = .004 and P = .009, respectively). Body weight, body composition, physical activity, or fuel oxidation did not differ between treatment modalities. Eight days of treatment with both olanzapine formulations similarly increased HOMA-IR and triglyceride concentrations and decreased FFA concentrations in response to standard meals without affecting anthropometrics or physical activity. These data suggest that olanzapine hampers insulin action via mechanistic routes other than body adiposity or physical inactivity. controlled-trials.com. Identifier: ISRCTN17632637.

Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations

BackgroundWeight regain after weight loss may not be due primarily to voluntary return to social habits but may be explained by changes in peripheral hormonal signals activating hunger and encouraging feeding behavior. ObjectiveThe objective of this study was to investigate physiologic adaptations to weight loss that may encourage weight regain. DesignThe study had a within-subject repeated-measure design [12 healthy, obese men, 33–64 y, body mass index (in kg/m2) 30–46] and was a clinical intervention investigation of circulating metabolites and hunger-satiety responses before and after weight loss. Measures included anthropometry (bioelectrical impedance, body weight, and waist circumference), concentrations of circulating hormones and metabolites [ketone bodies, free fatty acids (FFAs), insulin, leptin, glucose, and cholecystokinin (CCK)], and measures of hunger and satiety at baseline, 8 wk after weight loss with a very-low-energy diet, and 1 wk after weight maintenance. ResultsWeight loss led to a reduction in postprandial CCK secretion (P = 0.016). However, when subjects were ketotic (elevated circulating β-hydroxybutyrate concentrations), CCK secretion was sustained at concentrations before weight loss. After weight loss, there were reduced postprandial FFA concentrations (P = 0.0005). The presence of ketosis sustained FFA to concentrations before weight loss (P = 0.60). ConclusionRapid weight loss of ≈10% of initial body weight results in a reduction in postprandial CCK and FFA concentrations.

Rosiglitazone Improves Postprandial Triglyceride and Free Fatty Acid Metabolism in Type 2 Diabetes

Increased postprandial lipemia is part of diabetic dyslipidemia and is associated with accelerated atherosclerosis. We investigated the effects of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone on postprandial lipemia in patients with type 2 diabetes. A randomized, 8-week, crossover, placebo-controlled, double-blind trial was performed in which rosiglitazone at 4 mg was administrated twice daily in 19 patients with type 2 diabetes. Standardized 6-h oral fat-loading tests were performed after each treatment period. Postprandial curves were calculated as the total area under the curve (AUC) and the incremental area under the curve (dAUC). Rosiglitazone did not change fasting plasma triglycerides compared with placebo (1.97 +/- 0.22 vs. 1.88 +/- 0.20 mmol/l, respectively) but decreased postprandial triglyceride levels, leading to significantly lower triglyceride dAUC (-37%, P < 0.05), without changing total triglyceride AUC. Significant postprandial triglyceride reductions in the chylomicron fraction (Svedberg flotation rate [Sf] >400) were achieved with rosiglitazone, which resulted in a significant lower triglyceride AUC (-22%) in this fraction. The postprandial triglyceride increase in VLDL1 (Sf 60-400) was also lower after rosiglitazone (-27%), but this did not result in a significant lower triglyceride AUC. In VLDL2 (Sf 20-60), there were no significant differences in triglyceride AUC and triglyceride dAUC between rosiglitazone and placebo. Rosiglitazone decreased free fatty acid (FFA) AUC (-12%) and FFA dAUC (-18%) compared with placebo. Rosiglitazone improves the metabolism of large triglyceride-rich lipoproteins and decreases postprandial FFA concentrations in type 2 diabetes. This may have clinical implications, as these effects may contribute to cardiovascular risk reduction.

TRAINING-INDUCED CHANGES IN THE LIPOLYTIC RESPONSE TO AN EVENING MEAL ARE RELATED TO CHANGES IN NOCTURNAL GROWTH HORMONE AND CORTISOL.

Endurance exercise training alters lipid metabolism, however, little is known about the effect of exercise training on postprandial fatty acid metabolism and its modulation by nocturnal endocrine response. The purpose of this study was to determine the effect of exercise training intensity on the overnight fatty acid and endocrine response to an evening meal. To achieve different levels of endurance training, 18 postmenopausal women trained for 4 months at two levels of exercise intensity; 1) 95% of their ventilatory threshold (VT, n = 6, LOW) or 2) 125% of their VT (n = 12, HIGH). The training consisted of supervised walking 4.8 km/day, 5 days/week. After 4 months of training, all subjects were admitted to the hospital, provided a standard meal at 1800 h, and blood samples were obtained every ten minutes overnight (1800–0800 h) to measure plasma free fatty acid (FFA), cortisol, insulin, and GH concentrations. Postprandial FFA concentration was lower in the HIGH compared with the LOW group (P = 0.03). There was no difference in the postprandial insulin response to the meal. Additionally, postprandial FFA concentrations for all subjects were positively correlated with nocturnal plasma cortisol concentrations (area under the curve [AUC]) (r = 0.54; P = 0.03) and negatively correlated with nocturnal plasma GH concentrations (r = 0.48; P = 0.05). Nocturnal plasma FFA concentration was not related to the magnitude of the insulin response to the meal, nor was it related to nocturnal plasma cortisol or GH concentrations. These findings suggest that more intense endurance training may enhance the antilipolytic effect of insulin, resulting in lower postprandial plasma FFA concentration. Additionally, our findings suggest that these alterations in the lipolytic response to an evening meal may affect the nocturnal secretion of GH while nocturnal secretion of cortisol may affect the lipolytic response to the meal. Support: NIH M01-RR00042.

Regional postprandial fatty acid metabolism in different obesity phenotypes.

To examine if postprandial splanchnic/hepatic free fatty acid (FFA) delivery is increased in upper-body (UB) obesity, and to determine the adipose tissue depots responsible for the greater postprandial FFA availability, we measured systemic and regional uptake and release of FFAs ([1-(14)C]palmitate) before and during a 5-h frequent-feeding mixed meal in eight UB and eight lower-body (LB) obese women. Postabsorptive FFA flux and splanchnic FFA delivery were not different in UB and LB obese women; however, postprandial FFA concentrations (257 +/- 45 vs. 81 +/- 12 micromol/l, P < 0.0001), FFA flux (8.5 +/- 1.2 vs. 3.9 +/- 0.8 micromol x kg(-1) fat-free mass x min(-1), P < 0.0001), splanchnic FFA delivery (275 +/- 45 vs. 88 +/- 24 micromol/min, respectively, P < 0.005), and estimated hepatic FFA delivery were greater in UB than LB obese women. Nonsplanchnic UB adipose tissue FFA release was greater in UB than in LB obese women (276 +/- 71 vs. 97 +/- 37 micromol/min, respectively, P < 0.05) and accounted for the greater postprandial FFA availability in UB obesity. Postprandial leg glucose uptake was less in UB than in LB obese women (8.4 +/- 5.1 vs. 22.9 +/- 2.6 micromol x kg(-1) leg fat-free mass x min(-1), P < 0.05). We conclude that the elevated postprandial FFA release observed in UB obese women originates from the nonsplanchnic UB fat, not visceral fat. These results suggest that visceral fat may be a marker for, but not the source of, excess postprandial FFAs in obesity.

Effects of a cardioselective β-blocker on postprandial triglyceride-rich lipoproteins, low density lipoprotein particle size and glucose-insulin homeostasis in middle-aged men with modestly increased cardiovascular risk

β-adrenergic receptor-blocking agents are commonly used for treatment of hypertension, angina pectoris and arrhythmias and as secondary prevention after myocardial infarction. The modest protection against myocardial infarction conferred by these compounds in primary-preventive studies has suggested that beneficial effects of β-blockade are counteracted by known adverse influences on lipid and glucose metabolism. As most β-blockers increase plasma triglycerides and decrease the high density lipoprotein (HDL) cholesterol concentration, a randomized, double-blind, cross-over study was conducted to evaluate whether a 12-week treatment with metoprolol (100 mg o.d.) or placebo affected the metabolism of postprandial triglyceride-rich lipoproteins in 15 middle-aged men with a modestly increased cardiovascular risk. Metoprolol treatment significantly increased the postprandial responses of very low density lipoprotein (VLDL) and VLDL remnants to a mixed meal-type of oral fat tolerance test. The effect was particularly prominent for larger (Svedberg flotation rate (Sf)>400 and Sf 60–400) particle species ( P<0.001 in repeated measures ANOVA), whereas the smaller (Sf 20–60) particles were less affected ( P<0.05). The changes in the postprandial responses of the different VLDL species were mainly related to an effect on the fasting plasma concentrations, with limited or no influences on VLDL catabolism during the postprandial state. In contrast, metoprolol treatment did not significantly influence the postprandial responses of chylomicrons and chylomicron remnants. Notably, the enhanced fasting and postprandial triglyceridaemia during metoprolol treatment was neither accompanied by a rise in fasting or postprandial free fatty acid concentrations, nor by alterations of the glucose and insulin responses to a standard oral glucose challenge. The ensuing shift in the LDL particle size distribution towards smaller particles was limited (fraction small LDL: metoprolol 22.8±15.7% versus placebo 19.3±15.0%, P<0.05). In conclusion, metoprolol treatment primarily enhances fasting and postprandial triglyceridaemia in middle-aged men by increasing the basal hepatic production of VLDL.

The association between free fatty acid concentrations and triglyceride-rich lipoproteins in the post-prandial state is altered by a common deletion polymorphism of the apo B signal peptide

To investigate whether there were associations between the free fatty acid (FFA) response during a fat tolerance test and changes in concentrations of triglyceride-rich lipoproteins 57 healthy Caucasian men between 57 and 70 years of age underwent a fat tolerance test lasting 8 h. FFA concentrations initially decreased from 0.75 ± 0.03 to 0.64 ± 0.03 mmol/1 at 2 h and thereafter increased to 1.2 ± 0.04 mmol/1 at 8 h. Maximum FFA concentration was the only significant determinant of 8 h triglyceride-rich lipoprotein (TGRLP) concentrations (pooled chylomicron and VLDL fractions d < 1.006) (TGRLP-TG r = 0.33, P = 0.012; TGRLP apo B r = 0.37, P = 0.004; TGRLP cholesterol r = 0.38, P = 0.004). The strength of the association between FFA and TGRLP was affected by the apo B signal peptide genotype. Only in individuals who were homozygous for the 27 amino acid (SP27 or I) allele of the apo B signal peptide were there significant associations between maximum FFA concentration quartile and 8 h TGRLP concentration ( P value for linear trend = 0.025). In this genotypic group there were lower HDL cholesterol concentrations (1.16 mmol/1 compared to 1.38 mmol/ in subjects either heterozygous or homozygous for the SP24 [D] allele; P = 0.005) and there was a trend toward increased 8 h TGRLP concentrations. We propose that the association between post-prandial FFA concentrations and post-prandial TGRLP concentrations in individuals who are homozygous for the SP27 allele may be linked to the increased prevalence of ischemic heart disease (IHD) in this genotypic group.