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Dietary interventions to delay carbohydrate digestion or absorption can effectively prevent hyperglycaemia in the early postprandial phase. L-arabinose can specifically inhibit sucrase. It remains to be assessed whether co-ingestion of L-arabinose with sucrose delays sucrose digestion, attenuates subsequent glucose absorption and impacts hepatic glucose output. In this double-blind, randomised crossover study, we assessed blood glucose kinetics following ingestion of a 200-ml drink containing 50 g of sucrose with 7·5 g of L-arabinose (L-ARA) or without L-arabinose (CONT) in twelve young, healthy participants (24 ± 1 years; BMI: 22·2 ± 0·5 kg/m2). Plasma glucose kinetics were determined by a dual stable isotope methodology involving ingestion of (U-13C6)-glucose-enriched sucrose, and continuous intravenous infusion of (6,6–2H2)-glucose. Peak glucose concentrations reached 8·18 ± 0·29 mmol/l for CONT 30 min after ingestion. In contrast, the postprandial rise in plasma glucose was attenuated for L-ARA, because peak glucose concentrations reached 6·62 ± 0·18 mmol/l only 60 min after ingestion. The rate of exogenous glucose appearance for L-ARA was 67 and 57 % lower compared with CONT at t = 15 min and 30 min, respectively, whereas it was 214 % higher at t = 150 min, indicating a more stable absorption of exogenous glucose for L-ARA compared with CONT. Total glucose disappearance during the first hour was lower for L-ARA compared with CONT (11 ± 1 v. 17 ± 1 g, P < 0·0001). Endogenous glucose production was not differentially affected at any time point (P = 0·27). Co-ingestion of L-arabinose with sucrose delays sucrose digestion, resulting in a slower absorption of sucrose-derived glucose without causing adverse effects in young, healthy adults.
Lifestyle intervention may be effective in reducing type 2 diabetes mellitus incidence and cardiometabolic risk. A more personalised nutritional approach based on an individual or subgroup-based metabolic profile may optimise intervention outcome. Whole body insulin resistance (IR) reflects defective insulin action in tissues such as muscle, liver, adipose tissue, gut and brain, which may precede the development of cardiometabolic diseases. IR may develop in different organs but the severity may vary between organs. Individuals with more pronounced hepatic IR have a distinct plasma metabolome and lipidome profile as compared with individuals with more pronounced muscle IR. Additionally, genes related to extracellular modelling were upregulated in abdominal subcutaneous adipose tissue in individuals with more pronounced hepatic IR, whilst genes related to inflammation as well as systemic low-grade inflammation were upregulated in individuals with primarily muscle IR. There are indications that these distinct IR phenotypes may also respond differentially to dietary macronutrient composition. Besides metabolic phenotype, microbial phenotype may be of importance in personalising the response to diet. In particular fibres or fibre mixtures, leading to a high distal acetate and SCFA production may have more pronounced effects on metabolic health. Notably, individuals with prediabetes may have a reduced response to diet-induced microbiota modulation with respect to host insulin sensitivity and metabolic health outcomes. Overall, we need more research to relate metabolic subphenotypes to intervention outcomes to define more optimal diets for individuals with or predisposed to chronic metabolic diseases.
The obese insulin resistant and/or prediabetic state is characterised by systemic lipid overflow, mainly driven by an impaired lipid buffering capacity of adipose tissue, and an impaired capacity of skeletal muscle to increase fat oxidation upon increased supply. This leads to the accumulation of bioactive lipid metabolites in skeletal muscle interfering with insulin sensitivity via various mechanisms. In this review, the contribution of dietary v. endogenous fatty acids to lipid overflow, their extraction or uptake by skeletal muscle as well as the fractional synthetic rate, content and composition of the muscle lipid pools is discussed in relation to the development or presence of insulin resistance and/or an impaired glucose metabolism. These parameters are studied in vivo in man by combining a dual stable isotope methodology with [2H2]- and [U-13C]-palmitate tracers with the arterio-venous balance technique across forearm muscle and biochemical analyses in muscle biopsies. The insulin-resistant state is characterised by an elevated muscle TAG extraction, despite similar supply, and a reduced skeletal muscle lipid turnover, in particular after intake of a high fat, SFA fat meal, but not after a high fat, PUFA meal. Data are placed in the context of current literature, and underlying mechanisms and implications for long-term nutritional interventions are discussed.
The importance of chronic low-grade inflammation in the pathology of numerous age-related chronic conditions is now clear. An unresolved inflammatory response is likely to be involved from the early stages of disease development. The present position paper is the most recent in a series produced by the International Life Sciences Institute's European Branch (ILSI Europe). It is co-authored by the speakers from a 2013 workshop led by the Obesity and Diabetes Task Force entitled ‘Low-grade inflammation, a high-grade challenge: biomarkers and modulation by dietary strategies’. The latest research in the areas of acute and chronic inflammation and cardiometabolic, gut and cognitive health is presented along with the cellular and molecular mechanisms underlying inflammation–health/disease associations. The evidence relating diet composition and early-life nutrition to inflammatory status is reviewed. Human epidemiological and intervention data are thus far heavily reliant on the measurement of inflammatory markers in the circulation, and in particular cytokines in the fasting state, which are recognised as an insensitive and highly variable index of tissue inflammation. Potential novel kinetic and integrated approaches to capture inflammatory status in humans are discussed. Such approaches are likely to provide a more discriminating means of quantifying inflammation–health/disease associations, and the ability of diet to positively modulate inflammation and provide the much needed evidence to develop research portfolios that will inform new product development and associated health claims.
High-fibre diets offer several beneficial health effects. The objective of the present study was to investigate whether replacement of 30 % of the available carbohydrates with polydextrose (PDX) or soluble maize fibre (SCF) at breakfast and lunch would result in an increased fat oxidation rate and satiety, which may be of relevance for body weight control and diabetes prevention. In a single-blind, randomised cross-over study, eighteen overweight men and women underwent four different dietary interventions, which consisted of a PDX diet, a SCF diet and two control diets (full energetic and isoenergetic, comparable with PDX with respect to g or energy percentage of macronutrients, respectively). Glycaemic profile, energy expenditure and substrate oxidation were measured for 24 h in a respiration chamber. Circulating insulin, NEFA and TAG concentrations were determined over a 14 h period during daytime. Appetite ratings were assessed using visual analogue scales. The replacement of available carbohydrates with PDX or SCF reduced the peak glucose response, which was accompanied by reduced postprandial insulin responses. Moreover, higher concentrations of circulating NEFA were observed after consumption of both fibre diets, which were accompanied by an increased fat oxidation over 24 h. This effect was mainly attributed to the lower energetic value of the fibre diets and not to the fibres per se. Besides increasing fat oxidation, PDX exerted a pronounced suppressive effect on appetite ratings. The replacement of available carbohydrates with PDX may be of special interest because of its beneficial effects on metabolic profile and it may affect body weight control in the long term.
The impact of slowly digestible sugars in reducing the risk of developing obesity and related metabolic disorders remains unclear. We hypothesised that such carbohydrates (CHO), resulting in a lower glycaemic and insulinaemic response, may lead to greater postprandial fat oxidation rates in subjects with impaired glucose tolerance (IGT). The present study intends to compare the postprandial metabolic responses to the ingestion of glucose (GLUC) v. trehalose (TRE) and sucrose (SUC) v. isomaltulose (IMU). In a randomised, single-blind, cross-over design, ten overweight IGT subjects were studied four times, following ingestion of different CHO drinks either at breakfast or in combination with a mixed meal at lunch. Before and 3 h after CHO ingestion, energy expenditure, substrate utilisation and circulating metabolite concentrations were determined. Ingestion of CHO drinks with a meal resulted in an attenuated rise in GLUC ( − 33 %) and insulin ( − 14 %) concentrations following TRE when compared with GLUC and following IMU, an attenuation of 43 and 34 % when compared with SUC ingestion, respectively. Additionally, there was less inhibition of the rise in NEFA concentrations and less decline in postprandial fat oxidation (22 %) after IMU when compared with SUC, whereas TRE did not differ from GLUC. The attenuated rise in GLUC and insulin concentrations following IMU ingestion attenuated the postprandial inhibition of fat oxidation compared with SUC when co-ingested with a meal. This suggests that exchange of SUC in the diet for IMU may result in a more favourable metabolic response and may help to reduce the risks associated with obesity and type 2 diabetes.
Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF2α (a major F2-isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF2α (15-keto-dihydro-PGF2α, a major PGF2α metabolite and marker of cyclooxygenase-mediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α nor those of CRP differed between diet groups at baseline (P>0·07) or at the end of the study (P>0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF2α, P = 0·83; 15-keto-dihydro-PGF2α, P = 0·45; and CRP, P = 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.
Hypertension is a key feature of the metabolic syndrome. Lifestyle and dietary changes may affect blood pressure (BP), but the knowledge of the effects of dietary fat modification in subjects with the metabolic syndrome is limited. The objective of the present study was to investigate the effect of an isoenergetic change in the quantity and quality of dietary fat on BP in subjects with the metabolic syndrome. In a 12-week European multi-centre, parallel, randomised controlled dietary intervention trial (LIPGENE), 486 subjects were assigned to one of the four diets distinct in fat quantity and quality: two high-fat diets rich in saturated fat or monounsaturated fat and two low-fat, high-complex carbohydrate diets with or without 1·2 g/d of very long-chain n-3 PUFA supplementation. There were no overall differences in systolic BP (SBP), diastolic BP or pulse pressure (PP) between the dietary groups after the intervention. The high-fat diet rich in saturated fat had minor unfavourable effects on SBP and PP in males.
The impact of slow digestible sources of dietary carbohydrate in reducing the risk of developing obesity and related metabolic disorders is unclear. The aim of the present study was to compare the postprandial metabolic response to the ingestion of sucrose v. isomaltulose. We hypothesised that the reduced digestion and absorption rate of isomaltulose would result in lower glycaemic and insulinaemic responses when compared with the ingestion of sucrose, leading to greater postprandial fat oxidation rates. In a randomised, single-blind, cross-over study, ten overweight subjects ingested two different carbohydrate drinks (sucrose and isomaltulose, 75 g carbohydrate equivalents) following an overnight fast (08.40 hours) and with a standardised meal (12.30 hours, 25 % of total energy content was provided as either a sucrose or isomaltulose drink). Blood samples were taken before ingestion and every 30 min thereafter for a period of 3 h, substrate use was assessed by indirect calorimetry and breath samples were collected. Ingestion of carbohydrates with a mixed meal resulted in a lower peak glucose and insulin response and a lower change in area under the curve (ΔAUC) following isomaltulose when compared with sucrose. Together with the lower glucose and insulin responses, postprandial fat oxidation rates were higher (14 %) with isomaltulose when compared with sucrose when ingested with a mixed meal (P = 0·02). The attenuated rise in glucose and insulin concentrations following isomaltulose results in reduced inhibition of postprandial fat oxidation. The metabolic response to isomaltulose co-ingestion suggests that this may represent an effective nutritional strategy to counteract overweight-induced metabolic disturbances.
The proposed impact of slowly digestible sources of dietary carbohydrate in reducing the risk of developing obesity and related metabolic disorders remains unclear. The aim of the present study was to compare the postprandial metabolic response to the ingestion of glucose v. trehalose. We hypothesised that the reduced digestion and absorption rate of trehalose is accompanied by an attenuated glycaemic and insulinaemic response, leading to a less inhibited postprandial fat oxidation rate. In a randomised, single-blind, cross-over study, ten overweight subjects ingested two carbohydrate drinks (75 g carbohydrate equivalents of trehalose or glucose) following an overnight fast (08.40 hours) and together with a standardised mixed meal (12.30 hours; 25 % total energy content was provided as either glucose or trehalose). Blood samples were collected before ingestion and every 30 min thereafter for a period of 3 h; substrate use was assessed by indirect calorimetry and expired breath samples were collected. Ingestion of carbohydrates with a mixed meal resulted in a lower peak glucose response and a lower change in area under the curve (ΔAUC) following trehalose when compared with glucose. Differences in peak insulin response and ΔAUC were observed with trehalose when compared with glucose during the morning and afternoon. These differences were accompanied with a reduced carbohydrate oxidation after trehalose when ingested as a drink, whilst no significant differences in fat oxidation between drink were observed.
Controlled human intervention trials are required to confirm the hypothesis that dietary fat quality may influence insulin action. The aim was to develop a food-exchange model, suitable for use in free-living volunteers, to investigate the effects of four experimental diets distinct in fat quantity and quality: high SFA (HSFA); high MUFA (HMUFA) and two low-fat (LF) diets, one supplemented with 1·24 g EPA and DHA/d (LFn-3). A theoretical food-exchange model was developed. The average quantity of exchangeable fat was calculated as the sum of fat provided by added fats (spreads and oils), milk, cheese, biscuits, cakes, buns and pastries using data from the National Diet and Nutrition Survey of UK adults. Most of the exchangeable fat was replaced by specifically designed study foods. Also critical to the model was the use of carbohydrate exchanges to ensure the diets were isoenergetic. Volunteers from eight centres across Europe completed the dietary intervention. Results indicated that compositional targets were largely achieved with significant differences in fat quantity between the high-fat diets (39·9 (sem 0·6) and 38·9 (sem 0·51) percentage energy (%E) from fat for the HSFA and HMUFA diets respectively) and the low-fat diets (29·6 (sem 0·6) and 29·1 (sem 0·5) %E from fat for the LF and LFn-3 diets respectively) and fat quality (17·5 (sem 0·3) and 10·4 (sem 0·2) %E from SFA and 12·7 (sem 0·3) and 18·7 (sem 0·4) %E MUFA for the HSFA and HMUFA diets respectively). In conclusion, a robust, flexible food-exchange model was developed and implemented successfully in the LIPGENE dietary intervention trial.
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