Postprandial Metabolic Changes Research Articles

Post-Bariatric Hypoglycemia: an Impaired Metabolic Response to a Meal

Aims/HypothesisPost-bariatric hypoglycemia (PBH) is caused by postprandial hyperinsulinemia, due to anatomical alterations and changes in post-prandial metabolism after bariatric surgery. The mechanisms underlying the failing regulatory and compensatory systems are unclear. In this study, we investigated the differences in post-prandial hormones and metabolic profiles between patients with and without PBH.MethodsWe performed a mixed meal test (MMT) in 63 subjects before and 1 year after Roux-en-Y gastric bypass (RYGB) surgery. Blood was withdrawn at 0, 10, 20, 30, 60, and 120 min after ingestion of a standardized meal. Glucose, insulin, GLP-1, FGF-19, and FGF-21 were measured and untargeted metabolomics analysis was performed on blood plasma to analyze which hormonal and metabolic systems were altered between patients with and without PBH.ResultsOut of 63, a total of 21 subjects (33%) subjects developed PBH (glucose < 3.1 mmol/L) after surgery. Decreased glucose and increased insulin excursions during MMT were seen in PBH (p < 0.05). GLP-1, FGF-19, and FGF-21 were elevated after surgery (p < 0.001), but did not differ between PBH and non-PBH groups. We identified 20 metabolites possibly involved in carbohydrate metabolism which differed between the two groups, including increased carnitine and acylcholines in PBH.ConclusionOverall, 33% of the subjects developed PBH 1 year after RYGB surgery. While GLP-1, FGF-19, and FGF-21 were similar in PBH and non-PBH patients, metabolomics analysis revealed changes in carnitine and acyclcholines that are possibly involved in energy metabolism, which may play a role in the occurrence of PBH.Graphical

Abstract MP09: Diets Varying in Glycemic Index and Carbohydrates With Meal-Timing Specific 12-hour Postprandial Metabolic Changes: The Omnicarb Trial

Background: Both the glycemic index (GI) and amounts of carbohydrates are important determinants of postprandial glucose changes. Recent studies suggest the effects of carbohydrate intake on postprandial glucose metabolism may differ according to meal timing, showing circadian patterns. Hypothesis: We investigated whether the relations of altering both GI levels and the carbohydrate amount with postprandial response of glucose, insulin, and c-peptide differed by meal timing (breakfast, lunch, and dinner), in overweight and obese adults. Methods: The OmniCarb trial was a randomized trial with a crossover design in which participants were given 4 diets varying in GI levels and carbohydrate content. We included 61 participants attended the 12-h postprandial study and completed at least two diets. Area under the curve increment (AUCi) of glucose, insulin, and c-peptide after breakfast (180 min), lunch (240 min), and dinner (120 min), was calculated as outcome. Results: After consuming each diet for 5 weeks, we observed that the diet replacing effects on the postprandial responses in glucose, insulin and c-peptide significantly differed by meal timing. For postprandial glucose response to breakfast, the beneficial effects (lowered AUCi) of replacing high- by low-GI in high-carb diet, replacing high- by low-carb in high-GI diet, and replacing high-GI/high-carb by low-GI/low-carb diet were consistently observed. Such beneficial effects were less significant for lunch and dinner (Figure). For the response of insulin, the beneficial effects of the corresponding diet replacements were more consistently observed in dinner, followed by breakfast. For the response of C-peptide, similar beneficial effects of the corresponding diet replacements were observed for breakfast and dinner, but not lunch. Conclusion: Our results indicate that the beneficial effects of replacing high-GI and/or high-carbohydrate diets by low-GI and/or low-carbohydrate diets on postprandial metabolic changes may differ according to meal timing.

Menopause is associated with postprandial metabolism, metabolic health and lifestyle: The ZOE PREDICT study.

The menopause transition is associated with unfavourable alterations in health. However, postprandial metabolic changes and their mediating factors are poorly understood. The PREDICT 1 UK cohort (n=1002; pre- n=366, peri- n=55, and post-menopausal females n=206) assessed phenotypic characteristics, anthropometric, diet and gut microbiome data, and fasting and postprandial (0-6h) cardiometabolic blood measurements, including continuous glucose monitoring (CGM) data. Differences between menopausal groups were assessed in the cohort and in an age-matched subgroup, adjusting for age, BMI, menopausal hormone therapy (MHT) use, and smoking status. Post-menopausal females had higher fasting blood measures (glucose, HbA1c and inflammation (GlycA), 6%, 5% and 4% respectively), sugar intakes (12%) and poorer sleep (12%) compared with pre-menopausal females (p<0.05 for all). Postprandial metabolic responses for glucose2hiauc and insulin2hiauc were higher (42% and 4% respectively) and CGM measures (glycaemic variability and time in range) were unfavourable post- versus pre-menopause (p<0.05 for all). In age-matched subgroups (n=150), postprandial glucose responses remained higher post-menopause (peak0-2h 4%). MHT was associated with favourable visceral fat, fasting (glucose and insulin) and postprandial (triglyceride6hiauc) measures. Mediation analysis showed that associations between menopause and metabolic health indicators (visceral fat, GlycA360mins and glycaemia (peak0-2h)) were in part mediated by diet and gut bacterial species. Findings from this large scale, in-depth nutrition metabolic study of menopause, support the importance of monitoring risk factors for type-2 diabetes and cardiovascular disease in mid-life to older women to reduce morbidity and mortality associated with oestrogen decline. Zoe Ltd.

Immune and hormonal regulation of the Boa constrictor (Serpentes; Boidae) in response to feeding

Feeding upregulates immune function and the systemic and local (gastrointestinal tract) concentrations of some immunoregulatory hormones, as corticosterone (CORT) and melatonin (MEL), in mammals and anurans. However, little is known about the immune and hormonal regulation in response to feeding in other ectothermic vertebrates, especially snakes, in which the postprandial metabolic changes are pronounced. Here, we investigated the effects feeding have on hormonal and innate immune responses in the snake, Boa constrictor. We divided juvenile males into two groups: fasting and fed with mice (30% of body mass). We measured the rates of oxygen consumption, plasma CORT levels, heterophil/lymphocyte ratio (HL ratio), plasma bacterial killing ability (BKA), and stomach and intestine MEL in fasting snakes and 48 h after meal intake. We observed increased rates of oxygen consumption, plasma CORT levels, and HL ratio, along with a tendency of decreased stomach and intestine MEL in fed snakes compared to fasting ones. BKA was not affected by feeding. Overall, we found that feeding modulates metabolic rates, CORT levels, and immune cell distribution in boas. Increased baseline CORT may be important to mobilize energy to support the metabolic increment during the postprandial period. Increased HL ratio might be an immunoregulatory effect of increased CORT, which has been shown in different physiological situations such as in response to immune challenge. Our results suggest that feeding activates the hypothalamic-pituitary-adrenal axis and modulates immune cell redistribution, possibly contributing to fighting potential injuries and infections derived from predation and from pathogens present in ingested food.

Fortifying a meal with oyster mushroom powder beneficially affects postprandial glucagon-like peptide-1, non-esterified free fatty acids and hunger sensation in adults with impaired glucose tolerance: a double-blind randomized controlled crossover trial

PurposeImpaired glucose tolerance (IGT) is a pathophysiological condition characterized by insulin resistance with known metabolic consequences such as postprandial hyperglycemia and hypertriglyceridemia. We hypothesized that fortifying a meal with mushrooms rich in β-glucans may diminish glucose and triglyceride responses by improving postprandial gastrointestinal hormone release.MethodsIn a randomized controlled crossover study, 22 subjects with IGT ingested a meal either enriched with 20 g powder (8.1 g β-glucans) of oven-dried Pleurotus ostreatus (enriched meal, EN) or without enrichment (control meal, CON). Blood was collected before and repeatedly within 4 h after the meal to determine AUC of glucose (primary outcome), insulin, triglycerides, non-esterified free fatty acids (NEFAs), glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and ghrelin. Appetite sensations (hunger, satiety, fullness, and desire to eat) were assessed before and after meal consumption by visual analog scales.ResultsPostprandial glucose, insulin, triglycerides, GIP and ghrelin concentrations as well as the corresponding AUCs did not differ between EN and CON. NEFAs-AUC was 14% lower (P = 0.026) and GLP-1-AUC 17% higher (P = 0.001) after EN compared to CON. Appetite ratings did not differ between treatments, except for hunger (AUC 22% lower after EN vs. CON; P = 0.031).ConclusionThe observed immediate postprandial metabolic changes indicate that an easily manageable fortification of a single meal with powder from dried oyster mushrooms as β-glucan source may improve postprandial metabolism. If the effect is preserved long term, this measure can diminish the risk for further development of overweight/obesity and type 2 diabetes in subjects with IGT.Clinical trial registrationGerman Clinical Trial Register on 09/08/2018; trial-ID: DRKS00015244.

Effect of maternal supplementation with essential fatty acids and conjugated linoleic acid on metabolic and endocrine development in neonatal calves

We tested the hypothesis that the maternal supply of essential fatty acids (EFA), especially α-linolenic acid, and conjugated linoleic acid (CLA), affects glucose metabolism, the endocrine regulation of energy metabolism and growth, and the intestinal development of neonatal calves. We studied calves from dams that received an abomasal infusion of 76 g/d coconut oil (CTRL; n = 9), 78 g/d linseed oil and 4 g/d safflower oil (EFA; n = 9), 38 g/d Lutalin (BASF SE) containing 27% cis-9,trans-11 and trans-10,cis-12 CLA (CLA; n = 9), or a combination of EFA and CLA (EFA+CLA; n = 11) during the last 63 d of gestation and early lactation. Calves received colostrum and transition milk from their own dam for the first 5 d of life. Insulin-like growth factor (IGF)-I, leptin, and adiponectin concentrations were measured in milk. Blood samples were taken before first colostrum intake, 24 h after birth, and from d 3 to 5 of life before morning feeding to measure metabolic and endocrine traits in plasma. On d 3 of life, energy expenditure was evaluated by a bolus injection of NaH13CO3 and determination of CO2 appearance rate. On d 4, additional blood samples were taken to evaluate glucose first-pass uptake and 13CO2 enrichment after [13C6]-glucose feeding and intravenous [6,6-2H2]-glucose bolus injection, as well as postprandial changes in glucose, nonesterified fatty acids (NEFA), insulin, and glucagon. On d 5, calves were killed 2 h after feeding and samples of small intestinal mucosa were taken for histomorphometric measurements. The concentrations of IGF-I, adiponectin, and leptin in milk decreased during early lactation in all groups, and the concentrations of leptin in first colostrum was higher in EFA than in CTRL cows. Plasma glucose concentration before first colostrum intake was higher in EFA calves than in non-EFA calves and was lower in CLA calves than in non-CLA calves. Plasma IGF-I concentration was higher on d 1 before colostrum intake in EFA calves than in EFA+CLA calves and indicated an overall CLA effect, with lower plasma IGF-I in CLA than in non-CLA calves. Postprandial NEFA concentration was lowest in EFA and CLA calves. The postprandial rise in plasma insulin was higher in EFA than in non-EFA calves. Plasma adiponectin concentration increased from d 1 to d 2 in all groups and was higher on d 3 in CLA than in non-CLA calves. Plasma leptin concentration was higher on d 4 and 5 in EFA than in non-EFA calves. Maternal fatty acid treatment did not affect energy expenditure and first-pass glucose uptake, but glucose uptake on d 4 was faster in EFA than in non-EFA calves. Crypt depth was lower, and the ratio of villus height to crypt depth was higher in the ilea of CLA than non-CLA calves. Elevated plasma glucose and IGF-I in EFA calves immediately after birth may indicate an improved energetic status in calves when dams are supplemented with EFA. Maternal EFA and CLA supplementation influenced postprandial metabolic changes and affected factors related to the neonatal insulin response.

Metabolomics of postprandial plasma alterations: a comprehensive Japanese study.

While endogenous metabolites in plasma can be used as clinical biomarkers, intra-day variations should be carefully considered. The postprandial effect is a large contributing factor and is dependent on regional features (e.g. meals, ethnicity). Thus, for clinical application, regional-specific postprandial baseline data are required. In this study, 10 healthy Japanese volunteers of different ages and genders ate the same meal, and blood samples were taken 30 min before and 1 h after the meal challenge. Plasma metabolomics was conducted and metabolites that significantly changed with the meal challenge were extracted. Principal component analysis of the data from 1101 metabolites showed a postprandial shift with a common direction despite marked individual variation. Pathway enrichment analysis demonstrated known postprandial effects, including the energy utilization shift from lipolysis to glycolysis and the elevation of bile acids for lipid absorption. Other postprandial metabolic changes were observed, including decreases in orexigenic signals and increases of food-derived components. The postprandial alteration accumulated in this study will be used for the understanding of Japanese clinical metabolomics for health promotion in Japan.

Acute effects of plant stanol esters on postprandial metabolism and its relation with changes in serum lipids after chronic intake.

Plant stanol esters lower serum low-density lipoprotein (LDL)-cholesterol (LDL-C), but responses between individuals vary widely. As the ability of subjects to respond to acute dietary challenges may reflect the flexibility to adapt to changes on the longer term, we related subjects' acute postprandial metabolic changes to changes in serum lipoproteins after chronic intake of plant stanol esters. In a double-blind crossover design, 20 healthy subjects received in random order a high-fat shake enriched with or without plant stanol esters (4 g). Blood samples were taken during 4 h to examine lipid, glucose and lipoprotein profiles. Two subjects dropped out. For the 3 weeks after this postprandial test, the subjects who received the shake with plant stanol esters continued the consumption of plant stanol-enriched (3g/day) margarine and subjects receiving the control shake in the postprandial test consumed for the next 3 weeks a control margarine. After the washout period, subjects received the other shake and margarines. The margarine enriched with plant stanol esters lowered concentrations of total cholesterol by 7.3% (P<0.01), LDL-C by 9.5% (P<0.01) and apoB100 by 8.6% (P<0.01). Furthermore, particle concentrations of total very low-density lipoprotein (VLDL), small VLDL and large LDL were reduced by 26.6% (P=0.02), 27.6% (P=0.02) and 12.3% (P=0.04), respectively. Plant stanol esters did not affect parameters related to lipid and glucose metabolism during the postprandial phase. However, the incremental area under the curve (iAUC) of the postprandial glucose concentration after consuming the control shake correlated positively with changes in fasting concentrations of total cholesterol, LDL-C, apoB100, total VLDL, small VLDL and intermediate-density lipoprotein after 3 weeks. A single dose of plant stanol esters does not change postprandial lipid and lipoprotein profiles. However, postprandial glucose responses may predict the effects of chronic plant stanol ester consumption.

Relationship between postprandial metabolomics and colon motility in children with constipation

The metabolic pathways associated with colonic motility are unknown. To identify potential metabolic targets for treatment of constipation, we examined the metabolic profile before and after a meal challenge in a cohort of children with constipation and determined its relationship with postprandial colon motility patterns. In this prospective study, 187 metabolites were measured by liquid chromatography-mass spectrometry at multiple time points before and after a standardized meal in constipated children undergoing a colon manometry. Postprandial metabolite levels were compared with baseline and also correlated with multiple manometric measurements, including the number, frequency, and amplitude of pressure peaks as well as the motility index (MI). A total of 20 subjects were included (mean age 13.1 ± 3.4 years). No significant metabolite changes were observed at 10 min after the meal, whereas 16 amino acid and 22 lipid metabolites had significant (P < 0.005) postprandial changes, including decreases in methylhistamine, histamine, and GABA, by 60 min. Correlations were observed between normal and abnormal postprandial motility patterns and changes in specific metabolites, including glycerol, carnosine, alanine, asparagine, cytosine, choline, phosphocholine, thyroxine, and triiodothyronine. Interestingly, subjects without the normal postprandial increase in area under the curve (AUC), had markedly increased levels of kynurenic acid and adenosyl-homocysteine. This is the first study to examine postprandial metabolic changes in children and also to correlate changes in specific metabolites with colonic motility. The results suggest possible metabolic pathways associated with motility and identify potential targets for the treatment of constipation.

The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism

Postprandially, the liver experiences an extensive metabolic reprogramming that is required for the switch from glucose production to glucose assimilation. Upon refeeding, the unfolded protein response (UPR) is rapidly, though only transiently, activated. Activation of the UPR results in a cessation of protein translation, increased chaperone expression, and increased ER-mediated protein degradation, but it is not clear how the UPR is involved in the postprandial switch to alternate fuel sources. Activation of the inositol-requiring enzyme 1 (IRE1) branch of the UPR signaling pathway triggers expression of the transcription factor Xbp1s. Using a mouse model with liver-specific inducible Xbp1s expression, we demonstrate that Xbp1s is sufficient to provoke a metabolic switch characteristic of the postprandial state, even in the absence of caloric influx. Mechanistically, we identified UDP-galactose-4-epimerase (GalE) as a direct transcriptional target of Xbp1s and as the key mediator of this effect. Our results provide evidence that the Xbp1s/GalE pathway functions as a novel regulatory nexus connecting the UPR to the characteristic postprandial metabolic changes in hepatocytes.

Effects of whole eggs combined with other cooked breakfast foods on postprandial metabolism in older, overweight adults

Adverse postprandial metabolic changes may contribute to the pathogenesis of chronic diseases. Eggs provide highly digestible protein, unsaturated fatty acids, carotenoids and other antioxidants that may act synergistically to antagonize these effects when combined with unhealthy breakfast foods. To determine the postprandial metabolic effects of a typical cooked American breakfast high in glycemic load either with no eggs (N), 2 eggs (E), or a nutrient‐poor protein + cholesterol egg substitute (ES), we conducted a 3‐way crossover pilot study in 7 subjects (age 50–70 y, BMI 28–34) with a 2‐d low antioxidant diet run‐in and 1 wk washout for each intervention. Blood and urine were collected before and for 4 h after each isocaloric breakfast. Compared to baseline, GLP‐1 increased 135, 78 and 61% at 2 h with E, ES, and N, respectively (E vs. ES, P&lt;0.05), while ghrelin decreased 6% for N (P&gt;0.05 vs. E and ES, 16% for each). Plasma total thiols also increased at 2 h by 7.4, 5.5 and 0.5% with E, N, and ES, respectively (E vs. ES, P&lt;0.05). At 2 and 4 h the increase in urinary isoprostanes was similar with each breakfast. Glucoregulation was better controlled with E compared to ES and N (HOMA‐IR: E&lt;ES&lt;N; AUCins/glu: E&lt;ES&lt;N; P&gt;0.05). These data suggest the positive postprandial effects of eggs on satiety and endogenous antioxidant defenses may be attributed to the whole food. (Supported by USDA and the Egg Nutrition Center)

Post-Challenge Hyperglycemia in Older Adults Is Associated with Increased Cardiovascular Risk Profile

Post-challenge hyperglycemia (PCH) is common in older adults and is associated with increased cardiovascular disease (CVD) risk and total mortality. However, PCH is rarely recognized in clinical settings, and the glycemic exposure and CVD risk profile of elderly individuals with PCH has not been defined. The aim of the study was to characterize metabolic and CVD risk profile of elderly subjects with PCH and to determine the effect of acute postprandial metabolic changes on vascular biomarkers. We conducted a cross-sectional study with a standard meal challenge protocol. Older adults with normal glucose tolerance (n = 30) or PCH (fasting glucose <126 mg/dl and 2-h glucose >or=170 mg/dl; n = 28) participated in the study. We assessed fasting and postprandial levels of glucose, insulin, lipids, high sensitivity C-reactive protein, plasminogen activator inhibitor-1, and adiponectin and endothelial function using reactive hyperemia peripheral arterial tonometry. Normal glucose tolerance and PCH subjects were matched for age, sex, body mass index, and ethnicity. Fasting glucose (102 +/- 3 vs. 93 +/- 2 mg/dl; P < 0.001) and glycosylated hemoglobin (5.7 vs. 5.4%; P = 0.01) were modestly higher in the PCH group, which was also more insulin resistant (homeostasis model assessment for insulin resistance, 7.0 +/- 1.3 vs. 4.1 +/- 0.6; P = 0.03). Fasting high sensitivity C-reactive protein was higher (2.6 +/- 0.5 vs. 1.3 +/- 0.2 mg/dl; P = 0.05), and adiponectin was lower (11.6 +/- 1.6 vs. 14.0 +/- 1.3 microg/ml; P = 0.03) in subjects with PCH. Peak and 6-h postprandial area under the curve glucose, insulin, and lipids were higher in PCH subjects, who also had higher fasting and postprandial levels of plasminogen activator inhibitor-1. Reactive hyperemia peripheral arterial tonometry declined postprandially only in PCH. Older adults with PCH experience significant fasting and postprandial metabolic dysregulation, which is accompanied by a proatherosclerotic and prothrombotic vascular profile.

Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin

This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to enterostatin remains to be determined. As lipid metabolism appeared to be altered by enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPARalpha, -beta, -gamma1, and -gamma2 expression were modified by enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPARgamma2 play a role in the control of insulin and amylin release from the pancreas. This implies that enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure.

Postprandial Lipaemia, Haemostasis, Inflammatory Response and other Emerging Risk Factors for Cardiovascular Disease: The Influence of Fatty Meals

Adverse changes in postprandial metabolism may promote the development of cardiovascular disease (CVD) through a range of mechanisms. Since a large proportion of our day is spent in the postprandial state it is important to understand these post meal changes with respect to both the amount and type of nutrient consumed. Of particular importance appear to be the fatty meals, commonly eaten and which can induce significant postprandial lipaemia, accumulation of potentially atherogenic triglyceride-rich lipoprotein (TRL) remnants and formation of highly oxidisable small, dense low-density lipoproteins (LDL). In addition to these relatively well established lipaemic effects there is growing evidence that high-fat foods also have adverse effects on a number of the emerging CVD risk factors including haemostasis, mediators of inflammation and endothelial function. This review will consider the acute effects of high-fat feeding, investigating any differential effects of saturated and unsaturated fatty acids, on postprandial lipaemic profile, haemostatic clotting factors fibrinogen and factor VII, acute phase C-reactive protein (C-RP), inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α), and vascular reactivity.

Metabolic and cognitive coefficients in the development of hunger sensations after pure macronutrient ingestion in the morning

The effect of pure carbohydrate, protein and fat ingestion on different aspects of short-term satiety and their relation to metabolic and cognitive performance indices were studied in 15 healthy male students. Subjects were tested in three sessions for short-term changes in blood indices, indirect calorimetry, different aspects of hunger sensations as well as mood and objective cognitive performance using a repeated-measures, counterbalanced cross-over design. Measurements were made after an overnight fast before and hourly during 3 h after macronutrient ingestion. Preloads were isoenergetic (1670 kJ) spoonable creams with similar sensory properties of either pure carbohydrates, protein or fat. Overall ‘desire to eat’ and ‘gastric emptiness’ represented principal components for overall ‘hunger’ ratings, which were larger after fat and carbohydrate compared with protein ingestion. In the first hour, the hunger suppression of carbohydrates was similar to that of protein and related to changes in β-hydroxybutyrate and insulin concentrations accompanied with a preference for carbohydrate-rich food. In the third hour, it was similar to the low satiating power of fat and related to diet-induced thermogenesis together with a preference for protein-rich food. For all macronutrients feelings of ‘energy’ were negatively related to hunger sensations, whereas objective cognitive performance was positively related. Our findings suggest that the subjective satiating effect of carbohydrates seems to change with time in relation to postprandial metabolic changes, presumably mainly dependent on the glycemic response and diet-induced thermogenesis.

Cognitive performance and its relationship with postprandial metabolic changes after ingestion of different macronutrients in the morning.

The effect of carbohydrate, protein and fat ingestion on simple as well as complex cognitive functions and the relationship between the respective postprandial metabolic changes and changes in cognitive performance were studied in fifteen healthy male students. Subjects were tested in three sessions, separated by 1 week, for short-term changes in blood variables, indirect calorimetry, subjective performance and different objective performance tasks using a repeated-measures counterbalanced cross-over design. Measurements were made after an overnight fast before and hourly during 3 h after test meal ingestion. Test meals consisted of either pure carbohydrates, protein or fat and were served as isoenergetic (1670 kJ) spoonable creams with similar sensory properties. Most aspects of subjective performance did not differ between test meals. For all objective tasks, however, postprandial cognitive performance was best after fat ingestion concomitant with an almost constant glucose metabolism and constant metabolic activation state measured by glucagon:insulin (G:I). In contrast, carbohydrate as well as protein ingestion resulted in lower overall cognitive performance, both together with partly marked changes in glucose metabolism and metabolic activation. They also differently affected specific cognitive functions in relation to their specific effect on metabolism. Carbohydrate ingestion resulted in relatively better short-term memory and accuracy of tasks concomitant with low metabolic activation, whereas protein ingestion resulted in better attention and efficiency of tasks concomitant with higher metabolic activation. Our findings support the concept that good and stable cognitive performance is related to a balanced glucose metabolism and metabolic activation state.

Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men

Adjustments of carbohydrate intake and oxidation occur in both normal-weight and overweight individuals. Nevertheless, the contribution of carbohydrates to the accumulation of fat through either reduction of fat oxidation or stimulation of fat synthesis in obesity remains poorly investigated. The objective of this study was to assess the postprandial metabolic changes and the fractional hepatic de novo lipogenesis (DNL) induced by a high-carbohydrate, low-fat meal in lean and overweight young men. A high-carbohydrate, low-fat meal was administered to 6 lean and 7 overweight men after a 17.5-h fast. During the fasting and postprandial periods, energy expenditure (EE), macronutrient oxidation, diet-induced thermogenesis, and serum insulin, glucose, triacylglycerol, and fatty acids were measured. To determine DNL, [1-13C]sodium acetate was infused and the mass isotopomer distribution analysis method was applied. After intake of the high-carbohydrate meal, the overweight men had hyperinsulinemia and higher fatty acid and triacylglycerol concentrations than did the lean men. The overweight group showed a greater EE, whereas there was no significant difference in carbohydrate oxidation between the groups. Nevertheless, the overweight men had a marginally higher protein oxidation and a lower lipid oxidation than did the lean men. DNL was significantly higher before and after meal intake in the overweight men and was positively associated with fasting serum glucose and insulin concentrations. Furthermore, postprandial DNL was positively correlated with body fat mass, EE, and triacylglycerol. After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional hepatic fat synthesis than did lean men.

Prolonged fasting significantly changes nutrient oxidation and glucose tolerance after a normal mixed meal.

The aim of this study was to establish the experimental paradigm of fasting, followed by refeeding, to investigate individual differences in nutrient partitioning. Eight nonobese men were fed a normal meal (25% of daily energy requirements) on two occasions, after an overnight (13-h) fast and after a prolonged (72-h) fast. During the entire fasting period, subjects were resident in a whole room indirect calorimeter, and blood samples were drawn periodically. Because no other food was consumed over the 12 h after either meal, negative energy balance was observed after the overnight and prolonged fast. Postprandial carbohydrate oxidation was significantly reduced after the 72- vs. 13-h fast (P < 0.0001), whereas fat oxidation was significantly increased (P < 0.0001). Interestingly, carbohydrate balance was positive after the prolonged fast but negative after the overnight fast (24 +/- 17 vs. -57 +/- 16 g/12 h, respectively; P < 0.001), whereas fat balance was negative under both conditions (-78 +/- 7 vs. -47 +/- 8 g/12 h, respectively; P < 0.002). With 72 h of fasting, the glucose and insulin excursions in response to the mixed meal were significantly greater compared with the 13-h fast (P < 0.001). In conclusion, prolonged fasting resulted in a significant decrease in carbohydrate oxidation and an increase in fat oxidation, after a normal mixed meal, in healthy men. This was associated with a significant decrease in glucose tolerance. Because circulating free fatty acids were greatly elevated at all times after the prolonged fast, these may be mediating some of the changes in postprandial metabolism.

Acarbose vs. bedtime NPH insulin in the treatment of secondary failures to sulphonylurea‐metformin therapy in type 2 diabetes mellitus

To evaluate the efficacy of acarbose in the treatment of secondary failures to sulphonylurea-metformin therapy, its comparison against bedtime NPH insulin, and to measure the changes in postprandial metabolism resulting from both treatments. One hundred type 2 diabetic patients in a secondary failure were included. The study begun with a run-in diet period of 6 weeks, in which an isocaloric diet was prescribed. Only subjects who continued hyperglycaemic were randomly assigned to placebo and acarbose (n = 17) or bedtime NPH insulin (n = 12). Acarbose (300 mg/day) or placebo were administered using a randomized, double blind, crossover design. Treatment periods of 3 months were separated by a 3-week washout period. Insulin was administered during 3 months. At the beginning and the end of each treatment period, an i.v. glucose tolerance test and a meal test were performed. Safety tests were done every 4 weeks. Acarbose resulted in a small but significant improvement in fasting plasma glucose (13.5 +/- 2.4 vs. 11.3 +/- 3.9 mmol/l, p = 0.05), HbA1c (11.1 +/- 3.4 vs. 10.3 +/- 2.5%, P = 0.3) and in a decreased plasma glucose during the meal test. Bedtime insulin significantly decreased fasting plasma glucose (13.1 +/- 2.9 vs. 8.2 +/- 2.3 mmol/l, p < 0.01), HbA1c (11.7 +/- 2.9 vs. 9.4 +/- 2.7%, p < 0.01) and plasma cholesterol. No change in insulin secretion resulted from insulin and acarbose treatment. Acarbose decreases blood glucose in secondary failure to sulphonylurea-metformin therapy; however, the decrease is not enough to reach the desired metabolic control. Bedtime NPH insulin is, by far, a more effective alternative.

Rearing of coregonid ( Coregonus schinzi palea Cuv. et Val.) larvae using dry and live food : II. Oxygen consumption and nitrogen excretion

Postprandial metabolic changes in 5-week-old coregonid fry were measured after feeding with live food, Artemia nauplii and three compound dry diets. Growth rates of fish were different and so were the mean weights of the different groups of fish used in these studies; 167 mg for fry fed Artemia and 53, 104 and 142 mg for fish fed diets 1, 2 and 3 respectively. During the week preceding the measurements, the growth rate was 8.12, 4.54, 6.51 and 9.03% day −1 respectively. There was an increase in ammonia and urea excretion in fed fish in comparison with fasted controls and, in the case of urea, this difference was maintained over 14 h after a meal at 13.5°C. An increase in nitrogen (ammonia + urea) excreted after 2 h of feeding in comparison with unfed fish accounted for 9.16–36.92% of nitrogen consumed. During the 5th week of the experiment, nitrogen retention (the proportion of nitrogen gain to nitrogen consumed) amounted to 38.2% in fish fed Artemia and between 11.5 and 20.9% in fish fed dry diets. Postprandial increase in oxygen consumption (specific dynamic action, SDA) was separated from an increase due to activity. SDA accounted for 28.7% of the energy consumed in fish fed live Artemia, whereas in fish fed artificial diets, the SDA was inversely related to their growth rate, and accounted for 4.9–12.7% of energy intake.