Postprandial Glucose Regulation Research Articles

Oat Beta-Glucan and Postprandial Blood Glucose Regulation: A Systematic Review and Meta-Analysis of Acute, Single-Meal Feeding, Controlled Trials

Abstract Objectives The efficacy of oat beta-glucan (OBG), a viscous soluble fibre, on postprandial glycemic outcomes may depend on the nature of the control and the dose and molecular weight (MW) utilized. We undertook a systematic review and meta-analysis of acute clinical trials to determine whether these features mediate the glycemic response to OBG. Methods MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through October 2, 2019. We included acute, single-meal feeding, controlled trials investigating the effect of OBG (concentrate or oat bran) added to a carbohydrate-containing meal compared to a comparable meal (matched control) or a different carbohydrate-containing meal (unmatched control). Two reviewers extracted the data and assessed the risk of bias. The primary outcome was incremental area under the curve (iAUC) for blood glucose. Data were pooled using the generic-inverse variance method with random effects model and expressed as ratio of means with [95% Cis]. Results We included 93 trial comparisons (N = 432). OBG reduced glucose iAUC by 23% (0.77 [0.73 to 0.81]). The effect was not significantly different between matched and unmatched controls (P = 0.17). Dose and MW were significant effect modifiers (P < 0.01). OBG doses per 30 g available carbohydrate of <1.5 g, 1.5 to <2.5 g, 2.5 to <3.5 g, 4.5 to <5.5 g, and >5.5 g OBG led to reductions of 9% (0.91 [0.81 to 1.02]), 14% (0.86 [0.80 to 0.93]), 17% (0.83 [0.76 to 0.90]), 31% (0.69 [0.64 to 0.74)], and 39% (0.61 [0.56 to 0.66]), respectively. Low MW OBG (<300,000 g/mol) had no effect (1.00 [0.94 to 1.07]) but medium MW (300,000 to <1000,000 g/mol) and high MW (>1000,000 g/mol) OBG led to significant reductions of 23% (0.77 [0.69 to 0.87]) and 32% (0.68 [0.63 to 0.73]), respectively. Conclusions Current evidence indicates that the addition of oat beta-glucan to carbohydrate-containing meals reduces the postprandial glycemic response. However, the magnitude of the reduction depends on the dose and the molecular weight of the oat beta-glucan. Funding Sources INQUIS Clinical Research Ltd. (formerly GI Labs), and PepsiCo Global R&D.

Effect of fructose and its epimers on postprandial carbohydrate metabolism: A systematic review and meta-analysis.

To synthesize the evidence of the effect of small doses (≤30-g/meal) of fructose and its epimers (allulose, tagatose, and sorbose) on the postprandial glucose and insulin response to carbohydrate-containing meals. MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through to April 9, 2019. We included randomized (RCTs) and non-randomized acute, single-meal, controlled feeding trials that added ≤30-g of fructose or its epimers either prior to or with a carbohydrate-containing meal compared with the same meal alone. Outcomes included the incremental area under the curve (iAUC) for glucose and insulin, the Matsuda Insulin Sensitivity Index, and the Early Insulin Secretion Index. Data were expressed as ratio of means (RoM) with 95% CIs and pooled using the inverse variance method. The overall certainty of the evidence was evaluated using GRADE. Forty trial comparisons (n=400) were included (none for sorbose). Allulose significantly reduced the postprandial iAUC glucose response by 10% (0.90 [0.84 to 0.96], P<0.01). Tagatose significantly reduced the postprandial iAUC insulin response by 25% (0.75 [0.62 to 0.91], P<0.01) and showed a non-significant 3% reduction in the postprandial iAUC glucose response (0.97 [0.94 to 1.00], P=0.07). There was no effect of fructose on any outcome. The certainty of the evidence was graded as low to moderate for fructose, moderate for allulose, and low for tagatose. Small doses of allulose and tagatose, but not fructose, lead to modest improvements on postprandial glucose and insulin regulation. There is a need for long-term RCTs to confirm the sustainability of these improvements.

Glycative stress and anti-aging: 13. Regulation of Glycative stress. 1. Postprandial blood glucose regulation

Glycative stress and anti-aging: 13. Regulation of Glycative stress. 1. Postprandial blood glucose regulation

Postprandial glycaemic responses in women co-ingesting green leafy vegetables with a carbohydrate meal: interactions with the sirtuin system

AbstractThe addition of vegetable to carbohydrate-based meals has been shown to improve postprandial glucose homeostasis. Inter-individual variation in responses preclude conclusive evidence, particularly in women. The sirtuins and associated genes involved in producing the chemical, nicotinamide adenine dinucleotide (NAD), are emerging as key players in blood glucose control and may contribute to variable responses. This study aimed to investigate effects of co-ingesting green leafy vegetables (GLV) on postprandial glucose regulation following a carbohydrate meal and factors affecting inter-individual variation particularly around the sirtuin system.Twenty-five women (BMI 24.8–30.5 kg/m2) were recruited to ‘The impact of Vegetables’ (VegGI) study on acute glycaemia and Glycaemia induced CVD risk in women: metabolic effects and Inter-individual variations. Postprandial glycaemic responses (GR) following rice (75 g of available carbohydrate), rice with bok choy (150g) or spinach (150g) were measured every 5 minutes for 4 hours using a Continuous Glucose Monitoring system (Medtronic Ltd). Anthropometric, cholesterol (Cholestech LDX, Alere), HbA1c (Afinion AS100, Alere) and insulin (Mercodia AB) measures were made in a fasted state. Oestradiol, progesterone, follicular stimulating hormone and testosterone were measured (ADVIA Centaur). Total RNA was extracted from postprandial blood collected at 0 h, 30 min, 1 h and 2 h in PAXgene blood RNA tubes (PreAnalytiX GmbH) using a Blood RNA Kit (Qiagen, Crawley, UK) and quality assessed by Agilent Bioanalyser (Agilent Technologies, Bracknell, UK). Gene expression was measured using the GenomeLab System and a custom designed multiplex assay, the hSIRTNADPlex (25 targets involved in the sirtuin signalling).Linear mixed models (ver.24.0; SPSS Inc) revealed no effect of GLV consumption on postprandial GR. Principal component analysis (SIMCA-P + 12.0 software, MKS Instruments UK Ltd.) of postprandial GR indicated inter-individual variation in the responses associated with the test meals. Partial Least Square (PLS) stratified the cohort into two subgroups based on sirtuin system gene expression profiles. Postprandial GR was a contributing factor in the stratification observed, together with BMI, plasma lipid, insulin and glucose levels, but not menopausal status.Preliminary evidence indicates that co-ingesting GLV with a carbohydrate meal does not reduce postprandial GR in women (BMI 24.8–30.5 kg/m2) and that significant inter-individual variation in postprandial GR may be linked to the sirtuin system, BMI, plasma lipid, insulin, and glucose levels but not menopausal status. Recruitment and data analysis are ongoing to increase group size and further assess contributing factors.This work was supported by Scottish Government's Rural and Environment Science and Analytical Services Division

N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis

Fatty acid amide hydrolase (FAAH) degrades 2 major classes of bioactive fatty acid amides, the N-acylethanolamines (NAEs) and N-acyl taurines (NATs), in central and peripheral tissues. A functional polymorphism in the human FAAH gene is linked to obesity and mice lacking FAAH show altered metabolic states, but whether these phenotypes are caused by elevations in NAEs or NATs is unknown. To overcome the problem of concurrent elevation of NAEs and NATs caused by genetic or pharmacological disruption of FAAH in vivo, we developed an engineered mouse model harboring a single-amino acid substitution in FAAH (S268D) that selectively disrupts NAT, but not NAE, hydrolytic activity. The FAAH-S268D mice accordingly show substantial elevations in NATs without alterations in NAE content, a unique metabolic profile that correlates with heightened insulin sensitivity and GLP-1 secretion. We also show that N-oleoyl taurine (C18:1 NAT), the most abundant NAT in human plasma, decreases food intake, improves glucose tolerance, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice. Together, these data suggest that NATs act as a class of lipid messengers that improve postprandial glucose regulation and may have potential as investigational metabolites to modify metabolic disease.

Insulin Action in the Hypothalamus Increases Second-Phase Insulin Secretion in Humans

Background: Animal studies and initial correlative data in humans indicate that insulin action in the brain may affect pancreatic insulin secretion. An important brain region for this process is the hypothalamus, an area that can develop insulin resistance. Methods: Fifteen young, healthy men (27 ± 3 years) with a wide BMI spectrum (20–30 kg/m²) underwent 2 hyperglycemic clamps (target blood glucose: 10 mmol/L). In this double-blind study, subjects received 160 U of insulin or placebo as a nasal spray on 2 days in randomized order. On another day, insulin sensitivity of the hypothalamus was determined by functional magnetic resonance imaging. Results: Glucose levels were comparable on both study days. In the whole group, C-peptide levels were not significantly different between conditions. Though, there was a significant interaction between insulin sensitivity of the hypothalamus × nasal spray × time on C-peptide levels (p = 10^–6). The group was therefore divided according to median hypothalamic insulin sensitivity. C-peptide concentrations were higher after intranasal insulin compared to placebo spray in the group with a strong hypothalamic insulin response (p < 0.0001, β = 6.00 ± 1.24) and lower in the brain insulin-resistant group (p = 0.005, β = –2.68 ± 0.95). Neither somatostatin nor glucagon kinetics was altered by the nasal spray. Conclusions: In participants with high hypothalamic insulin sensitivity, insulin action in the brain enhanced second-phase insulin secretion from pancreatic beta cells. This reaction could, for example, contribute to late postprandial glucose regulation by suppressing hepatic glucose production by portal venous insulin.

Modest changes to glycemic regulation are sufficient to maintain glucose fluxes in healthy young men following overfeeding with a habitual macronutrient composition

Currently, it is unclear whether short-term overfeeding in healthy people significantly affects postprandial glucose regulation, as most human overfeeding studies have utilized induced experimental conditions such as the euglycemic-hyperinsulinemic clamp technique to assess glucoregulation. The aim of this study was to quantify glucose fluxes [rates of meal glucose appearance (Ra), disposal (Rd), and endogenous glucose production (EGP)] in response to 5 and 28 days of overfeeding (+45% energy) while maintaining habitual macronutrient composition (31.0 ± 1.9% fat, 48.6 ± 2.2% carbohydrate, 16.7 ± 1.4% protein) in healthy, lean young men. Meal tolerance testing was combined with the triple-stable isotope glucose tracer approach. Visceral adipose volume increased by ~15% with 5 days of overfeeding, while there was no further change at 28 days. In contrast, body mass (+1.6 kg) and fat mass (+1.3 kg) were significantly increased only after 28 days of overfeeding. Fasting EGP, Rd, and insulin were increased at 5 but unchanged after 28 days. Postprandial glucose and insulin responses were unaltered by 5 days of overfeeding but were modestly increased after 28 days (P < 0.05). However, meal Ra and glucose Rd were significantly increased after both 5 and 28 days of overfeeding (P < 0.05). Despite this, overfeeding did not lead to alterations to postprandial EGP suppression. Thus, in contrast to findings from euglycemic-hyperinsulinemic clamp studies, chronic overfeeding did not affect the ability to suppress EGP or stimulate Rd under postprandial conditions. Rather, glucose flux was appropriately maintained following 28 days of overfeeding through modest increases in postprandial glycemia and insulinemia.

Postprandial Glucose Regulation via KNN Meal Classification in Type 1 Diabetes

Blood glucose concentration control is a classic negative feedback problem with insulin secreted by the pancreas as a control variable. Type 1 Diabetes is a chronic metabolic disease caused by a cellular-mediated autoimmune destruction of the pancreas beta-cells, so exogenous insulin administration is needed to regulate the glycaemia. Postprandial glucose regulation is typically based on the knowledge of an estimation of the ingested carbohydrates, of the Carbohydrate-to-insulin ratio, of the correction factor, of the insulin still active and of a measure of the glycaemia just before the meal. Despite the use of this information meal compensation is yet a key unsolved issue. In this letter a new approach based on machine-learning methodologies is proposed to improve postprandial glucose regulation. The proposed approach uses the multiple K-nearest neighbors classification algorithm to predict postprandial glucose profile due to the nominal therapy and to suggest a correction to time and/or amount of the meal bolus. This approach has been successfully validated on the adult in silico population of the UVA/PADOVA simulator, which has been accepted by the Food and Drug Administration as a substitute to animal trials.

Peptide YY (PYY) Is Expressed in Human Skeletal Muscle Tissue and Expanding Human Muscle Progenitor Cells.

Peptide YY (PYY) is considered a gut peptide with roles in post-prandial appetite and glucose regulation. Circulating PYY protein levels increase during aerobic exercise. Furthermore, people who have greater increases in muscle progenitor cells (hMPCs), the adult stem cell population responsible for skeletal muscle (SkM) repair, after resistance training have higher PYY transcript levels in SkM prior to training. Currently, examination of PYY expression patterns in SkM and/or hMPCs is lacking. Our objective was to identify the expression patterns of PYY in SkM and hMPCs. PYY and the associated Y receptors were analyzed in SkM biopsy tissue and cultured hMPCs from young and old human participants. Additional experiments to assess the role and regulation of PYY in hMPCs were performed. In SkM, PYY and one of the three Y receptors (Y1r) were detectable, but expression patterns were not affected by age. In expanding hMPCs, PYY and all three Y receptor (Y1r, Y2r, and Y5r) proteins were expressed in a temporal fashion with young hMPCs having greater levels of Y receptors at various time points. Exogenous PYY did not affect hMPC population expansion. hMPC PYY levels increased following the metabolic stimulus, 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), but were not affected by the inflammatory stimulus, tumor necrosis factor alpha (TNFα). In conclusion, PYY and Y receptor expression are not impacted by age in SkM tissue but are reduced in old vs. young expanding hMPCs. Furthermore, endogenous PYY production is stimulated by low energy states and thus may be integral for skeletal muscle and hMPC responses to metabolic stimuli.

Effect of dairy and nondairy snacks on postprandial blood glucose regulation in 9-14-year-old children.

In adults, dairy consumption improves short-term blood glucose regulation. It is unknown if these short-term benefits extend to children of different weight statuses. The objective of this study was to investigate the effect of a dairy and nondairy snack in both normal-weight (NW) and overweight/obese (OW/OB) children on blood glucose regulation and food intake (FI). In a repeated-measures crossover design, 11 NW and 7 OW/OB children (age: 9-14 years), consumed, in random order, a dairy (Greek yogurt, 198.9 g, 171 kcal, 0 g fat, 17 g protein) or nondairy (mini sandwich-type cookies, 37.5 g, 175 kcal, 7.5 g fat, 1.3 g protein) snack containing 25 g of available carbohydrates. Ad libitum FI was measured 120 min after snack consumption. Blood glucose, insulin, C-peptide, and glucagon-like peptide-1 (GLP-1) were measured at 0 min (before the snack), and at 30, 60, 90, and 120 min after snack consumption. Insulin secretion was calculated from deconvolution of C-peptide. Hepatic insulin extraction was calculated as C-peptide divided by insulin. FI did not differ between snacks (P = 0.55). Mean blood glucose was lower (P < 0.001) and insulin higher (P < 0.0001) in the 120 min after consuming the dairy snack. C-Peptide concentrations (P = 0.75) and insulin secretion (P = 0.37) were not different between snacks. The increase in insulin was explained by reduced hepatic insulin extraction (P < 0.01). Consumption of the dairy snack also increased mean GLP-1 concentrations (P < 0.001). In conclusion, consumption of a dairy snack by NW and OW/OB children results in reduced postprandial blood glucose concentrations and elevated circulating insulin compared with a nondairy snack possibly because of delayed hepatic insulin extraction.

Regulations on glucose metabolism affected by dietary carbohydrate in different strains of juvenile gibel carp (Carassius gibelio)

This experiment was conducted to study the effects of dietary carbohydrate on glucose metabolism in gibel carp (Carassius gibelio) as well to investigate if different clones had different responses to carbohydrate intake. Unselected Dongting strain (DT strain), selected gibel carp “CAS III” (A strain) and gibel carp “CAS V” (F strain) were fed with no corn starch diet (0C), 30% corn starch diet (30C) and 45% corn starch diet (45C) for 8 weeks. The results showed that selected F strain showed higher growth performance. F strain and A strain showed better control on postprandial glucose regulation by increasing plasma triglyceride, plasma cholesterol, liver and muscle glycogen contents and also enhancing glycolysis and restraining gluconeogenesis. DT strain had higher body lipid and lipid utilization. In conclusion, gibel carp could tolerate 45% dietary carbohydrate and F strain showed better growth by increasing glycolysis while decreasing glycogenesis.

Separate and Combined Glucometabolic Effects of Endogenous Glucose-Dependent Insulinotropic Polypeptide and Glucagon-like Peptide 1 in Healthy Individuals.

The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted postprandially and contribute importantly to postprandial glucose tolerance. In this study, we assessed the individual and combined contributions of endogenous GIP and GLP-1 to the postprandial changes in glucose and glucoregulatory hormones using the novel GIP receptor antagonist GIP(3-30)NH2 and the well-established GLP-1 receptor antagonist exendin(9-39)NH2 During 4-h oral glucose tolerance tests (75 g) combined with an ad libitum meal test, 18 healthy men received on four separate days in randomized, double-blinded order intravenous infusions of A) GIP(3-30)NH2 (800 pmol/kg/min) plus exendin(9-39)NH2 (0-20 min: 1,000 pmol/kg/min; 20-240 min: 450 pmol/kg/min), B) GIP(3-30)NH2, C) exendin(9-39)NH2, and D) saline, respectively. Glucose excursions were significantly higher during A than during B, C, and D, while glucose excursions during B were higher than during C and D. Insulin secretion (assessed by C-peptide/glucose ratio) was reduced by 37 ± 16% (A), 30 ± 17% (B), and 8.6 ± 16% (C) compared with D (mean ± SD). A and C resulted in higher glucagon levels and faster gastric emptying. In conclusion, endogenous GIP affects postprandial plasma glucose excursions and insulin secretion more than endogenous GLP-1, but the hormones contribute additively to postprandial glucose regulation in healthy individuals.

Effects of starvation and short-term refeeding on gastric emptying and postprandial blood glucose regulation in adolescent girls with anorexia nervosa.

Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying, and glucoregulatory hormone changes in malnourished patients with AN and during 2 wk of acute refeeding compared with healthy controls (HCs). Twenty-two female adolescents with AN and 17 age-matched female HCs were assessed after a 4-h fast. Patients were commenced on a refeeding protocol of 2,400 kcal/day. Gastric emptying (13C-octanoate breath test), glucose absorption (3-O-methylglucose), blood glucose, plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin, C-peptide, and glucagon responses to a mixed-nutrient test meal were measured on admission and 1 and 2 wk after refeeding. HCs were assessed once. On admission, patients had slower gastric emptying, lower postprandial glucose and insulin, and higher glucagon and GLP-1 than HCs ( P < 0.05). In patients with AN, the rise in glucose (0-30 min) correlated with gastric emptying ( P < 0.05). With refeeding, postprandial glucose and 3-O-methylglucose were higher, gastric emptying faster, and baseline insulin and C-peptide less ( P < 0.05), compared with admission. After 2 wk of refeeding, postprandial glucose remained lower, and glucagon and GLP-1 higher, in patients with AN than HCs ( P < 0.05) without differences in gastric emptying, baseline glucagon, or postprandial insulin. Delayed gastric emptying may underlie reduced postprandial glucose in starved patients with AN; however, postprandial glucose and glucoregulatory hormone changes persist after 2 wk of refeeding despite improved gastric emptying. Future research should explore whether reduced postprandial glucose in AN is related to medical risk by examining associated symptoms alongside continuous glucose monitoring during refeeding.

The effect of visceral fat and elevated blood glucose on anxiety levels in college age students

Anxiety is prevalent among young adults; research shows metabolic inflexibility, the inability to oxidize fat, can increase the occurrence of hyper-aroused states. Fasting blood glucose is the current protocol for assessing metabolic impairment. However, recent studies have shown young adults may have normal fasting blood glucose levels with underlying irregularities in postprandial glucose regulation, insulin secretion and cortisol release, which causes a pattern of visceral fat accumulation. Visceral fat of the volunteers was assessed using the DXA (Dual-energy X-ray absorptiometry) full body scanning method; the waist was assessed by taking the circumference at the midpoint between the lower margin of the last palpable rib and the top of the iliac crest to formulate a waist to height ratio (WHtR); fasting glucose levels were measured via point-of-care (POC) finger-stick method using the Abbott Precision blood glucose meter and anxiety levels. The Pearson R correlation test showed significance between GAD-7 and VAT Volume at r = 0.513 VAT Mass r = 0.514 body fat percentage r = 0.407 and Android r = 0.419. This correlation between GAD-7 and VAT Volume and VAT Mass shows the physiological connection between elevated visceral fat and heightened anxiety. High amounts of visceral fat may lead to an increase in insulin and cortisol levels. The study may suggest that increased fasting blood glucose is not necessarily the best predictor of metabolic dysregulation in a population of healthy college students.

Effect of High ß-Glucan Barley on Postprandial Plasma Glucose Levels in Subjects with Normal Glucose Tolerance and Patients with Type 2 Diabetes

Increasing evidence supports a more prominent role for postprandial glucose (PPG) regulation in the management of type 2 diabetes. Viscous dietary fibers including oat and barley β-glucan are one of the most effective classes of functional food ingredients for reducing PPG. We investigated the effect of high β-glucan barley on postprandial plasma glucose and C-peptide levels using a meal tolerance test and continuous glucose monitoring (CGM) in 15 subjects with normal glucose tolerance (NGT) and 29 type 2 diabetic patients. A 500-kcal meal tolerance test, using white rice alone (white rice) or white rice mixed with 50% of barley (Kirari-mochi®) containing 1.5-times β-glucan higher than usual barley (barley), was performed, and plasma glucose and C-peptide levels were measured every 30 minutes for 180 minutes. Daily glucose variability was measured using CGM over two days, while subjects consumed 1600-kcal or 1800-kcal test meals consisting of white rice or barley. Subsequently, a meal tolerance test with identical carbohydrate quantity (52g carbohydrate) with or without 1.8g of β-glucan, was performed in 7 diabetic patients. In NGT subjects and diabetic patients, the incremental area under the curve (AUC) of plasma glucose and C-peptide levels for 180 minutes after the meal tolerance test were significantly decreased following the consumption of barley compared to the consumption of white rice alone. The studies using CGM have demonstrated that the consumption of barley lead to a significant decrease in the 24-h standard deviation of blood glucose (24-h SDBG) and mean amplitude of glycemic excursion (MAGE) in diabetic patients. Similar results were obtained in subsequent tests with identical carbohydrate quantity but with β-glucan. In conclusion, these results suggest that high-β-glucan barley may contribute to decreased PPG levels and endogenous insulin secretion in both patients with type 2 diabetes and the subjects with NGT. Disclosure M. Higa: None. A. Hashimoto: None. M. Hayasaka: None. M. Hijikata: None. A. Ueda: None. K. Oda: None. D. Kato: None. K. Yamashita: None. T. Ichijo: None.

Effects of 6 vs 3 eucaloric meal patterns on glycaemic control and satiety in people with impaired glucose tolerance or overt type 2 diabetes: A randomized trial

Background/objectivesThe study aimed to compare the effects of two eucaloric meal patterns (3 vs 6 meals/day) on glycaemic control and satiety in subjects with impaired glucose tolerance and plasma glucose (PG) levels 140–199mg/dL at 120min (IGT-A) or PG levels 140–199mg/dL at 120min and >200mg/dL at 30/60/90min post-oral glucose load on 75-g OGTT (IGT-B), or overt treatment-naïve type 2 diabetes (T2D). Subjects/methodsIn this randomized crossover study, subjects with IGT-A (n=15, BMI: 32.4±5.2kg/m2), IGT-B (n=20, BMI: 32.5±5kg/m2) or T2D (n=12, BMI: 32.2±5.2kg/m2) followed a weight-maintenance diet (45% carbohydrates, 20% proteins, 35% fats) in 3 or 6 meals/day (each intervention lasting 12 weeks). Anthropometrics, diet compliance and subjective appetite were assessed every 2 weeks. OGTT and measurements of HbA1c and plasma lipids were performed at the beginning and end of each intervention period. ResultsBody weight and physical activity levels remained stable throughout the study. In T2D, HbA1c and PG at 120min post-OGTT decreased with 6 vs 3 meals (P<0.001 vs P=0.02, respectively). The 6-meal intervention also improved post-OGTT hyperinsulinaemia in IGT-A subjects and hyperglycaemia in IGT-B subjects. In all three groups, subjective hunger and desire to eat were reduced with 6 vs 3 meals/day (P<0.05). There were no differences in HOMA-IR or plasma lipids between interventions. ConclusionAlthough weight loss remains the key strategy in hyperglycaemia management, dietary measures such as more frequent and smaller meals may be helpful for those not sufficiently motivated to adhere to calorie-restricted diets. Our study shows that 6 vs 3 meals a day can increase glycaemic control in obese patients with early-stage T2D, and may perhaps improve and/or stabilize postprandial glucose regulation in prediabetes subjects.

Erythritol Attenuates Postprandial Blood Glucose by Inhibiting α-Glucosidase.

Diabetes mellitus (DM) is a serious metabolic disorder, where impaired postprandial blood glucose regulation often leads to severe health complications. The natural chemical erythritol is a C4 polyol approved by the U.S. Food and Drug Administration for use as a sweetener. Here, we examined a potential role for erythritol in the control of postprandial blood glucose levels in DM. An anti-postprandial hyperglycemia effect upon erythritol administration (500 mg kg-1) was demonstrated in alloxan-induced DM model mice by monitoring changes in blood glucose after intragastric administration of drugs and starch. We also found that erythritol most likely exerts its anti-postprandial hyperglycemic activities by inhibiting α-glucosidase in a competitive manner. This was supported by enzyme activity assays and molecular modeling experiments. In the latter experiments, it was possible to successfully dock erythritol into the catalytic pocket of α-glucosidase, with the resultant interaction likely driven by electrostatic interactions involving Asp215, Asp69, and Arg446 residues. This study suggests that erythritol may not only serve as a glucose substitute but also be a useful agent in the treatment of DM to help manage postprandial blood glucose levels.

The Artificial Pancreas and Meal Control: An Overview of Postprandial Glucose Regulation in Type 1 Diabetes

In healthy individuals, plasma glucose concentration is tightly regulated by the action of the hormones secreted by the endocrine pancreas, principally, insulin and glucagon. Insulin is secreted by the pancreatic beta cells to signal organs to absorb glucose, and glucagon is secreted by the pancreatic alpha cells to signal the liver to produce glucose [1]. In type 1 diabetes (T1D), insulin secretion is lost due to the autoimmune destruction of the beta cells [2]. T1D accounts for 5-15% of the 366 million people with diabetes worldwide [3].

High intake of fatty fish, but not of lean fish, improved postprandial glucose regulation and increased the n-3 PUFA content in the leucocyte membrane in healthy overweight adults: a randomised trial.

The prevalence of type 2 diabetes (T2D) is low in populations with a high fish intake; however prospective studies with fish intake have shown positive, negative or no association between fish intake and the risk for T2D. The aim of this study was to investigate the effects of high intake of lean or fatty fish on glucose tolerance, leucocyte membrane fatty acid composition and leucocyte function in overweight/obese adults. In this randomised clinical trial, sixty-eight healthy overweight/obese participants consumed 750 g/week of either lean or fatty fish as dinners, or were instructed to continue their normal eating habits but to avoid fish intake (control group), for 8 weeks. Energy and macronutrient intake and physical activity were not changed within the groups during the study period. High intake of fatty fish, but not of lean fish, significantly improved glucose regulation 120 min postprandially (P=0·012), but did not affect fasting glucose concentration. A smaller increase in fasting to 120 min postprandial insulin C-peptide concentration was seen after fatty fish intake (P=0·012). Lean fish increased the DHA content in leucocyte membranes (P=0·010), and fatty fish increased the total content of n-3 PUFA (P=0·00016) and reduced the content of n-6 PUFA (P=0·00057) in leucocyte membranes. Lean and fatty fish intake did not affect phagocytosis of bacteria ex vivo. The findings suggest that high intake of fatty fish, but not of lean fish, beneficially affected postprandial glucose regulation in overweight/obese adults, and may therefore prevent or delay the development of T2D in this population.

High intake of fatty fish, but not of lean fish, affects serum concentrations of TAG and HDL-cholesterol in healthy, normal-weight adults: a randomised trial

The aim of the present study was to examine whether high intake of lean or fatty fish (cod and farmed salmon, respectively) by healthy, normal-weight adults would affect risk factors of type 2 diabetes and CVD when compared with lean meat (chicken). More knowledge is needed concerning the potential health effects of high fish intake (>300 g/week) in normal-weight adults. In this randomised clinical trial, thirty-eight young, healthy, normal-weight participants consumed 750 g/week of lean or fatty fish or lean meat (as control) for 4 weeks at dinner according to provided recipes to ensure similar ways of preparations and choices of side dishes between the groups. Energy and macronutrient intakes at baseline and end point were similar in all groups, and there were no changes in energy and macronutrient intakes within any of the groups during the course of the study. High intake of fatty fish, but not lean fish, significantly reduced TAG and increased HDL-cholesterol concentrations in fasting serum when compared with lean meat intake. When compared with lean fish intake, fatty fish intake increased serum HDL-cholesterol. No differences were observed between lean fish, fatty fish and lean meat groups regarding fasting and postprandial glucose regulation. These findings suggest that high intake of fatty fish, but not of lean fish, could beneficially affect serum concentrations of TAG and HDL-cholesterol, which are CVD risk factors, in healthy, normal-weight adults, when compared with high intake of lean meat.