Postprandial Glycemia In Type Research Articles

Manipulation of Post-Prandial Hyperglycaemia in Type 2 Diabetes: An Update for Practitioners.

This review paper explores post-prandial glycemia in type 2 diabetes. Post-prandial glycemia is defined as the period of blood glucose excursion from immediately after the ingestion of food or drink to 4 to 6 hours after the end of the meal. Post-prandial hyperglycemia is an independent risk factor for cardiovascular disease with glucose "excursions" being more strongly associated with markers of oxidative stress than the fasting or pre-prandial glucose level. High blood glucose is a major promoter of enhanced free radical production and is associated with the onset and progression of type 2 diabetes. Oxidative stress impairs insulin action creating a vicious cycle where repeated post-prandial glucose spikes are key drivers in the pathogenesis of the vascular complications of type 2 diabetes, both microvascular and macrovascular. Some authors suggest post-prandial hyperglycemia is the major cause of death in type 2 diabetes. Proper management of post-prandial hyperglycemia could yield up to a 35% cut in overall cardiovascular events, and a 64% cut in myocardial infarction. The benefits of managing post-prandial hyperglycemia are similar in magnitude to those seen in type 2 diabetes patients receiving secondary prevention with statins - prevention which today is regarded as fundamental by all practitioners. Given all the evidence surrounding the impact of post-prandial glycemia on overall outcome, it is imperative that any considered strategy for the management of type 2 diabetes should include optimum dietary, pharma, and lifestyle interventions that address glucose excursion. Achieving a low post-prandial glucose response is key to prevention and progression of type 2 diabetes and cardiometabolic diseases. Further, such therapeutic interventions should be sustainable and must benefit patients in the short and long term with the minimum of intrusion and side effects. This paper reviews the current literature around dietary manipulation of post-prandial hyperglycemia, including novel approaches. A great deal of further work is required to optimize and standardize the dietary management of post-prandial glycemia in type 2 diabetes, including consideration of novel approaches that show great promise.

Influence of resistant starch resulting from the cooling of rice on postprandial glycemia in type 1 diabetes

IntroductionCarbohydrates are one of the macronutrients which have the most substantial influence on glycemic response. The cooling of rice after cooking causes retrogradation of starch, which becomes a non-absorbable product in the human digestive tract.Aim of the studyThis study aimed to assess whether cooling of rice affects postprandial glycemia in subjects with type 1 diabetes.Materials and methodsThe study included 32 patients with type 1 diabetes. Each participant of the study consumed two standardized test meals consisting of long-grain white rice. One of the test meals was served immediately after preparation, and another was cooled for 24 h at 4 °C after preparation and reheated before being served. Postprandial glycemia was measured for 3 h using the FreeStyle Libre flash glucose monitoring system for each patient.ResultsAfter consumption of the test meal containing rice subjected to the cooling process when compared to fresh rice, a significantly lower value of maximum glycemia (11 vs. 9.9 mmol/L, p = 0.0056), maximum glycemic increase (2.7 vs. 3.9 mmol/L, p < 0.0001), areas under the glycemic curve (135 vs. 336 mmol/L * 180 min, p < 0.0001) and significantly shorter time to peak (35 vs. 45 min, p = 0.031) was observed. There was a significantly higher number of hypoglycemic episodes among the patients after consuming test meals with cooled rice compared to fresh ones during 180 min of observation (12(38) vs. 3(9), p = 0.0039).ConclusionsConsumption of rice subjected to the cooling process results in a lower increase of postprandial blood glucose in subjects with type 1 diabetes. At the same time it increases the risk of postprandial hypoglycemia using a standard insulin dose.

Wholegrain Particle Size Influences Postprandial Glycemia in Type 2 Diabetes: A Randomized Crossover Study Comparing Four Wholegrain Breads.

Wholegrain foods vary in the extent of processing. We investigated whether wholegrain particle size in bread influences postprandial glycemia in type 2 diabetes. Postprandial glycemia (incremental area under the blood glucose curve [iAUC]) was measured after consumption of three breads made with roller-milled wholegrain flour and added grains and a fourth made with stone-ground flour. All flours and grains were 100% wholegrain wheat. Breads were nutrient matched. Fifteen adults (64 ± 10 years, HbA1c 58 ± 13 mmol/mol) completed the study. iAUC for the three breads made with roller-milled flour ranged from 376 to 641 mmol-1min-1, inverse linear trend for grain particle size P = 0.039. The iAUC for stone-ground wholegrain bread (503) was smaller than predicted from mean particle size. Wholegrain structural integrity in bread is a determinant of glycemic response. These findings have implications for dietary advice and the definition of the term "'wholegrain."

Insulin Dosing for Fat and Protein: Is it Time?

The impact of dietary fat and protein on postprandial glycemia in type 1 diabetes (T1D) and the need to adjust for them in the mealtime insulin dose have been controversial (1,2). Recently, carefully designed randomized trials in individuals living with T1D have shown protein and fat consumed in meals with carbohydrate reduce the early postprandial rise (1–2 h) and contribute to postprandial hyperglycemia in the late (3–6 h) postprandial period (3–5). In clinical practice, continuous glucose monitoring highlights the glycemic effects of different meal types demonstrating that mealtime insulin dosing strategies based on carbohydrate counting alone have limitations. There is a need for an evidence-based, safe, and practical method to guide insulin adjustments for high-fat, high-protein meals. In this issue of Diabetes Care , Bell et al. (6) address the pressing clinical question of optimal insulin adjustments for meals containing differing amounts of dietary fat. This is important because postprandial hyperglycemia has been identified as a risk factor for the development of long-term complications of diabetes (7), and higher fat diets have increased in popularity in recent years. The mechanisms by which all three macronutrients impact blood glucose levels in people with T1D is shown in Fig. 1. Dietary carbohydrate is absorbed and rapidly increases the blood glucose concentration (8). Dietary protein results in a delayed and more prolonged increase in blood glucose levels by conversion of amino acids to glucose through gluconeogenesis, as well as an influence on multiple hormones including glucagon, cortisol, growth hormone, insulin-like growth factor 1, and ghrelin, thus increasing insulin resistance (9). Dietary fat also results in a delayed glycemic response by a number of mechanisms. Free fatty acids act via peroxisome proliferator–activated receptors and free fatty acid receptors to impact …

The Effects of a Whey Protein and Guar Gum-Containing Preload on Gastric Emptying, Glycaemia, Small Intestinal Absorption and Blood Pressure in Healthy Older Subjects.

A whey protein/guar gum preload reduces postprandial glycaemia in type 2 diabetes through slowing gastric emptying. However, gastric emptying has previously been assessed using a stable isotope breath test technique, which cannot discriminate between slowing of gastric emptying and small intestinal absorption. This preload also may be useful in the management of postprandial hypotension. We evaluated the effects of a whey protein/guar preload on gastric emptying, glucose absorption, glycaemic/insulinaemic and blood pressure (BP) responses to an oral glucose load. Eighteen healthy older participants underwent measurements of gastric emptying (scintigraphy), plasma glucose and insulin, glucose absorption, superior mesenteric artery (SMA) flow, BP and heart rate (HR) after ingesting a 50 g glucose drink, with or without the preload. The preload reduced plasma glucose (p = 0.02) and serum 3-O-methylglucose (3-OMG) (p = 0.003), and increased plasma insulin (p = 0.03). There was no difference in gastric emptying or BP between the two days. The reduction in plasma glucose on the preload day was related to the reduction in glucose absorption (r = 0.71, p = 0.002). In conclusion, the glucose-lowering effect of the preload may relate to delayed small intestinal glucose absorption and insulin stimulation, rather than slowing of gastric emptying.

Title: Differentiating the effects of whey protein and guar gum preloads on postprandial glycemia in type 2 diabetes

Background and aimsWhey protein and guar gum have both been reported to reduce postprandial glycemia in health and type 2 diabetes, associated with stimulation of glucagon-like peptide-1 (GLP-1) and/or slowing of gastric emptying. Our aim was to evaluate, in type 2 diabetes, the acute effects of low dose “preloads” of whey and guar, given alone or in combination before a meal, on postprandial glycemia, insulin, GLP-1, and gastric emptying. Methods21 patients with type 2 diabetes, managed by diet or metformin alone, were each studied on 4 days. They received a preload “shake” 15min before a mashed potato meal (368.5 kcal) labeled with 13C-octanoic-acid. The preloads comprised either (i) 17 g whey (W), (ii) 5 g guar (G), (iii) 17 g whey + 5 g guar (WG) each sweetened with 60 mg sucralose, and (iv) 60 mg sucralose alone (control; C), all dissolved in 150 mL water. Venous blood was sampled frequently for measurements of glucose, insulin, and GLP-1 concentrations. Gastric half-emptying time (T50) was calculated from breath 13CO2 excretion over 240 min. ResultsPostprandial blood glucose concentrations were lower with W and WG compared to C (each P < 0.0001, treatment × time interaction), and lower after G than C only at 30min. Insulin, GLP-1, and glucagon concentrations were higher after W than WG, G, or C (P < 0.05, treatment × time interaction), without differences between the latter three. Gastric emptying was slower with W (T50: 179.6 ± 6.1 min, P < 0.05) and WG (T50: 197.6 ± 9.7 min, P < 0.0001) when compared to C (T50: 162.9 ± 6.2 min), but did not differ between G (T50: 171.3 ± 7.0) and C (P > 0.99). ConclusionBoth whey and whey/guar preloads reduced postprandial glycemia, associated with slowing of gastric emptying. Low dose guar was less effective as a preload for glucose-lowering and did not slow gastric emptying. Clinical Trial Registry number and websiteAustralian and New Zealand Clinical Trials Registry, Trial ID ACTRN12615001272583, http://www.anzctr.org.au

Gastrointestinal effects of extra-virgin olive oil associated with lower postprandial glycemia in type 1 diabetes

To explore the possible mechanisms behind the lower glycemic response observed when extra-virgin olive oil (EVOO) is added to a high-glycemic index meal in patients with type 1 diabetes (T1D). According to a randomized cross-over design, eleven T1D patients (6 women, 5 men) on insulin pump consumed in the metabolic ward, one week apart, three high-glycemic index meals differing only for amount and quality of fat: high-monounsaturated fat (EVOO), high-saturated fat (Butter), and low-fat (LF). Before and after the meals, blood glucose (continuous glucose monitoring), gastric emptying rate (ultrasound technique), and plasma concentrations of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide GIP (ELISA), glucagon (RIA), and lipids (colorimetric assays) were evaluated. Blood glucose iAUC (mmol/lx360min) was lower after the EVOO (690±431) than after the Butter (1320±600) and LF meals (1007±990) (M±SD, p=0.041 by repeated measures ANOVA). Gastric antrum volume was significantly larger in the early (60-90min) postprandial phase (106±21 vs. 90±16ml, p=0.048) and significantly smaller in the late phase (330-360min) (46±10 vs. 57±22ml, p=0.045) after the EVOO than after Butter meal. EVOO significantly increased postprandial GLP-1 iAUC (261±311) compared to Butter (189±349) (pmol/Lx180min, p=0.009). Postprandial GIP and glucagon responses were not significantly different between EVOO and Butter. Postprandial triglyceride iAUC was significantly higher after EVOO (100±53) than after Butter (65±60) (mmol/l×360min, p=0.048). Changes in gastric emptying and GLP-1 secretion and reduced glucose absorption through glucose-lipid competition may contribute to lower glycemia after a high-glycemic index meal with EVOO in T1D patients. NCT02330939.

Effects of acute ingestion of whey protein with or without prior aerobic exercise on postprandial glycemia in type 2 diabetics.

Acute protein co-ingestion or a single bout of aerobic exercise can attenuate postprandial glycemia, but their combined effect has not been investigated in type 2 diabetics. Using a randomised crossover design, male type 2 diabetics (n = 8) [mean (95% CI); age, 55.0 (45.2, 64.8) year; BMI, 33.7 (25.6, 41.8) kg·m- 2; 2h glucose 14.0 (12.5, 15.5) mM] completed (1) 75g oral glucose tolerance test (OGTT) (CON); (2) OGTT supplemented with 0.33 g·kg BM- 1 of whey protein concentrate (PRO); or OGTT supplemented with PRO but preceded by a bout of aerobic cycling exercise (PRO + EX). Postprandial venous blood samples were collected for glucose, insulin, C-peptide and glucagon. Despite a fold-increase of 1.90 (1.26, 2.56; p < 0.05) in postprandial insulin compared to CON, PRO failed to attenuate postprandial glycemia measured by 2h glucose area under the curve. During PRO + EX, plasma glucose was elevated by 1.51 (0.5, 2.5) mM and 1.3 (0.3, 2.3) mM at 15 and 30min, respectively, compared to CON, but was lower by 1.60 (0.6, 2.6) mM and 1.5 (0.5, 2.5) mM at 90 and 120min, respectively (all p < 0.01). The additive effect of exercise and protein ingestion resulted in a fold-increase of 1.67 (1.35, 2.00; p < 0.05) in postprandial glucagon compared to CON. In type 2 diabetics, prior aerobic exercise altered the humoral response to co-ingestion of whey protein with a carbohydrate load, but neither protein ingestion alone nor when preceded by prior exercise attenuated postprandial glycemia.

A small dose of whey protein co-ingested with mixed-macronutrient breakfast and lunch meals improves postprandial glycemia and suppresses appetite in men with type 2 diabetes: a randomized controlled trial

Large doses of whey protein consumed as a preload before single high-glycemic load meals has been shown to improve postprandial glycemia in type 2 diabetes. It is unclear if this effect remains with smaller doses of whey co-ingested at consecutive mixed-macronutrient meals. Moreover, whether hydrolyzed whey offers further benefit under these conditions is unclear. The aim of this study was to investigate postprandial glycemic and appetite responses after small doses of intact and hydrolyzed whey protein co-ingested with mixed-nutrient breakfast and lunch meals in men with type 2 diabetes. In a randomized, single-blind crossover design, 11 men with type 2 diabetes [mean±SD age: 54.9±2.3 y; glycated hemoglobin: 6.8%±0.3% (51.3±3.4 mmol/mol)] attended the laboratory on 3 mornings and consumed 1) intact whey protein (15 g), 2) hydrolyzed whey protein (15 g), or 3) placebo (control) immediately before mixed-macronutrient breakfast and lunch meals, separated by 3 h. Blood samples were collected periodically and were processed for insulin, intact glucagon-like peptide 1 (GLP-1), gastric inhibitory polypeptide (GIP), leptin, peptide tyrosine tyrosine (PYY3-36), and amino acid concentrations. Interstitial glucose was measured during and for 24 h after each trial. Subjective appetite was assessed with the use of visual analog scales. Total postprandial glycemia area under the curve was reduced by 13%±3% after breakfast following the intact whey protein when compared with control (P<0.05). Hydrolyzed whey attenuated early glucose after breakfast when compared with control (P<0.05). Glycemia was improved postlunch after the intact whey protein only when compared with control (P<0.05). Greater satiety was observed after the intact whey protein only after both meals when compared with control (P<0.05). Insulin concentrations increased after both the intact and hydrolyzed whey protein, showing strong positive correlations with increases in valine and isoleucine (P<0.05). Incretin and appetite regulatory hormone responses were similar across trials (P>0.05). The consumption of a small 15-g dose of intact whey protein immediately before consecutive mixed-macronutrient meals improves postprandial glycemia, stimulates insulin release, and increases satiety in men with type 2 diabetes. This trial was registered at www.clinicialtrials.gov as NCT02903199.

Diabetes medication pharmacology

Diabetes medication pharmacology

Advice to walk after meals is more effective for lowering postprandial glycaemia in type 2 diabetes mellitus than advice that does not specify timing: a randomised crossover study

Regular physical activity is a cornerstone of diabetes management. We conducted a study to evaluate whether specifying the timing of walking in relation to meals enhances the benefits conferred by current physical activity guidelines. A total of 41 adults with type 2 diabetes mellitus (mean ± SD age 60 ± 9.9years; mean diabetes duration 10years) participated in this randomised, crossover study. Randomisation was by a computer-generated protocol. For periods of 2weeks, advice to walk 30min each day was compared with advice to walk for 10min after each main meal. Both sets of advice met current physical activity guidelines for people with type 2 diabetes mellitus. Physical activity was measured by accelerometry over the full intervention, and glycaemia was measured using continuous glucose monitoring in 5min intervals over 7days. The primary outcome of postprandial glycaemia was assessed during the 3h after a meal by the incremental area under the blood glucose curve (iAUC). The iAUC was significantly lower when participants walked after meals compared with on a single daily occasion (ratio of geometric means 0.88, 95% CI 0.78, 0.99). The improvement was particularly striking after the evening meal (0.78, 95% CI 0.67, 0.91) when the most carbohydrate was consumed and sedentary behaviours were highest. One participant died during the 30day washout period between interventions, but participation in this study was not judged to contribute to this unfortunate event. The benefits relating to physical activity following meals suggest that current guidelines should be amended to specify post-meal activity, particularly when meals contain a substantial amount of carbohydrate. ACTRN12613000832774 FUNDING: : This study was supported by grants from the University of Otago and the New Zealand Artificial Limb Service. Glycated albumin reagents were provided by Asahi Kasei.

A Protein Preload Enhances the Glucose-Lowering Efficacy of Vildagliptin in Type 2 Diabetes.

Nutrient "preloads" given before meals can attenuate postprandial glycemic excursions, at least partly by slowing gastric emptying and stimulating secretion of the incretins (i.e., glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]). This study was designed to evaluate whether a protein preload could improve the efficacy of the dipeptidyl peptidase-4 (DPP-4) inhibitor vildagliptin to increase incretin concentrations, slow gastric emptying, and lower postprandial glycemia in type 2 diabetes. Twenty-two patients with type 2 diabetes treated with metformin were studied on four occasions, receiving either 50 mg vildagliptin (VILD) or placebo (PLBO) on both the evening before and the morning of each study day. The latter dose was followed after 60 min by a preload drink containing either 25 g whey protein (WHEY) or control flavoring (CTRL), and after another 30 min by a (13)C-octanoate-labeled mashed potato meal. Plasma glucose and hormones, and gastric emptying, were evaluated. Compared with PLBO/CTRL, PLBO/WHEY reduced postprandial peak glycemia, increased plasma insulin, glucagon, and incretin hormones (total and intact), and slowed gastric emptying, whereas VILD/CTRL reduced both the peak and area under the curve for glucose, increased plasma intact incretins, and slowed gastric emptying but suppressed plasma glucagon and total incretins (P < 0.05 each). Compared with both PLBO/WHEY and VILD/CTRL, VILD/WHEY was associated with higher plasma intact GLP-1 and GIP, slower gastric emptying, and lower postprandial glycemia (P < 0.05 each). In metformin-treated type 2 diabetes, a protein preload has the capacity to enhance the efficacy of vildagliptin to slow gastric emptying, increase plasma intact incretins, and reduce postprandial glycemia.

Glycemic effects and safety of L-Glutamine supplementation with or without sitagliptin in type 2 diabetes patients-a randomized study.

Background and AimsL-glutamine is an efficacious glucagon-like peptide (GLP)-1 secretagogue in vitro. When administered with a meal, glutamine increases GLP-1 and insulin excursions and reduces postprandial glycaemia in type 2 diabetes patients. The aim of the study was to assess the efficacy and safety of daily glutamine supplementation with or without the dipeptidyl peptidase (DPP)-4 inhibitor sitagliptin in well-controlled type 2 diabetes patients.MethodsType 2 diabetes patients treated with metformin (n = 13, 9 men) with baseline glycated hemoglobin (HbA1c) 7.1±0.3% (54±4 mmol/mol) received glutamine (15 g bd)+ sitagliptin (100 mg/d) or glutamine (15 g bd) + placebo for 4 weeks in a randomized crossover study.ResultsHbA1c (P = 0.007) and fructosamine (P = 0.02) decreased modestly, without significant time-treatment interactions (both P = 0.4). Blood urea increased (P<0.001) without a significant time-treatment interaction (P = 0.8), but creatinine and estimated glomerular filtration rate (eGFR) were unchanged (P≥0.5). Red blood cells, hemoglobin, hematocrit, and albumin modestly decreased (P≤0.02), without significant time-treatment interactions (P≥0.4). Body weight and plasma electrolytes remained unchanged (P≥0.2).ConclusionsDaily oral supplementation of glutamine with or without sitagliptin for 4 weeks decreased glycaemia in well-controlled type 2 diabetes patients, but was also associated with mild plasma volume expansion.Trial RegistrationClincalTrials.gov NCT00673894

Incretin, insulinotropic and glucose-lowering effects of whey protein pre-load in type 2 diabetes: a randomised clinical trial.

Since protein ingestion is known to stimulate the secretion of glucagon-like peptide-1 (GLP-1), we hypothesised that enhancing GLP-1 secretion to harness its insulinotropic/beta cell-stimulating activity with whey protein pre-load may have beneficial glucose-lowering effects in type 2 diabetes. In a randomised, open-label crossover clinical trial, we studied 15 individuals with well-controlled type 2 diabetes who were not taking any medications except for sulfonylurea or metformin. These participants consumed, on two separate days, 50 g whey in 250 ml water or placebo (250 ml water) followed by a standardised high-glycaemic-index breakfast in a hospital setting. Participants were randomised using a coin flip. The primary endpoints of the study were plasma concentrations of glucose, intact GLP-1 and insulin during the 30 min following meal ingestion. In each group, 15 patients were analysed. The results showed that over the whole 180 min post-meal period, glucose levels were reduced by 28% after whey pre-load with a uniform reduction during both early and late phases. Insulin and C-peptide responses were both significantly higher (by 105% and 43%, respectively) with whey pre-load. Notably, the early insulin response was 96% higher after whey. Similarly, both total GLP-1 (tGLP-1) and intact GLP-1 (iGLP-1) levels were significantly higher (by 141% and 298%, respectively) with whey pre-load. Dipeptidyl peptidase 4 plasma activity did not display any significant difference after breakfast between the groups. In summary, consumption of whey protein shortly before a high-glycaemic-index breakfast increased the early prandial and late insulin secretion, augmented tGLP-1 and iGLP-1 responses and reduced postprandial glycaemia in type 2 diabetic patients. Whey protein may therefore represent a novel approach for enhancing glucose-lowering strategies in type 2 diabetes. Trial registration ClinicalTrials.gov NCT01571622 Funding The Israeli Ministry of Health and Milk Council funded the research.

Safety and Efficacy of the Nonsystemic Chewable Complex Carbohydrate Dietary Supplement PAZ320 on Postprandial Glycemia When Added to Oral Agents or Insulin in Patients with Type 2 Diabetes Mellitus

Our primary objective was to evaluate the effect of the dietary supplement PAZ320 on postprandial glucose excursion. PAZ320 is derived from glucomannan and acts by blocking carbohydrate hydrolyzing enzymes and by binding to ingested polysaccharides. Endpoints included area under the curve during postprandial glucose excursion (gAUC) and adverse reactions. In an open-label, sequential dose-escalation, prospective study, we examined the efficacy and safety of PAZ320 in 24 subjects with type 2 diabetes treated with oral agents and/or insulin. Subjects consumed 75 g jasmine rice alone or with low-dose (8 g) or high-dose (16 g) PAZ320. A real-time blinded continuous glucose monitor (CGM) was used to assess 3-hour postprandial glycemia. We found that 45% of subjects responded to high-dose PAZ320 as evidenced by a decrease in gAUC of 40% compared to baseline in a dose-dependent manner. The effect of PAZ320 does not correlate with duration of diabetes and seems to work regardless of concurrent diabetes medications. The responders had higher postmeal glucose elevation at baseline, while the nonresponders showed no effect or paradoxic glucose response to PAZ320. There was no severe hypoglycemia, and the gastrointestinal side effects were mild. PAZ320 may be useful as an adjunct to decrease postprandial glycemia in type 2 diabetes, although patients should verify its effect on postprandial glucose due to a possible paradoxic response. Its safety profile is reassuring. Further study is required to determine its long-term effects on glycated hemoglobin (HbA1c) and to further define which subpopulation may respond to PAZ320.

Effects of a d-Xylose Preload With or Without Sitagliptin on Gastric Emptying, Glucagon-Like Peptide-1, and Postprandial Glycemia in Type 2 Diabetes

OBJECTIVEMacronutrient “preloads” can reduce postprandial glycemia by slowing gastric emptying and stimulating glucagon-like peptide-1 (GLP-1) secretion. An ideal preload would entail minimal additional energy intake and might be optimized by concurrent inhibition of dipeptidyl peptidase-4 (DPP-4). We evaluated the effects of a low-energy d-xylose preload, with or without sitagliptin, on gastric emptying, plasma intact GLP-1 concentrations, and postprandial glycemia in type 2 diabetes.RESEARCH DESIGN AND METHODSTwelve type 2 diabetic patients were studied on four occasions each. After 100 mg sitagliptin (S) or placebo (P) and an overnight fast, patients consumed a preload drink containing either 50 g d-xylose (X) or 80 mg sucralose (control [C]), followed after 40 min by a mashed potato meal labeled with 13C-octanoate. Blood was sampled at intervals. Gastric emptying was determined.RESULTSBoth peak blood glucose and the amplitude of glycemic excursion were lower after PX and SC than PC (P < 0.01 for each) and were lowest after SX (P < 0.05 for each), while overall blood glucose was lower after SX than PC (P < 0.05). The postprandial insulin-to-glucose ratio was attenuated (P < 0.05) and gastric emptying was slower (P < 0.01) after d-xylose, without any effect of sitagliptin. Plasma GLP-1 concentrations were higher after d-xylose than control only before the meal (P < 0.05) but were sustained postprandially when combined with sitagliptin (P < 0.05).CONCLUSIONSIn type 2 diabetes, acute administration of a d-xylose preload reduces postprandial glycemia and enhances the effect of a DPP-4 inhibitor.

Off-line control of the postprandial glycemia in type 1 diabetes patients by a fuzzy logic decision support

The target of this paper is to describe the use of fuzzy techniques in the development of a decision support system that allows the optimization of postprandial glycemia in type 1 diabetes patients taking into account the kind of meal taken by patients, the preprandial glycemia and the insulin resistance (the response of the body to insulin dose injection therapy). The decision support system can, in many cases, provide patients with the correct number of rapid insulin units that must be assumed to assure an optimal glycemic profile, keeping the blood glucose level close to the homeostatic condition, several hours after the meal.

Glutamine Reduces Postprandial Glycemia and Augments the Glucagon-Like Peptide-1 Response in Type 2 Diabetes Patients

Impaired glucagon-like peptide (GLP-1) secretion or response may contribute to ineffective insulin release in type 2 diabetes. The conditionally essential amino acid glutamine stimulates GLP-1 secretion in vitro and in vivo. In a randomized, crossover study, we evaluated the effect of oral glutamine, with or without sitagliptin (SIT), on postprandial glycemia and GLP-1 concentration in 15 type 2 diabetes patients (glycated hemoglobin 6.5 ± 0.6%). Participants ingested a low-fat meal (5% fat) after receiving either water (control), 30 g L-glutamine (Gln-30), 15 g L-glutamine (Gln-15), 100 mg SIT, or 100 mg SIT and 15 g L-glutamine (SIT+Gln-15). Studies were conducted 1–2 wk apart. Blood was collected at baseline and postprandially for 180 min for measurement of circulating glucose, insulin, C-peptide, glucagon, and total and active GLP-1. Gln-30 and SIT+Gln-15 reduced the early (t = 0–60 min) postprandial glycemic response compared with control. All Gln treatments enhanced the postprandial insulin response from t = 60–180 min but had no effect on the C-peptide response compared with control. The postprandial glucagon concentration was increased by Gln-30 and Gln-15 compared with control, but the insulin:glucagon ratio was not affected by any treatment. In contrast to Gln-30, which tended to increase the total GLP-1 AUC, SIT tended to decrease the total GLP-1 AUC relative to control (bothP= 0.03). Gln-30 and SIT increased the active GLP-1 AUC compared with control (P= 0.008 andP= 0.01, respectively). In summary, Gln-30 decreased the early postprandial glucose response, enhanced late postprandial insulinemia, and augmented postprandial active GLP-1 responses compared with control. These findings suggest that glutamine may be a novel agent for stimulating GLP-1 concentration and limiting postprandial glycemia in type 2 diabetes.

Effects of a Protein Preload on Gastric Emptying, Glycemia, and Gut Hormones After a Carbohydrate Meal in Diet-Controlled Type 2 Diabetes

OBJECTIVEWe evaluated whether a whey preload could slow gastric emptying, stimulate incretin hormones, and attenuate postprandial glycemia in type 2 diabetes.RESEARCH DESIGN AND METHODSEight type 2 diabetic patients ingested 350 ml beef soup 30 min before a potato meal; 55 g whey was added to either the soup (whey preload) or potato (whey in meal) or no whey was given.RESULTSGastric emptying was slowest after the whey preload (P < 0.0005). The incremental area under the blood glucose curve was less after the whey preload and whey in meal than after no whey (P < 0.005). Plasma glucose-dependent insulinotropic polypeptide, insulin, and cholecystokinin concentrations were higher on both whey days than after no whey, whereas glucagon-like peptide 1 was greatest after the whey preload (P < 0.05).CONCLUSIONSWhey protein consumed before a carbohydrate meal can stimulate insulin and incretin hormone secretion and slow gastric emptying, leading to marked reduction in postprandial glycemia in type 2 diabetes.

Effect of exenatide on gastric emptying and relationship to postprandial glycemia in type 2 diabetes

Objectives To evaluate the effect of exenatide on gastric emptying (GE) in type 2 diabetes using scintigraphy. Methods Seventeen subjects with type 2 diabetes participated in a randomized, single-blind, 3-period, crossover study. In each 5-day period, 5 or 10 µg exenatide or placebo was administered subcutaneously BID. Oral antidiabetic treatments were continued. The presence of cardiac autonomic neuropathy was assessed during screening. On day 5, after the morning dose, subjects consumed a 450-kcal breakfast containing 99mTc-labeled eggs and 111In-labeled water, and GE was measured by scintigraphy. Plasma glucose and insulin, perceptions of appetite, and plasma exenatide were also quantified. Results Exenatide slowed GE of both solid and liquid meal components [solid ( T 50(90% confidence interval [CI]); placebo, 60(50–70) min; 5 µg exenatide, 111(94–132) min; 10 µg exenatide, 169(143–201) min; both P < 0.01); liquid ( T 50(90% CI), placebo, 34(25–46) min; 5 µg exenatide, 87(65–117) min; 10 µg exenatide, 114(85–154) min; both P < 0.01)]. GE was not different between subjects with cardiac autonomic neuropathy ( n = 7), compared with those without ( n = 10) ( P ≥ 0.68). Exenatide reduced postprandial glucose (area under the curve [AUC (0–6 h)]) by 69–76% and peak insulin ( C max) by 84–86% compared with placebo. There was an inverse relationship between the postprandial rise in glucose (AUC (0–3 h)) and GE (solid T 50, r = − 0.49, P < 0.001). Conclusions Exenatide slows GE substantially in type 2 diabetes, which could be an important mechanism contributing to the beneficial effect of exenatide on postprandial glycemia.