Effect of Partially Depolymerized Guar Gum on Acute Metabolic Variables in Patients with Non-insulin-dependent Diabetes

Fourteen patients with non-insulin-dependent diabetes (NIDDM) attended the study centre on 4 mornings separated by at least 3 days, to receive in random order 75 g carbohydrate breakfast meals of control or guar breads with jam and butter. Guar gum flours of low, medium, and high molecular weight (MW) were incorporated into wheat bread rolls to provide 7.6 g guar per meal. Venous blood samples were taken via an indwelling cannula in a forearm vein at fasting and at eight postprandial times and then analysed for blood glucose, plasma insulin, C-peptide, and gastric inhibitory polypeptide (GIP). Guar gum bread significantly reduced the postprandial rise in blood glucose, plasma insulin, and, except for bread containing low MW guar gum, plasma GIP levels compared to the control. Thus, the partial depolymerization of guar gum does not diminish its physiological activity. No reductions in postprandial plasma C-peptide levels were seen after any of the guar bread meals. This suggests that guar gum attenuates the insulin concentration in peripheral venous blood in patients with NIDDM by increasing the hepatic extraction of insulin.     

Rye products in the diabetic diet. Postprandial glucose and hormonal responses in non-insulin-dependent diabetic patients as compared to starch availability in vitro and experiments in rats

Rye flakes, rye bread and white wheat bread were given as suspensions to rats and in standardized breakfast meals to non-insulin-dependent diabetics. In both cases the postprandial glucose response was lower after rye bread than after wheat bread. A larger amount of starch remained in the stomach of the rats 15 min after ingesting rye bread compared to wheat bread, indicating that delayed gastric emptying may be one factor explaining the lower response after rye bread. Although the incremental postprandial glucose areas after rye flakes and wheat bread were similar, the rate of decrease of the glucose curve was slower after flaked rye. This would point to a prolonged absorption of some starch in the rye flakes, also indicated by higher late immunoreactive insulin (IRI) values after that product. In the rats the content of starch in the stomachs 15 min after feeding was higher after rye flakes compared to wheat bread. In vitro incubations with alpha-amylase showed lower availability of the starch in rye flakes than in the breads, indicating that several factors may contribute to the differential postprandial glucose response after the wheat and rye products. The levels of insulin, C-peptide, gastric inhibitory polypeptide (GIP), glucagon, somatostatin, triglyceride and glycerol were followed after the breakfast meals. No pronounced differences of these parameters were seen. However, wheat bread gave significantly higher glucagon and GIP responses than did rye flakes. In conclusion, the absorption pattern and metabolic response after rye bread seems preferable to that after wheat bread. The flaked rye on the other hand was not effective in reducing postprandial glycaemia despite a lower availability of starch in vitro.     

The effect of unabsorbable carbohydrate on gut hormones

Summary Five healthy volunteers and 6 diabetics were given a mixed test meal on two occasions — once with and once without 10 g guar flour. Addition of guar caused a 47% decrease in maximum post-prandial GIP levels, a 48% decrease in blood glucose and a 48% decrease in plasma insulin in normal subjects. In diabetics, addition of guar caused a 30% reduction in maximum post-prandial GIP and 58% decrease in blood glucose. Four normal and 6 diabetic subjects were given a predominantly carbohydrate meal, again with and without 10 g guar. Addition of guar caused a 78% decrease in blood glucose and a 59% decrease in plasma insulin in normal subjects. In diabetics addition of guar caused a 71% decrease in maximum post-prandial plasma GIP and a 68% decrease in blood glucose. Lowering of post-prandial blood glucose, plasma insulin and GIP levels by guar was statistically significant in every case. Addition of guar to the predominantly carbohydrate meal caused a decrease in total plasma GLI in both normal and diabetic subjects but reached statistical significance only in the normal subjects. There was a highly significant correlation (r=0.83; p<0.0005) between peak post-prandial insulin levels in normal subjects and the corresponding plasma GIP concentration. The reduction in GIP or GLI secretion may, therefore, be partly responsible for the smaller rise in plasma insulin observed in normal volunteers when guar is added to meals.     

Effect of high protein and fat diet on postprandial blood glucose levels in children and adolescents with type 1 diabetes in Cairo,Egypt

Background and aimsTo determine the effect of high protein and high fat meals on post prandial glycemia in patients with type 1 diabetes.MethodsThis study included 51 children and adolescents with type 1 diabetes who were following up at Diabetes, Endocrine and Metabolism Pediatric Unit (DEMPU), Abo Elrish Children’s hospital, Cairo University.Post prandial blood glucose levels were recorded and compared following three breakfast meals with varying protein and fat content (standard carbohydrate meal, high fat meal, and high protein meal) over a period of 5 hours on 3 consecutive days.ResultsHigh protein meal resulted in hyperglycemia with the peak level at 3.5 hours and continued for 5 hours post prandial while high fat meal caused early hyperglycemia reached the peak at 2 hours then declined towards 5 hours.Comparison of the three different breakfast meals revealed statistically significant difference regarding the postprandial glycemia at 30, 60, 90,120, 180, 210, 240, 270, 300 min.ConclusionMeals high in protein caused sustained increase in postprandial glucose levels over a period of 5 h. However, high fat meals caused early postprandial hyperglycemia. Protein and fat content of meals affect the timing and values of the peak blood glucose as well as the duration of postprandial hyperglycemia. Therefore, fat/protein unit should be taken in consideration while calculating the bolus insulin dose and anticipating the postprandial glucose response.     

Effects of meal size and composition on incretin, α-cell, and β-cell responses

The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate postprandial insulin release from the β-cells. We investigated the effects of 3 standardized meals with different caloric and nutritional content in terms of postprandial glucose, insulin, glucagon, and incretin responses. In a randomized crossover study, 18 subjects with type 2 diabetes mellitus and 6 healthy volunteers underwent three 4-hour meal tolerance tests (small carbohydrate [CH]-rich meal, large CH-rich meal, and fat-rich meal). Non-model-based and model-based estimates of β-cell function and incremental areas under the curve of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP were calculated. Mixed models and Friedman tests were used to test for differences in meal responses. The large CH-rich meal and fat-rich meal resulted in a slightly larger insulin response as compared with the small CH-rich meal and led to a slightly shorter period of hyperglycemia, but only in healthy subjects. Model-based insulin secretion estimates did not show pronounced differences between meals. Both in healthy individuals and in those with diabetes, more CH resulted in higher GLP-1 release. In contrast with the other meals, GIP release was still rising 2 hours after the fat-rich meal. The initial glucagon response was stimulated by the large CH-rich meal, whereas the fat-rich meal induced a late glucagon response. Fat preferentially stimulates GIP secretion, whereas CH stimulates GLP-1 secretion. Differences in meal size and composition led to differences in insulin and incretin responses but not to differences in postprandial glucose levels of the well-controlled patients with diabetes.     

The effects of carbohydrate-enriched meals on glucose turnover and metabolic clearance rates of glucose in Type 2 diabetic patients

Summary The addition of fructose to natural meals elicits lower serum glucose and immunoreactive insulin responses when compared with that of sucrose and starch meals. Differences in rates of splanchnic glucose appearance and peripheral glucose disposal may be partly responsible. To evaluate the role of both parameters after different carbohydrate-enriched meals, we measured the arterialized venous blood glucose, immunoreactive insulin and gastric inhibitory polypeptide concentrations in seven Type 2 diabetic patients after ingestion of isocaloric test meals. Measurements were made in a random manner on three separate occasions. Fructose, sucrose, and bread supplementation constituted 68% of the total carbohydrate content of each meal. Rates of total glucose appearance, glucose utilization and metabolic clearance rates of glucose were determined by the D³-H-3glucose prime-continuous infusion technique. The mean fasting glucose levels were similar in the three groups. Mean peak glucose concentrations and integrated incremental areas were significantly lower (p < 0.02) after the fructose-enriched meals compared with that of either sucrose or bread. The basal arterialized venous blood glucose levels were similar in all three groups. The mean incremental integrated arterialized venous blood glucose area was significantly lower in the fructose group when compared with the sucrose (p < 0.05) and bread (p < 0.02) groups. The mean fasting gastric inhibitory polypeptide levels were similar in the three groups. However, the mean incremental integrated gastric inhibitory polypeptide areas were significantly lower in the fructose group compared with the sucrose and bread groups (p < 0.01 and p < 0.05 respectively). Basal hepatic glucose outputs were not significantly different in the three groups. After each test meal ingestion, the rate of total glucose appearance was lowest for the fructose group, intermediate for the bread group and highest for the sucrose group. However, the metabolic clearance rate did not change from the baseline despite variable arterialized venous blood glucose responses after each test meal. We conclude that the differences in glycaemic responses after carbohydrate-enriched meals cannot be ascribed solely to differences in peripheral glucose disposal in Type 2 diabetic patients. Rather, the rates of total splanchnic glucose output appear to determine the ultimate glycaemic responses after different carbohydrate-enriched meals in Type 2 diabetic patients.     

Development of a Smartphone Application to Capture Carbohydrate,Lipid, and Protein Contents of Daily Food: Need for Integration in Artificial Pancreas for Patients With Type 1 Diabetes?

Background:Meal lipids (LIP) and proteins (PRO) may influence the effect of insulin doses based on carbohydrate (CHO) counting in patients with type 1 diabetes (T1D). We developed a smartphone application for CHO, LIP, and PRO counting in daily food and assessed its usability in real-life conditions and potential usefulness.Methods:Ten T1D patients used the android application for 1 week to collect their food intakes. Data included meal composition, premeal and 2-hour postmeal blood glucose, corrections for hypo- or hyperglycemia after meals, and time for entering meals in the application. Meal insulin doses were based on patients’ CHO counting (application in blinded mode). Linear mixed models were used to assess the statistical differences.Results:In all, 187 meals were analyzed. Average computed CHO amount was 74.37 ± 31.78 grams; LIP amount: 20.26 ± 14.28 grams and PRO amount: 25.68 ± 16.68 grams. Average CHO, LIP, and PRO contents were significantly different between breakfast and lunch/dinner. The average time for meal entry in the application moved from 3-4 minutes to 2.5 minutes during the week. No significant impact of LIP and PRO was found on available blood glucose values.Conclusion:Our study shows CHO, LIP, and PRO intakes can be easily captured by an application on smartphone for meal entry used by T1D patients. Although LIP and PRO meal contents did not influence glucose levels when insulin doses were based on CHO in this pilot study, this application could be used for further investigation of this topic, including in closed-loop conditions.     

Beyond fasting plasma glucose: The association between coronary heart disease risk and postprandial glucose,postprandial insulin and insulin resistance in healthy,nondiabetic adults

Objective

Prediabetes is defined by elevations of plasma glucose concentration, and is aimed at identifying individuals at increased risk of type 2 diabetes and coronary heart disease (CHD). However, since these individuals are also insulin resistant and hyperinsulinemic, we evaluated the association between several facets of carbohydrate metabolism and CHD risk profile in apparently healthy, nondiabetic individuals.

Methods

Plasma glucose and insulin concentrations were measured before and at hourly intervals for eight hours after two test meals in 281 nondiabetic individuals. Insulin action was quantified by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test. CHD risk was assessed by measurements of blood pressure and fasting lipoprotein profile.

Results

For purposes of analysis, the population was divided into tertiles, and the results demonstrated that the greater the 1) fasting plasma glucose (FPG) concentration, 2) incremental plasma insulin response to meals, and 3) SSPG concentration, the more adverse the CHD risk profile (p < 0.05). In contrast, the CHD risk profile did not significantly worsen with increases in the incremental plasma glucose response to meals.

Conclusions

In nondiabetic individuals, higher FPG concentrations, accentuated daylong incremental insulin responses to meals, and greater degrees of insulin resistance are each associated with worse CHD risk profile (higher blood pressures, higher triglycerides, and lower high density lipoprotein cholesterol concentrations). Interventional efforts aimed at decreasing CHD in such individuals should take these abnormalities into consideration.     

Effect of pretreatment with a high fat diet on the gastric inhibitory polypeptide and insulin responses to oral triolein and glucose in rats

Summary Male Wistar rats were pretreated with 3 ml triolein orally for 4 days in addition to their normal diet. A similar control group were allowed free access to normal laboratory food. When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide (GIP) and triglyceride levels were significantly higher in the fat pretreated group. Inhibition of fat-stimulated GIP release by exogenous insulin was demonstrated in the untreated control group (plasma GIP: 663±49 versus 853±92 ng/l, mean ± SEM p < 0.025), but pretreatment with an oral fat load abolished this effect (plasma GIP: 1008±95 versus 1116±100 ng/l, p NS). Plasma glucose levels were significantly higher in fat pretreated rats given oral fat and intraperitoneal insulin compared with untreated controls (plasma glucose nadir 2.6±0.48 versus 1.6±0.15 mmol/l, p < 0.05). Fat-pretreated rats showed significantly higher insulin and glucose levels compared with the untreated rats when given oral glucose (plasma insulin: 6.2±1.2 versus 2.5±0.59 n.g/l, p < 0.01; plasma glucose: 10.2±0.39 versus 8.9±0.41 mmol/l, p < 0.025). Pretreatment of rats on a high fat diet causes (1) increased GIP secretion in response to an oral fat load, (2) abolition of the feed-back inhibition of exogenous insulin on fat-stimulated GIP release, and (3) some degree of insulin resistance.     

Clinical Update on Optimal Prandial Insulin Dosing Using a Refined Run-to-Run Control Algorithm

Background

This article provides a clinical update using a novel run-to-run algorithm to optimize prandial insulin dosing based on sparse glucose measurements from the previous day''s meals. The objective was to use a refined run-to-run algorithm to calculate prandial insulin-to-carbohydrate ratios (I:CHO) for meals of variable carbohydrate content in subjects with type 1 diabetes (T1DM).

Method

The open-labeled, nonrandomized study took place over a 6-week period in a nonprofit research center. Nine subjects with T1DM using continuous subcutaneous insulin infusion participated. Basal insulin rates were optimized using continuous glucose monitoring, with a target fasting blood glucose of 90 mg/dl. Subjects monitored blood glucose concentration at the beginning of the meal and at 60 and 120 minutes after the start of the meal. They were instructed to start meals with blood glucose levels between 70 and 130 mg/dl. Subjects were contacted daily to collect data for the previous 24-hour period and to give them the physicianapproved, algorithm-derived I:CHO ratios for the next 24 hours. Subjects calculated the amount of the insulin bolus for each meal based on the corresponding I:CHO and their estimate of the meal''s carbohydrate content. One- and 2-hour postprandial glucose concentrations served as the main outcome measures.

Results

The mean 1-hour postprandial blood glucose level was 104 ± 19 mg/dl. The 2-hour postprandial levels (96.5 ± 18 mg/dl) approached the preprandial levels (90.1 ± 13 mg/dl).

Conclusions

Run-to-run algorithms are able to improve postprandial blood glucose levels in subjects with T1DM.     

Impact of high‐fat /low‐carbohydrate,high‐, low‐glycaemic index or low‐caloric meals on glucose regulation during aerobic exercise in Type 2 diabetes

Aims A decrement in blood glucose (BG) may be observed in patients with Type 2 diabetes (T2DM) when exercise is performed after a meal, in contrast to fasting. We determined the impact of different pre‐exercise meal macronutrient compositions with modulation of the glycaemic index (GI) on glucose regulation during exercise in patients with T2DM. Methods Using a randomized, single‐blind crossover design, 10 sedentary men performed five exercise sessions, once after an overnight fast, and also after each of four test meals, consisting of a high‐fat/low‐carbohydrate meal, a high‐GI meal, a low‐GI meal, and a low‐calorie meal. Results Pre‐exercise BG and insulin levels were comparable for all four meals. Exercise decreased BG and insulin levels during all meal conditions (all P < 0.001) compared with the fasting state in which BG levels did not change. The magnitude of BG and insulin decrements was similar after consuming the low‐calorie, the high‐GI and the high‐fat/low‐carbohydrate meals, whereas the low‐GI meal induced the lowest BG fall. Adrenaline response was higher after consumption of the high‐, the low‐GI and the low‐caloric meals compared with the high‐fat/low‐carbohydrate meal and with the fasting state (P < 0.05). Conclusions This study underlines the beneficial effect of low‐GI foods and the differential impact of pre‐exercise meal macronutrient composition on BG decrease. This may protect against exercise‐induced hypoglycaemia, and reiterates the safety of exercising while fasting in T2DM patients.     

Effects of late evening snack on diurnal plasma glucose profile in patients with chronic viral liver disease

Aim: Glycemic control is important to improve the prognosis in cirrhotic patients with complications from diabetes. A late evening snack (LES) has been recommended for cirrhotic patients. We investigated the effects of LES on diurnal plasma glucose levels. Methods: Subjects comprised 47 patients with chronic viral liver disease (chronic hepatitis, n = 11; cirrhosis, n = 36) treated in the Department of Gastroenterology & Hepatology, Dokkyo Medical University Koshigaya Hospital. Diurnal variations in plasma glucose were first investigated with three meals/day, in accordance with the European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines. Starting the next day, patients were given four meals including a LES, without changing meal content. Diurnal variations in plasma glucose were examined on day 7, and urine C‐peptide immunoreactivity (CPR), and homeostasis model assessment insulin resistance (HOMA‐IR) were investigated. Results: With a LES, plasma glucose levels in patients with chronic hepatitis were significantly lower 2 hours before and 2 hours after dinner. In cirrhotic patients, significant decreases in plasma glucose levels were seen 2 hours after breakfast, before lunch, and before dinner. Significant decreases were noted in average plasma glucose levels and highest plasma glucose levels with four meals including a LES in patients with liver cirrhosis. This decrease was greater when maximum plasma glucose levels were higher on the three‐meal regimen. Conclusions: Improvements in plasma glucose levels were seen with four meals per day, including a LES, in viral chronic liver disease, particularly cirrhosis.     

The influence of the colon on postprandial glucagon-like peptide 1 (7-36) amide concentration in man

Glucagon-like peptide (7-36) amide (GLP-1) is an incretin hormone of the enteroinsular axis released rapidly after meals despite the fact that GLP-1 secreting cells (L-cells) occur predominantly in the distal gut. The importance of these colonic L-cells for postprandial GLP-1 was determined in healthy control subjects and in ileostomy patients with minimal small bowel resection (<5 cm). Subjects were fed a high complex carbohydrate test meal (15.3 g starch) followed by two carbohydrate-free, high fat test meals (25 g and 48.7 g fat respectively). Circulating levels of glucose, insulin, glucagon, glucose insulinotrophic peptide (GIP) and GLP-1 were measured over a 9-h postprandial period. For both subject groups the complex carbohydrate test meal failed to elicit a rise in either GIP or GLP-1. However, both hormones were elevated after the fat load although the GLP-1 concentration was significantly reduced in the ileostomist group when compared with controls (P=0.02). Associated with this reduction in circulating GLP-1 was an elevation in glucagon concentration (P=0.012) and a secondary rise in the plasma glucose concentration (P=0.006). These results suggest that the loss of colonic endocrine tissue is an important determinant in the postprandial GLP-1 concentration. Ileostomists should not be assumed to have normal enteroinsular function as the colon appears to have an important role in postprandial metabolism.     

Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy

Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. Fasting serum glucose concentrations fell an average of 167 mg/dl (P less than 0.001), and there was a 67% reduction (P less than 0.001) in the postprandial glucose response. Mean hemoglobin A1c declined and paralleled the fall in serum glucose concentrations (9.2 +/- 0.5% to 5.9% +/- 0.3%; P less than 0.01). This improvement in glycemic control, however, was not associated with any appreciable change in GIP secretion. Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. Insulin administration did not alter these elevated GIP levels. These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion.     

Impaired incretin secretion and pancreatic dysfunction with older age and diabetes

Objective

To estimate the impact of aging and diabetes on insulin sensitivity, beta-cell function, adipocytokines, and incretin production.

Methods

Hyperglycemic clamps, arginine tests and meal tolerance tests were performed in 50 non-obese subjects to measure insulin sensitivity (IS) and insulin secretion as well as plasma levels of glucagon, GLP-1 and GIP. Patients with diabetes and healthy control subjects were divided into the following groups: middle-aged type 2 diabetes (MA-DM), aged Type 2 diabetes (A-DM) and middle-aged or aged subjects with normal glucose tolerance (MA-NGT or A-NGT).

Results

IS, as determined by the homeostasis model assessment, glucose infusion rate, and oral glucose insulin sensitivity, was reduced in the aged and DM groups compared with MA-NGT, but it was similar in the MA-DM and A-DM groups. Insulinogenic index, first and second phase insulin secretion and the disposition indices, but not insulin response to arginine, were reduced in the aged and DM groups. Postprandial glucagon production was higher in MA-DM compared to MA-NGT. Whereas the GLP-1 production was reduced in A-DM, no differences between groups were observed in GIP production.

Conclusions

In non-obese subjects, diabetes and aging impair insulin sensitivity. Insulin production is reduced by aging, and diabetes exacerbates this condition. Aging associated defects superimposed diabetic physiopathology, particularly regarding GLP-1 production. On the other hand, the glucose-independent secretion of insulin was preserved. Knowledge of the complex relationship between aging and diabetes could support the development of physiopathological and pharmacological based therapies.     

Postprandial plasma glucose,insulin, glucagon and triglyceride responses to a standard diet in normal subjects

Summary Postprandial plasma glucose, insulin and triglyceride responses were determined in 12 normal subjects (7 male and 5 female) fed a standard diet composed of typical American foods; the three meals were identical for each subject. A significant post-prandial rise in glucose and insulin was observed. They were closely related temporally in the early post-absorptive period. However, in the late post-absorptive phase insulin decline was generally slower than the glucose decline. A considerable difference in the glucose and insulin response was observed between males and females. Fasting plasma glucose and insulin concentrations were lower in the women. Following each meal the peak plasma glucose was lower in the women, but the difference was significant only following breakfast (p < 0.02). The area under the glucose curve following breakfast was also lower (p < 0.01) in the women. In the men the maximal postprandial glucose concentration and the postprandial glucose area remained stable throughout the day, but there was an increase in peak insulin concentration and insulin area after dinner. In contrast, in the women the maximal postprandial glucose concentration and the postprandial glucose area increased throughout the day, but the peak insulin concentration and insulin area did not change. Plasma triglycerides increased with breakfast and remained elevated throughout the day. Both fasting and postprandial mean triglycerides were higher in the men, but this did not reach statistical significance. The circulating pancreatic glucagon concentration, determined in 4 subjects, was unaffected by meals and remained stable throughout the day.     

Daily profile of plasma %CoQ10 level, a biomarker of oxidative stress, in patients with diabetes manifesting postprandial hyperglycaemia

Abstract The purpose of this study was to investigate the effect of regular meals on the daily profile of blood oxidative stress markers in type 2 diabetic patients with postprandial hyperglycaemia. %CoQ10, calculated as the ratio of ubiquinone-10 (oxidised form of coenzyme Q10) to ubiquinol-10 (reduced form), was used as a sensitive marker of oxidative stress. Blood samples were collected from patients before and 2 h after breakfast, lunch and supper, and at 10 p.m. Patients were selected for the study if their blood glucose levels were <7 mmol/l before breakfast and ≥11.1 mmol/l on at least one occasion after breakfast. %CoQ10 levels after breakfast and throughout the day were significantly higher than those before breakfast (p=0.006–0.04). In contrast to the wave-like changes in plasma glucose levels, %CoQ10 levels increased after breakfast and remained at high levels throughout the day. These results indicated that diabetic patients with postprandial hyperglycaemia were exposed to meal-induced periods of oxidative stress during the day. Postprandial hyperglycaemia therefore has the potential to increase the risk of atherosclerotic cardiovascular disease through induction of oxidative stress.     

Enteral supplementation with glutamine,fiber, and oligosaccharide modulates incretin and glucagon‐like peptide‐2 secretion

Aims/Introduction

A dietary supplementation product enriched with glutamine, dietary fiber and oligosaccharide (GFO) is widely applied for enteral nutrition support in Japan. The aim of the present study was to evaluate the effects of GFO ingestion on secretion of incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and glucagon-like peptide-2 (GLP-2).

Materials and Methods

We carried out a cross-over study involving 20 healthy Japanese volunteers. The participants received GFO or 17 g of glucose, the equivalent carbohydrate in GFO as the control. Plasma glucose, serum insulin, and plasma total GIP, total GLP-1 and total GLP-2 levels during GFO or glucose loading were determined.

Results

GFO loading produced significantly higher plasma GLP-1 levels at 30 min and 60 min, area under the curve-GLP-1 value, and area under the curve-GLP-2 value after administration compared with those by glucose loading. In contrast, plasma GIP levels at both 30 and 60 min, and area under the curve-GIP value after glucose loading were significantly higher than those after GFO loading.

Conclusions

These results show that GFO ingestion stimulates GLP-1 and GLP-2 secretion, and reduces GIP secretion compared with glucose ingestion. Therefore, GFO could have an intestinotrophic effect as well as an ameliorating effect on metabolic disorders through modification of release of gut hormones.     

Effect of co-ingestion of fat on the metabolic responses to slowly and rapidly absorbed carbohydrates

Summary The present study examined the acute effects of coingestion of fat (37.5 g) on the post-prandial metabolic responses to 75 g of carbohydrate which was either slowly absorbed (lentils) or rapidly absorbed (potatoes). Co-ingestion of fat resulted in a significant flattening of the post-prandial glucose curves, the effect being more pronounced for the rapidly absorbed potatoes. This was probably due to delayed gastric emptying. However, the post-prandial insulin responses to either carbohydrate were not significantly reduced by fat, suggesting that the insulin response to a given glucose concentration was potentiated in the presence of fat. The gastric inhibitory polypeptide (GIP) responses to both carbohydrates were greatly increased in the presence of fat. To investigate further the possible roles of GIP in the entero-insular axis, a 5-g bolus of glucose was injected intravenously 1 h after lentils ± fat. This was sufficient to raise the glucose levels above the threshold reported for GIP to potentiate insulin secretion. However, despite the large differences in circulating GIP levels, the insulin response to glucose was not affected by the presence of fat. These results suggest that (1) the rate of absorption of carbohydrate is a major determinant of post-prandial metabolic responses even in the presence of fat, (2) fat-stimulated GIP secretion does not potentiate glucose-induced insulin secretion, and (3) the potentiation of the insulin response to glucose when carbohydrate is co-ingested with fat is consistent with the well-documented insulin resistance associated with high fat diets.     

What is the effect of rosiglitazone treatment on insulin secretory function in insulin-resistant individuals? It depends on how you measure it

The goal of this study was to compare methods used to quantify the effect of rosiglitazone (RSG) on insulin secretory function, particularly estimates based on changes in fasting plasma glucose and insulin concentration vs daylong insulin responses to meals. To do this, we compared these measures of insulin secretion before and 3 months after RSG treatment in insulin-resistant individuals, subdivided into nondiabetic subjects (n = 29) and patients with type 2 diabetes mellitus (2DM) (n = 22). Insulin resistance was quantified by determining the steady-state plasma glucose concentration during the insulin suppression test and insulin secretory function by homeostasis model assessment of β-cell function (HOMA-β) and the total integrated daylong plasma insulin responses to mixed meals (insulin area under the curve). Baseline fasting and daylong plasma glucose concentrations were higher (P < .001) in patients with 2DM, associated with lower HOMA-β values (P < .001). However, neither fasting nor daylong insulin concentrations after mixed meals differed in the 2 groups. Insulin sensitivity improved (P < .001) after RSG administration, with decreases of 31% ± 23% and 21% ± 14% in steady-state plasma glucose concentration in nondiabetic and diabetic subjects, respectively. Although fasting and daylong plasma glucose and insulin concentrations fell (P < .001) in both groups of RSG-treated individuals, HOMA-β decreased in nondiabetic subjects and did not change in those with 2DM. In conclusion, RSG administration improved insulin sensitivity in both groups, associated with lower fasting and daylong glucose concentrations. Fasting and daylong insulin concentrations were also lower in both groups of RSG-treated subjects, but the values of HOMA-β indicated either a decrease (nondiabetics) or no change (diabetics) in insulin secretory function. These results suggest that measurements of HOMA-β may not provide a complete view of insulin secretory function, either when comparing diabetic with nondiabetic individuals or when assessing the response to RSG treatment in insulin-resistant individuals.