The effect of combination treatment with acarbose and glibenclamide on postprandial glucose and insulin profiles: additive blood glucose lowering effect and decreased hypoglycaemia

This study compared the effects of acarbose plus glibenclamide combination therapy with acarbose or glibenclamide treatment alone on postprandial blood glucose, serum insulin and C-peptide levels, and the tendency to develop hypoglycaemia. A total of 84 patients with Type 2 diabetes (fasting blood glucose: 120-180 mg/dl; postprandial blood glucose: 140-240 mg/dl) was included in this two-centre, double-blind, double-dummy, placebo-controlled study. Patients were randomised to one of 4 treatment groups: acarbose (100 mg); glibenclamide (3.5 mg); acarbose plus glibenclamide; or placebo. Treatment was administered before a standard breakfast, and fasting (07.30 h, 08.00 h) and postprandial (09.00, 10.00, 11.00, 12.00 h) blood glucose, serum insulin and C-peptide levels were determined. Acarbose plus glibenclamide treatment significantly reduced the mean increase in postprandial blood glucose levels (23.7+/-17.3 mg/dl) compared with either acarbose (58.4+/-31.6 mg/dl), glibenclamide (56.9+/-42.8 mg/dl) or placebo (101.6+/-49.2 mg/dl) (p<0.05 for all). Serum insulin levels (mean AUC(7.30-12 h)) observed with acarbose plus glibenclamide combination therapy were significantly lower than those observed with glibenclamide monotherapy (243.5+/-161.1 vs 383.4+/-215.8 hr x microU/ml; p=0.02), and comparable with the values seen with placebo (226.0+/-166.6 hr x microU/ml), suggesting that acarbose modifies the insulin secretion induced by glibenclamide. Glibenclamide monotherapy resulted in a significantly higher rate of decrease in blood glucose level than with acarbose plus glibenclamide (71.8+/-29.9 vs 46.2+/-18.0 mg/dl x h(-1); p=0.0003), and blood glucose levels at 11.00 h were also markedly lower with glibenclamide (84.4+/-29 mg/dl) than acarbose plus glibenclamide (102.0+/-41 mg/dl), suggesting a reduced tendency for hypoglycaemic episodes with acarbose plus glibenclamide than with glibenclamide alone. In all, 6 (29%) hypoglycaemic episodes occurred with glibenclamide, 2 (10%) with acarbose plus glibenclamide and none with acarbose. Acarbose plus glibenclamide combination therapy results in an additive glucose lowering effect and reduced risk for hypoglycaemia. Acarbose modifies the insulin secretion induced by glibenclamide, which explains the lower risk of hypoglycaemia compared with glibenclamide monotherapy.     

Structural differences between rye and wheat breads but not total fiber content may explain the lower postprandial insulin response to rye bread

BACKGROUND: Rye bread has a beneficial effect on the postprandial insulin response in healthy subjects. The role of rye fiber in insulin and glucose metabolism is not known. OBJECTIVE: The aim of the study was to determine the effect of the content of rye fiber in rye breads on postprandial insulin and glucose responses. DESIGN: Nineteen healthy postmenopausal women aged 61 +/- 1 y, with a body mass index (in kg/m(2)) of 26.0 +/- 0.6, and with normal glucose tolerance participated in the study. The test products were refined wheat bread (control), endosperm rye bread, traditional rye bread, and high-fiber rye bread; each bread provided 50 g available carbohydrate and was served with breakfast. Plasma glucose, insulin, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and serum C-peptide were measured in fasting and 8 postprandial blood samples. In vitro starch hydrolysis and the microscopic structure of the breads were also determined. RESULTS: Postprandial insulin, glucose-dependent insulinotropic polypeptide, and C-peptide responses to the rye breads were significantly lower than the response to the control; no significant differences in insulin and C-peptide responses to the rye breads were found. Glucose and glucagon-like peptide 1 responses to the rye breads were not significantly different from those to the control, except at 150 and 180 min. In vitro starch hydrolysis was slower in all rye breads than in the control, and the structure of continuous matrix and starch granules differed between the rye and control breads. CONCLUSION: Total fiber content does not explain the lower postprandial insulin response to rye bread than to wheat bread, but structural differences between rye and wheat breads might.     

A MUFA-rich diet improves posprandial glucose, lipid and GLP-1 responses in insulin-resistant subjects

OBJECTIVE: To study the effects of three weight-maintenance diets with different macronutrient composition on carbohydrate, lipid metabolism, insulin and incretin levels in insulin-resistant subjects. METHODS: A prospective study was performed in eleven (7 W, 4 M) offspring of obese and type 2 diabetes patients. Subjects had a BMI > 25 Kg/m2, waist circumference (men/women) > 102/88, HBA1c < 6.5% and were regarded as insulin-resistant after an OGTT (Matsuda ISIm <4). They were randomly divided into three groups and underwent three dietary periods each of 28 days in a crossover design: a) diet high in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrate (CHO). RESULTS: Body weight and resting energy expenditure did not changed during the three dietary periods. Fasting serum glucose concentrations fell during MUFA-rich and CHO-rich diets compared with high-SAT diets (5.02 +/- 0.1, 5.03 +/- 0.1, 5.50 +/- 0.2 mmol/L, respectively. Anova < 0.05). The MUFA-rich diet improved insulin sensitivity, as indicated by lower homeostasis model analysis-insulin resistance (HOMA-ir), compared with CHO-rich and high-SAT diets (2.32 +/- 0.3, 2.52 +/- 0.4, 2.72 +/- 0.4, respectively, Anova < 0.01). After a MUFA-rich and high-SAT breakfasts (443 kcal) the postprandial integrated area under curve (AUC) of glucose and insulin were lowered compared with isocaloric CHO-rich breakfast (7.8 +/- 1.3, 5.84 +/- 1.2, 11.9 +/- 2.7 mmol . 180 min/L, Anova < 0.05; and 1004 +/- 147, 1253 +/- 140, 2667 +/- 329 pmol . 180 min/L, Anova <0.01, respectively); while the integrated glucagon-like peptide-1 response increased with MUFA and SAT breakfasts compared with isocaloric CHO-rich meals (4.22 +/- 0.7, 4.34 +/- 1.1, 1.85 +/- 1.1, respectively, Anova < 0.05). Fasting and postprandial HDL cholesterol concentrations rose with MUFA-rich diets, and the AUCs of triacylglycerol fell with the CHO-rich diet. Similarly fasting proinsulin (PI) concentration fell, while stimulated ratio PI/I was not changed by MUFA-rich diet. CONCLUSIONS: Weight maintenance with a MUFA-rich diet improves HOMA-ir and fasting proinsulin levels in insulin-resistant subjects. Ingestion of a virgin olive oil-based breakfast decreased postprandial glucose and insulin concentrations, and increased HDL-C and GLP-1 concentrations as compared with CHO-rich diet.     

Caffeine ingestion before an oral glucose tolerance test impairs blood glucose management in men with type 2 diabetes

Caffeine ingestion negatively affects insulin sensitivity during an oral glucose tolerance test (OGTT) in lean and obese men, but this has not been studied in individuals with type 2 diabetes. We examined the effects of caffeine ingestion on insulin and glucose homeostasis in obese men with type 2 diabetes. Men (n = 12) with type 2 diabetes (age = 49 +/- 2 y, BMI = 32 +/- 1 kg/m(2)) underwent 2 trials, 1 wk apart, in a randomized, double-blind design. Each trial was conducted after withdrawal from caffeine, alcohol, exercise, and oral hypoglycemic agents for 48 h and an overnight fast. Subjects randomly ingested caffeine (5 mg/kg body weight) or placebo capsules and 1 h later began a 3 h 75 g OGTT. Caffeine increased (P < 0.05) serum insulin, proinsulin, and C-peptide concentrations during the OGTT relative to placebo. Insulin area under the curve was 25% greater (P < 0.05) after caffeine than after placebo ingestion. Despite this, blood glucose concentration was also increased (P < 0.01) in the caffeine trial. After caffeine ingestion, blood glucose remained elevated (P < 0.01) at 3 h postglucose load (8.9 +/- 0.7 mmol/L) compared with baseline (6.7 +/- 0.4 mmol/L). The insulin sensitivity index was lower (14%, P = 0.02) after caffeine than after placebo ingestion. Overall, despite elevated and prolonged proinsulin, C-peptide, and insulin responses after caffeine ingestion, blood glucose was also increased, suggesting an acute caffeine-induced impairment in blood glucose management in men with type 2 diabetes.     

Increased dietary protein modifies glucose and insulin homeostasis in adult women during weight loss

Amino acids interact with glucose metabolism both as carbon substrates and by recycling glucose carbon via alanine and glutamine; however, the effect of protein intake on glucose homeostasis during weight loss remains unknown. This study tests the hypothesis that a moderate increase in dietary protein with a corresponding reduction of carbohydrates (CHO) stabilizes fasting and postprandial blood glucose and insulin during weight loss. Adult women (n = 24; >15% above ideal body weight) were assigned to either a Protein Group [protein: 1.6 g/(kg. d); CHO <40% of energy] or CHO Group [protein: 0.8 g/(kg. d); CHO >55%]. Diets were equal in energy (7100 kJ/d) and fat (50 g/d). After 10 wk, the Protein Group lost 7.53 +/- 1.44 kg and the CHO Group lost 6.96 +/- 1.36 kg. Plasma amino acids, glucose and insulin were determined after a 12-h fast and 2 h after a 1.67 MJ test meal containing either 39 g CHO, 33 g protein and 13 g fat (Protein Group) or 57 g CHO, 12 g protein and 14 g fat (CHO Group). After 10 wk, subjects in the CHO Group had lower fasting (4.34 +/- 0.10 vs 4.89 +/- 0.11 mmol/L) and postprandial blood glucose (3.77 +/- 0.14 vs. 4.33 +/- 0.15 mmol/L) and an elevated insulin response to meals (207 +/- 21 vs. 75 +/- 18 pmol/L). This study demonstrates that consumption of a diet with increased protein and a reduced CHO/protein ratio stabilizes blood glucose during nonabsorptive periods and reduces the postprandial insulin response.     

Quercetin attenuates fasting and postprandial hyperglycemia in animal models of diabetes mellitus

The objective of this study was to investigate the hypoglycemic effects of quercetin (QE) in animal models of diabetes mellitus (DM). A starch solution (1 g/kg) with and without QE (100 mg/kg) or acarbose (40 mg/kg) was orally administered to streptozotocin (STZ)-induced diabetic rats after an overnight fast. Postprandial plasma glucose levels were measured and incremental areas under the response curve were calculated. To study the effects of chronic feeding of QE, five-week-old db/db mice were fed an AIN-93G diet, a diet containing QE at 0.08%, or a diet containing acarbose at 0.03% for 7 weeks after 1 week of adaptation. Plasma glucose and insulin, blood glycated hemoglobin, and maltase activity of the small intestine were measured. Oral administration of QE (100 mg/kg) or acarbose (40 mg/kg) to STZ-treated rats significantly decreased incremental plasma glucose levels 30-180 min after a single oral dose of starch and the area under the postprandial glucose response, compared with the control group. QE (0.08% of diet) or acarbose (0.03% of diet) offered to db/db mice significantly reduced both plasma glucose and blood glycated hemoglobin compared to controls without significant influence on plasma insulin. Small intestine maltase activities were significantly reduced by consumption of QE or acarbose. Thus, QE could be effective in controlling fasting and postprandial blood glucose levels in animal models of DM.     

Lispro insulin treatment in comparison with regular human insulin in type 2 diabetic patients living in nursing homes

Lispro insulin has been demonstrated to be effective in reducing post-prandial blood glucose levels. Thirty Type 2 diabetic subjects (18 women and 12 men) living in nursing homes, aged 77 +/- 3 yr, mean systolic pressure 147 +/- 6 and diastolic 82 +/- 4 mmHg, body mass index 27.5 +/- 2 kg/m2, known diabetes duration 10.1+/- 0.7 yr, mean HbA1c 8.5 +/- 0.8%, fasting C-peptide 1.3 +/- 0.5 ng/ml, treated with intensive (4 insulin injections per day) therapy, mean insulin need 45 +/- 7 IU per day, with 2.0 +/- 0.6 hypoglycaemic (blood glucose level below 60 mg/dl) and 13 +/- 4 hyperglycaemic episodes (blood glucose level over 250 mg/dl) per wk, were studied. Their own informed consent or that provided by a family member was obtained before these patients took part in a therapy protocol divided into 3 four-mo periods; in the 1st and 3rd period regular insulin (75% of the total dose) was administered 30 min before each meal, in the second lispro insulin was administered immediately at the end of each meal, according to the carbohydrate quantity ingested with the meal. During the lispro treatment period there was a significant decrease of the mean daily blood glucose 166 +/- 12 regular vs 143 +/- 9 lispro; p<0.01, HbA1c 8.5 +/- 0.6 regular vs 7.6 +/- 0.5 % lispro; p<0.01, triglycerides 261 +/- 40 regular vs 218 +/- 20 mg/dl lispro; p<0.01, hypoglycaemic 2.1 +/- 0.2 regular vs 1.6 +/- 0.3 lispro; p<0.01 and hyperglicaemic 12 +/- 1 regular vs 8 +/- 0.3 lispro; p<0.01 episodes per wk. No statistical difference was recorded between the 1st and the 3rd treatment period. The lispro treatment produced a better metabolic control (mean blood glucose, HbA1c, triglycerides), better lifestyle (less hypo- and hyperglycaemic episodes), better nurse management (no waiting time before, but a more accurate calculation of the right dose administered immediately at the end of each meal). Lispro insulin seems to be a good therapeutic choice not only in Type 1, but also in the large population of elderly Type 2 diabetic patients.     

瑞格列奈或格列吡嗪联合甘精胰岛素治疗初诊2型糖尿病的观察

目的比较瑞格列奈或格列吡嗪联合甘精胰岛素治疗对初诊2型糖尿病患者降糖的疗效及对β细胞功能的影响。方法将笔者所在医院门诊初诊的2型糖尿病患者45例,随机分成瑞格列奈组（瑞格列奈＋甘精胰岛素,n=23）和格列吡嗪组（格列吡嗪＋甘精胰岛素,n=22）。结果两组治疗3个月后餐前和餐后的末梢血糖及HbA1c均较治疗前明显下降（P〈0．01）。结论瑞格列奈（1mg,3次／d）联合甘精胰岛素控制餐后血糖、HbA1c和改善胰岛β细胞分泌功能较格列吡嗪（5mg,1次／d）联合组更好。     

Metabolic effects of acarbose in young healthy men

To explore the long-term metabolic effects of acarbose in man, 6 healthy men (25 +/- 2 years; BMI: 21.6 +/- 2.7) were fed a controlled diet in a metabolic ward for 7 consecutive weeks. After an initial 3-week period to ensure a metabolic steady-state, they received 300 mg/d of acarbose (100 mg before each meal) for the remaining 4 weeks. Stool and urine collections were made over 7 d on weeks 3 and 7. Faecal excretion of water, nitrogen, carbohydrate, fat, zinc, magnesium, copper, chromium, iron, calcium and phosphorus and urinary excretion of nitrogen, urea and calcium were measured. In addition, fasting and postprandial blood glucose and insulin levels, as well as fasting triglycerides, total cholesterol, apolipoproteins (Apo) A-I, A-II, and B, zinc and copper, vitamins A, B1, B2, B6, C, and E concentrations were measured before and at the end of the acarbose period. Weight, food consumption, and water balance were not modified by acarbose. Faecal nitrogen excretion increased significantly but the nitrogen balance remained positive. Faecal excretion of carbohydrate, fat, iron and chromium were significantly increased by acarbose. Apos A-I and A-II decreased significantly. Plasma levels of vitamin B6 increased and vitamin A concentrations decreased with acarbose. This study provides new insights into the metabolic effects of acarbose with respect to nitrogen, mineral and vitamin metabolism.     

Insulin response and glycemic effects of meals in non-insulin-dependent diabetes

Glycemic and hormonal responses to two breakfast mixed meals were studied in six obese subjects with NIDDM. The study evaluated a high-glycemic-effect (HGE) and a low-glycemic-effect (LGE) meal, each with approximately 600 kcal and 12% protein, 15% fat, and 73% carbohydrate. Plasma insulin and counterregulatory hormones were measured at baseline and at 30-min intervals for 5 h after meals. Mean fasting plasma glucose and insulin concentrations were similar before both studies: for the LGE meal, 11.9 +/- 1.8 mmol/L and 261.9 +/- 50.1 pmol/L; for the HGE meal, 11.9 +/- 2.0 mmol/L and 262.6 +/- 43.1 pmol/L. Peak plasma glucose concentrations were approximately 25% lower with the LGE meal and the area under the glucose curve was 63% of that obtained for the HGE meal (p less than 0.05). Although the integrated insulin responses of the two meals did not differ, the peak occurred 60 min earlier in the LGE meal (p less than 0.05). The LGE meal may produce a lower glycemic response, in part because of earlier insulin secretion.     

地特胰岛素联合瑞格列奈对初发2型糖尿病疗效的观察

目的：评价地特胰岛素联合瑞格列奈对初发2型糖尿病患者血糖和体重的影响。方法：初发2型糖尿病患者60例,随机分为两组,分别于睡前皮下注射地特胰岛素（n=30）或甘精胰岛素（n=30）。两组均联合口服瑞格列奈（1mg,3次/d）治疗12周,比较两组治疗前后空腹血糖（FPG）、餐后2h血糖（2hPG）、糖化血红蛋白（HbA1c）、体重、低血糖的变化。结果：与治疗前比较,两组FPG、2hPG、HbA1c均明显下降,差异均有统计学意义（P〈0.05）。两组低血糖发生率差异无统计学意义（P〉0.05）,而地特胰岛素组体重增加明显低于甘精胰岛素组（P〈0.05）。结论：对初发2型糖尿病,与甘精胰岛素相比,地特胰岛素联合瑞格列奈可有效控制血糖,在减少体重增加方面更有优势。     

Postprandial lipemia in subjects with the threonine 54 variant of the fatty acid-binding protein 2 gene is dependent on the type of fat ingested

BACKGROUND: The alanine-for-threonine substitution at codon 54 (A54T polymorphism) in the fatty acid-binding protein 2 gene (FABP2) has been associated with hypertriglyceridemia and insulin resistance. Obese and diabetic T54 carriers have greater postprandial lipemia than do A54 homozygotes. The T54 protein isoform is also associated with increased triacylglycerol secretion in vitro. OBJECTIVE: We investigated diet-gene interactions by measuring postprandial lipids, glucose, insulin, and C-peptide in healthy, nonobese A54 homozygotes and T54 carriers after ingestion of 3 different fats. DESIGN: Eleven A54 homozygotes and 11 T54 carriers were given 3 oral-fat-tolerance tests (butter, safflower oil, and olive oil). Cholesterol and triacylglycerol were measured in plasma and in chylomicron fractions. RESULTS: There was no main effect of FABP2 genotype for chylomicron triacylglycerol, glucose, or C-peptide. The area under the insulin curve and the ratio of insulin to C-peptide were lower in T54 carriers than in A54 homozygotes [312 +/- 29 ( +/- SEM) compared with 425 +/- 31 pmol. h/L (P = 0.05) and 0.23 +/- 0.03 compared with 0.40 +/- 0.05 (P = 0.04), respectively], which suggests greater hepatic insulin clearance in T54 carriers. An association between genotype and chylomicron cholesterol was seen only after olive oil: values were higher (P = 0.02) in T54 carriers (0.087 +/- 0.006 mmol. h/L) than in A54 homozygotes (0.058 +/- 0.004 mmol. h/L). The main effect of fat was significant for the areas under the chylomicron cholesterol and chylomicron triacylglycerol curves [higher values for safflower (0.635 +/- 0.053 and 2.48 +/- 0.30 mmol. h/L, respectively) and olive (0.592 +/- 0.052 and 2.48 +/- 0.32 mmol. h/L, respectively) oils than for butter (0.425 +/- 0.043 and 1.69 +/- 0.20 mmol. h/L, respectively); P < 0.05]. CONCLUSIONS: The A54T polymorphism results in a diet-gene interaction: the T54 group had increased chylomicron cholesterol after olive oil only. Nevertheless, the greater hepatic insulin clearance in T54 carriers suggests that the polymorphism may not be deleterious in nonobese subjects.     

Hypoglycemic and antioxidant effects of Daraesoon (Actinidia arguta shoot) in animal models of diabetes mellitus

BACKGROUND/OBJECTIVES

The primary objective of the treatment of diabetes mellitus is the attainment of glycemic control. Hyperglycemia increases oxidative stress which contributes to the progression of diabetic complications. Thus, the purpose of this study was to investigate the hypoglycemic and antioxidant effects of Daraesoon (Actinidia arguta shoot) in animal models of diabetes mellitus.

MATERIALS/METHODS

Rats with streptozotocin-induced diabetes received an oral administration of a starch solution (1 g/kg) either with or without a 70% ethanol extract of Daraesoon (400 mg/kg) or acarbose (40 mg/kg) after an overnight fast and their postprandial blood glucose levels were measured. Five-week-old C57BL/6J mice were fed either a basal or high-fat/high-sucrose (HFHS) diet with or without Daraesoon extract (0.4%) or acarbose (0.04%) for 12 weeks after 1 week of adaptation to determine the effects of the chronic consumption of Daraesoon on fasting hyperglycemia and antioxidant status.

RESULTS

Compared to the control group, rats that received Daraesoon extract (400 mg/kg) or acarbose (40 mg/kg) exhibited a significant reduction in the area under the postprandial glucose response curve after the oral ingestion of starch. Additionally, the long-term consumption of Daraesoon extract or acarbose significantly decreased serum glucose and insulin levels as well as small intestinal maltase activity in HFHS-fed mice. Furthermore, the consumption of Daraesoon extract significantly reduced thiobarbituric acid reactive substances and increased glutathione levels in the livers of HFHS-fed mice compared to HFHS-fed mice that did not ingest Daraesoon.

CONCLUSIONS

Daraesoon effectively suppressed postprandial hyperglycemia via the inhibition of α-glucosidase in STZ-induced diabetic rats. Chronic consumption of Daraesoon alleviated fasting hyperglycemia and oxidative stress in mice fed a HFHS diet.     

Time course of oxidative stress status in the postprandial and postabsorptive states in type 1 diabetes mellitus: relationship to glucose and lipid changes

OBJECTIVE: The aim of this study was to compare oxidative stress status (OSS) with blood glucose and lipid changes during the fasting, postprandial and postabsorptive phases in type 1 diabetes mellitus. METHODS: Twenty-three patients on intensive insulin treatment received a standard fat-rich breakfast and lunch. OSS was monitored at fasting (F), just after the post-breakfast glycemia peak (BP) (identified by continuous subcutaneous glucose monitoring), 3.5-h post-breakfast (B3.5), just after the post-lunch peak (LP), just after the post-lunch dale (LD) and 5 hours after lunch (L5). RESULTS: Whereas whole blood glutathione and plasma protein thiols increased in the postprandial period (from 6.52 +/- 1.20 (F) to 7.08 +/- 1.45 micromol/g Hb (BP), p = 0.005), ascorbate decreased gradually from 44 +/- 17 (F) to 39 +/- 19 micromol/L (LD), p = 0.015. Retinol and alpha-tocopherol also decreased from 27.1 +/- 7.0 (F) to 25.3 +/- 5.2 micromol/L (BP), p = 0.005. Uric acid decreased later, from 213 +/- 77 (BP) to 204 +/- 68 micromol/L (B3.5), p = 0.01, but then increased in LP (231 +/- 70 micromol/L) and LD to values higher than F (215 +/- 64, micromol/L, p = 0.01). Malondialdehyde increased gradually from 1.02 +/- 0.36 (F) to a maximum of 1.14 +/- 0.40 micromol/L (LP). In the postabsorptive phase (L5) all parameters except for thiols reverted to fasting concentrations. CONCLUSIONS: In type 1 diabetes lipid peroxidation increases during the postprandial phase in parallel to glucose and triglyceride changes. Blood antioxidants, however, followed diverse patterns of change.     

Effects of short-chain fructo-oligosaccharides on glucose and lipid metabolism in mild hypercholesterolaemic individuals

BACKGROUND: The intake of 10 g/day of short-chain-fructo-oligosaccharides (sc-FOS) has been shown to increase significantly bifidus counts and to produce high amounts of short-chain fatty acids (SCFA), presumed to influence glucose and lipid metabolism. AIM: To evaluate the effects of moderate intake of sc-FOS on glucose and lipid metabolism in individuals with mild hypercholesterolaemia. Design: A randomized double-blind sequential cross-over study. SUBJECTS AND METHODS: Thirty subjects of both genders (20 M/10 F), mean age 45.5+/-9.9 years (M+/-SD), BMI 26.6+/-2.2 kg/m(2), with plasma cholesterol >5.17 and <7.76 mmol/l and plasma triglycerides <3.45 mmol/l, participated in the study. The study was performed after a wash-out period of 1 month and a run-in period of 1 month to stabilize patients on a standard diet (CHO 50%, fat 30%, protein 20%, fibre 20 g/day) plus placebo (maltodextrine plus aspartame 15 g/day). At the end of run-in, subjects were randomly assigned to receive sc-FOS (Actilight) (10.6g/day) or placebo (maltodextrine plus aspartame 15 g/day) with tea and/or coffee for a duration of 2 months and thereafter switched to the other treatment for additional 2 months. Plasma glucose, total and lipoprotein (VLDL, LDL, HDL) cholesterol and triglyceride concentrations were measured in the fasting state at the end of run-in and of each treatment period. At the end of the two treatment periods, patients consumed a standard test meal (protein 15%, carbohydrate 34%, fat 51%, kJ 3988) 1h after the administration of 5.3g of sc-FOS or placebo; plasma glucose, insulin, free fatty acid (FFA) and triglyceride responses to the test meal were evaluated. RESULTS: No significant difference in fasting parameters was detected between the two treatments. After sc-FOS and placebo plasma cholesterol levels were, respectively, 6.47+/-0.70 and 6.44+/-0.78 mmol/l (n.s.) and plasma triglycerides were 1.53+/-0.71 and 1.56+/-0.53 mmol/l (n.s.). No significant differences were observed in cholesterol and triglyceride content of VLDL, LDL and HDL and in plasma Apo A1 levels; conversely, fasting plasma Lp(a) concentrations were significantly increased after sc-FOS (37+/-38 vs. 33+/-35 mg/dl; P<0.005). Postprandial responses of glucose, FFA and triglycerides were not significantly different between sc-FOS and placebo, while postprandial insulin response (incremental area) was significantly reduced after sc-FOS compared to placebo (14,490+/-7416 vs. 17,760+/-7710 pmol/l x 300 min; P<0.02). CONCLUSIONS: A moderate intake of sc-FOS has no major effects on lipid metabolism, both in the fasting and in the postprandial period, in individuals with mild hypercholesterolaemia. A small but significant increase of Lp(a) concentrations was observed with sc-FOS consumption together with a reduction of the postprandial insulin response; however, the clinical relevance of these small effects is unclear.     

Palatability and glucose, insulin and satiety responses of chickpea flour and extruded chickpea flour bread eaten as part of a breakfast

OBJECTIVE: To determine the effect of adding chickpea flour or extruded chickpea flour to white bread on palatability and postprandial glycaemia, insulinaemia and satiety. DESIGN: A randomised, single-blind, cross-over study of four 50 g available carbohydrate breakfasts. SETTING: School of Exercise and Nutrition Sciences, Deakin University. SUBJECTS: In all, 12 healthy subjects were recruited through posted notices. Totally, 11 (nine male, two female) completed the study (mean+/-s.e.m.; age 32+/-2 y; body mass index, 24.7+/-0.8 kg/m(2)). INTERVENTION: After overnight fasting, subjects consumed a control (white) bread (WB) breakfast twice, a chickpea bread (CHB) breakfast once and an extruded chickpea bread (EXB) breakfast once. Palatability and postprandial blood glucose, insulin and satiety responses were determined. Following this, food intakes from an ad libitum buffet and for the remainder of the day were assessed. RESULTS: A trend towards a lower incremental area under the curve (IAUC) of glucose for the CHB breakfast compared to the WB breakfast was observed (P=0.087). The IAUC of insulin and insulinaemic index (II) of the CHB breakfast were higher (P<0.05) than for the WB breakfast. No differences in glycaemic index (GI), satiety response, food intake or palatability were observed. CONCLUSIONS: CHB and EXB demonstrated acceptable palatability. CHB demonstrated some hypoglycaemic effect compared to WB, but neither CHB nor EXB demonstrated effects on satiety or food intake. The hyperinsulinaemic effect of CHB observed in this study requires further investigation.     

Dietary manipulation as a primary treatment strategy for pregnancies complicated by diabetes

The mainstay of management for gestational diabetic women (GDM) has been dietary. If it is inadequate to sustain normoglycemia, insulin therapy must be initiated. We studied whether we could prevent macrosomia by insulin therapy based on four daily self blood glucose levels (SBG). Fifty GDM, ages 28-39 years were, recruited to the study. They were divided based on fasting glucose (FBS) level on the glucose tolerance test (GTT): those with FBS less than 90 mg/dl were managed by diet alone; those with FBS greater than 90 mg/dl were immediately started on insulin. The four SBG checks [FBS and 1 hour after each meal (lhpc)] correlated with the continuous glucose monitor with r = 0.91. The women were asked to perform a dipstick for ketones on their urine upon awakening and whenever a meal or snack had been missed. Insulin was initiated when the SBG monitoring indicated that: (1) the FBS was 80 mg/dl whole blood from fingerstick (WBG) or the plasma glucose (PG) greater than 90 mg/dl and/or (2) the lhpc was greater than 140 mg/dl WBG and/or (3) the patient had persistent ketonuria on the prescribed diet which cleared only when the caloric intake was increased to a point which precipitated postprandial hyperglycemia. The prescribed diet was calculated based on body weight to be 30 kcal/kg if the women were between 80 and 120% ideal body weight; or was calculated to be 24 kcal/kg if their weight was greater than 120% ideal body weight. The calories were divided such that 40% was carbohydrate, 20% protein, and 40% fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary manipulation as a primary treatment strategy for pregnancies complicated by diabetes.

The mainstay of management for gestational diabetic women (GDM) has been dietary. If it is inadequate to sustain normoglycemia, insulin therapy must be initiated. We studied whether we could prevent macrosomia by insulin therapy based on four daily self blood glucose levels (SBG). Fifty GDM, ages 28-39 years were, recruited to the study. They were divided based on fasting glucose (FBS) level on the glucose tolerance test (GTT): those with FBS less than 90 mg/dl were managed by diet alone; those with FBS greater than 90 mg/dl were immediately started on insulin. The four SBG checks [FBS and 1 hour after each meal (lhpc)] correlated with the continuous glucose monitor with r = 0.91. The women were asked to perform a dipstick for ketones on their urine upon awakening and whenever a meal or snack had been missed. Insulin was initiated when the SBG monitoring indicated that: (1) the FBS was 80 mg/dl whole blood from fingerstick (WBG) or the plasma glucose (PG) greater than 90 mg/dl and/or (2) the lhpc was greater than 140 mg/dl WBG and/or (3) the patient had persistent ketonuria on the prescribed diet which cleared only when the caloric intake was increased to a point which precipitated postprandial hyperglycemia. The prescribed diet was calculated based on body weight to be 30 kcal/kg if the women were between 80 and 120% ideal body weight; or was calculated to be 24 kcal/kg if their weight was greater than 120% ideal body weight. The calories were divided such that 40% was carbohydrate, 20% protein, and 40% fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fructose-induced in vivo insulin resistance and elevated plasma triglyceride levels in rats

Insulin action was assessed by using the hyperinsulinemic (approximately 800 pmol/L) euglycemic clamp in rats fed equal amounts of glucose or fructose (35% of calories) for 4 wk. The glucose infusion rate required to maintain euglycemia was decreased in fructose-fed animals (14.6 +/- 1.4 vs 21.8 +/- 1.1 for glucose-fed rats, p less than 0.001) with this whole-body effect contributed to equally by an impairment in hepatic insulin action and a reduction in peripheral glucose disposal in a range of tissues. There was no difference in basal glucose turnover, energy expenditure, or postprandial blood glucose and insulin responses to the diets. In the fructose-fed rats there was an increase in fasting triglyceride levels by 2 wk. Euglycemic clamp glucose disposal correlated positively and clamp hepatic glucose output correlated negatively with fasting triglyceride levels. In summary, fructose but not glucose feeding led to impaired insulin action in both the liver and peripheral tissues, effects that may depend on antecedent circulating triglyceride levels.     

Effect of meal sequence on postprandial lipid, glucose and insulin responses in young men

OBJECTIVE: To investigate whether the postprandial changes in plasma triacylglycerol (TAG), nonesterified fatty acids (NEFA), glucose and insulin concentrations in young men were the same if an identical meal was fed at breakfast and lunch, and if the response to lunch was modified by consumption of breakfast. METHODS: In two trials (1 and 2) healthy subjects (age 22+/-1 y, body mass index 22+/-2 kg/m(2)) were fed the same mixed macronutrient meal at breakfast at 08:00 h and lunch at 14:00 h. In the third trial, no breakfast was fed and the overnight fast extended until lunch at 14:00 h. Addition of [1,1,1-(13)C]tripalmitin to one meal in each trial was used to distinguish between endogenous and meal-derived lipids. RESULTS: The postprandial changes in TAG, NEFA and glucose concentrations were similar in trials 1 and 2. The change in plasma total TAG concentration was about two fold less (P<0.05) after lunch compared to breakfast. Postprandial NEFA suppression was the same after breakfast and lunch. Glucose and insulin responses were significantly greater following lunch suggesting decreasing insulin sensitivity during the day. Consumption of breakfast did not alter the postprandial total TAG or NEFA responses after lunch. Measurement of [(13)C]palmitic acid concentration showed that handling of TAG and NEFA from the meal was the same after breakfast and lunch, and was not altered by consumption of breakfast. CONCLUSIONS: Overall, these data suggest that in young, healthy men regulation of plasma TAG from endogenous sources, principally VLDL, but not chylomicrons during the postprandial period leads to differences in the magnitude of lipaemic response when the same meal was consumed at breakfast or at lunch 6 h later.