Modification of beta-cell response to different postprandial blood glucose concentrations by prandial repaglinide and combined acarbose/repaglinide application

This study was designed to compare the effects of repaglinide plus acarbose combination treatment to repaglinide alone on postprandial glucose, serum insulin, C-peptide and proinsulin concentrations. A total of 40 patients with Type 2 diabetes (T2DM) (fasting blood glucose: 120-180 mg/dl; postprandial blood glucose: 140-240 mg/dl) were included in this single-centre, controlled, randomised, single-dose, cross-over study. On two consecutive days, patients either received 2 mg repaglinide 15 min before breakfast followed by 100 mg acarbose with breakfast or repaglinide alone. Two fasting (7.30 h, 8.00 h) and five postprandial blood samples (from 8.30 h to 12.00 h) were taken for blood glucose, serum insulin, C-peptide and proinsulin determination. Repaglinide plus acarbose treatment significantly reduced the mean increase in postprandial blood glucose levels (24.2+/-18.2 mg/dl) compared to repaglinide alone (51.1+/-29.0 mg/dl; p<0.001). Serum insulin, C-peptide and proinsulin levels [mean area under the curve (AUC7.30-12.00h)] were significantly lower than those observed with repaglinide monotherapy (e.g. insulin: 1089.2+/-604.5 hr x pmol/l and 1596.8+/-1080.6 hr x pmol/l, resp., p<0.001), suggesting that acarbose modifies the rapid insulin release induced by repaglinide. Prandial treatment with a combination of acarbose and repaglinide results in an additive glucose lowering effect and modified insulin secretion compared to repaglinide alone. Postprandial hyperglycaemia is not abolished by rapid stimulation of insulin release induced by repaglinide. Additional reduction of postprandial blood glucose by acarbose modifies the stimulation of insulin release.     

Influence of acarbose on post-prandial insulin requirements in patients with Type 1 diabetes

The primary objective of this double-blind, placebo-controlled, randomised cross-over study was to investigate the influence of acarbose on insulin requirement in patients with Type 1 diabetes (T1DM) following a standardised meal. In addition, the study assessed the effects of acarbose on post-prandial triglyceride, glucagon and gastrointestinal peptide levels, gastric emptying, and oxidative glucose metabolism. Following normalisation of their blood glucose, 10 patients received a standardised meal together with acarbose (100 mg) or placebo. Each patient was evaluated twice (separated by 10+/-3 days), and the cross-over study design ensured that they received both acarbose and placebo. The insulin requirement for maintenance of normoglycaemia was assessed using a closed-loop insulin infusion system (artificial pancreas, Biostator). Acarbose produced a statistically significant reduction in mean insulin requirement over a 3-hr period following the meal compared with placebo (5171.7+/-2282.6 mU vs 8074.5+/-3045.4 mU; p=0.003). The level of blood glucose control over the same period was similar in the two groups. Gastric inhibitory polypeptide levels also showed a statistically significant decrease with acarbose treatment compared with placebo for AUC (area under the curve; p=0.006) and Cmax (maximum plasma concentration; p=0.022), but not tmax (time to reach Cmax from the start of the standardised meal; p>0.05). Analysis of the other efficacy parameters revealed no statistically significant differences between acarbose treatment and placebo (p>0.05). These results indicate that acarbose decreases insulin requirement in patients with T1DM without affecting gastric emptying.     

Insulin and glucose responses to glucose injection in fed and fasted obese and lean sheep

Effects of short-term fasting on the insulin and glucose responses to injected glucose were determined in obese (n = 6) and lean (n = 6) Dorset ewes that were fed a maintenance level of energy intake. Sheep were assigned by Latin-square design to be fasted for 0 (fed), 12 or 24 h before glucose (350 mg/kg) was injected via jugular cannula at 2000 h with at least 7 d between successive tests. Insulin and glucose were quantified in jugular plasma samples. Pretreatment concentrations of insulin were affected (P less than 0.005) only by body condition with higher mean values in obese (23.5 +/- 3.3 microU/ml) than in lean (9.4 +/- 1.0 microU/ml) sheep. Pretreatment concentrations of glucose (53.6 +/- 1.8 mg/dl) were unaffected by body condition and fasting. The insulin responses to glucose, whether determined as absolute levels or response areas above base-line levels, were greater (P less than 0.005) in obese than in lean sheep regardless of fasting period. Insulin and glucose concentrations after glucose injection in lean sheep were unaffected by fasting. In contrast, the insulin response to glucose was greater (P less than 0.005) in fed obese than 12- or 24-h fasted obese sheep while glucose levels in the fed sheep were similar to those in the fasted obese sheep. Thus, factors associated with feeding enhanced the insulin response to glucose in obese sheep. In addition, obesity in sheep was associated with insulin resistance because basal hyperinsulinemia coexisted with euglycemia and because fractional removal rates of injected glucose were similar in obese and lean sheep despite much greater concentrations of insulin in obese sheep.     

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.     

阿卡波糖对糖耐量减低患者血管内皮功能的保护

目的 观察阿卡波糖对糖耐量减低患者血管内皮功能的影响.方法 根据口服葡萄糖耐量试验选择56例糖耐量减低(IGT)患者,按系统抽样法随机分为对照组27例和治疗组29例.对照组口服安慰剂,治疗组口服阿卡波糖25～50 mg,3次/d,连续12周.测定两组治疗前后体质指数、血脂、空腹血糖(FPG)、空腹胰岛素、糖化血红蛋白(HbA1c)、高敏C反应蛋白(hs-CRP)、血管性血友病因子(vWF)、餐后2h血糖和餐后2h胰岛素及肱动脉内皮依赖性舒张功能(EDD).结果 与治疗前比较,治疗组患者治疗后体质指数、餐后2h血糖、餐后2h胰岛素、HbA1c、hs-CRP、vWF明显降低[(24.69±2.62) kg/m2比(22.02±2.59) kg/m2; (9.26±1.02) mmol/L比(7.43±0.95) mmol/L;(42.17±9.98) U/L比(34.76±9.86) U/L; (6.03±0.67)％比(5.37±0.56)％;(5.45±1.93) mg/L比(4.52±1.55) mg/L;( 187.22±26.57)％比(165.13±23.86)％] (P＜ 0.05或＜0.01),EDD明显增大[(6.08±1.22)％比(7.94±1.25)％](P＜0.01).对照组治疗前后各指标比较差异无统计学意义(P＞0.05).结论 阿卡波糖可以降低IGT患者餐后血糖,并减轻机体胰岛素抵抗,减少炎性因子,改善血管内皮功能,延缓糖尿病的发生及动脉粥样硬化的发展.     

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.     

The effect of acarbose and miglitol (BAY-M-1099) on postprandial glucose levels following ingestion of various sources of starch by nondiabetic and streptozotocin-induced diabetic rats

The effect of two alpha-glucosidase inhibitors, acarbose (BAY-G-5421) and miglitol (BAY-M-1099), on postprandial glucose levels following intubation of corn, rice, spaghetti and potato (0.5 g/100 g body wt) was evaluated in nondiabetic and diabetic rats. The peak plasma glucose level and total incremental glucose were significantly decreased following ingestion of each starch source when acarbose (8 mg/100 g body wt) or BAY-M-1099 (2 mg/100 g body wt) were simultaneously intubated. The effect of both inhibitors was more pronounced in diabetic rats than in nondiabetic rats, and their effect on digestion was in a substrate-specific manner. Potato starch digestion was inhibited 58 +/- 11% by BAY-M-1099, and by acarbose, 38 +/- 9%. Rice starch digestion was inhibited by 65 +/- 2% by acarbose, and by BAY-M-1099, only 30 +/- 9%. Both drugs had a similar inhibitory effect when corn or spaghetti was ingested. BAY-M-1099 appears to be more potent than acarbose on both a weight-per-weight basis and on a molar basis. When corn or rice was used, only 2 mg of BAY-M-1099 was required to achieve a similar inhibitory effect to that of 8 mg of acarbose (9.7 X 10(-3) M) vs. 12.2 X 10(-3) M). Since both drugs blunted to varying degrees the rise in glucose level following starch ingestion, they may be a useful adjuvant in the treatment of diabetic subjects. Simultaneous use of both drugs in therapeutic treatment should be seriously considered.     

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.     

Association of serum phosphate levels with glucose tolerance, insulin sensitivity and insulin secretion in non-diabetic subjects

BACKGROUND: Hypophosphatemia is associated with impaired glucose tolerance and insulin resistance in primary hyperparathyroidism. However, little is known about the association between serum phosphate and glucose metabolism in healthy subjects. METHODS: We measured fasting serum phosphate levels (SP, normal range 2.6-4.5 mg/dl) and serum calcium (S-Ca, normal range 2.1-2.6 mmol/l) in 881 non-diabetic subjects (341 male/540 female, age: 38+/-1 years, body mass index 25.9+/-0.2 kg/m(2) (mean+/-standard error of the mean). An oral glucose tolerance test (OGTT) with determination of glucose and insulin every 30 min was performed in all subjects. Insulin secretion and insulin sensitivity (IS) were estimated from the OGTT using validated indices. Furthermore, we tested whether serum phosphate predicts glucose tolerance in 115 subjects during a lifestyle intervention program (LIP). RESULTS: Serum phosphate was negatively correlated with 2-h blood glucose levels independent of age, gender and percent body fat (r=-0.13, P<0.0001). This association remained significant after additional adjustment for S-Ca, creatinine and parathyroid hormone. Serum phosphate was positively correlated with IS (r=0.10, P=0.0006), but not with insulin secretion. This was independent of age, gender, percent body fat, S-Ca and serum creatinine. In the subjects taking part in the LIP low serum phosphate levels at baseline were associated with higher postprandial glucose levels. CONCLUSIONS: In non-diabetic subjects, low serum phosphate levels are associated with high 2-h blood glucose levels and reduced IS. Whether low serum phosphate levels are a cause or a consequence of low IS and impairment of glucose tolerance needs to be tested in further studies.     

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.     

Maitake (Grifola frondosa) improve glucose tolerance of experimental diabetic rats

We have previously reported that rats with diabetes induced by injecting streptozotocin into neonates showed remarkably lower blood glucose, urine volume, and glucosuria after administration of Maitake (Grifola frondosa). In the present study, we investigated the effects of Maitake on insulin concentration, organ weight, serum composition, and islets of Langerhans in streptozotocin-induced diabetic rats using the same method. The diabetic rats were produced by injecting 80 mg/kg B.W. streptozotocin into 2-d-old neonates. From the age of 9 wk, the rats were given experimental diets for 100 d. The diabetes and control groups were given either diets containing 20% Maitake (DM and CM groups) or control diets (D and C groups). During administration of the experimental diets, we measured body weight, food intake, amount of feces, and serum insulin concentration at glucose loading. The glucose tolerance test was performed at the 10th week after the start of the experimental diets. The D group had an initial fasting blood glucose of 225+/-49 mg/dL, and a maximum blood glucose of 419+/-55 mg/dL at 60 min. In the DM group, however, the initial fasting blood glucose was 170+/-23 mg/dL, and the maximum blood glucose was 250+/-41 mg/dL at 15 min. Both values were markedly lower than those in the D group (p<0.05). The insulin concentration at 15 min. after glucose loading in the DM group was 41+/-16 microU/mL, which was significantly higher than that in the D group (15+/-7 microU/mL) (p<0.05). After the 100-d experimental period, blood samples were collected. The fructosamine level was significantly lower in the DM group (152+/-21 mmol/L) than in the D group (185+/-13 mmol/L). The concentration of 1.5-A.G. (1.5-anhydro glucitol) was significantly higher in the DM group (9.33+/-2.42 microg/mL) than in the D group (1.33+/-0.52 microg/mL). Observation of insulin antibody stain in the Langerhans cells of the pancreas using ABC method showed a decrease insulin antibody stain in the D group. The cells of the DM group were stained more darkly than those of the D group. From these results, we postulated that the bioactive substances present in Maitake can ameliorate the symptoms of diabetes.     

共轭亚油酸对胰岛素抵抗大鼠葡萄糖运载体4蛋白表达影响的研究

目的通过研究共轭亚油酸（conjugated linoleic acid,CLA）对饮食诱导胰岛素抵抗大鼠葡萄糖运载体4（glucose transporter4,GLUT4）蛋白表达的影响,探讨CLA抗糖尿病作用的机制。方法选用雄性Wistar大鼠,用随机数字表法按体重随机分为对照组、高脂组、高脂＋CLA组（每100g饲料含CLA分别为0．75g、1．50g．3．00g）,每组动物10只,观察CLA对胰岛素抵抗大鼠胰岛素、血糖水平的影响,并应用Western blot方法检测大鼠骨骼肌GLUT4蛋白的表达水平。结果高脂组大鼠血清胰岛素和糖血水平分别为（11．11±2．73）μU／ml、（5．09±0．66）mmol／L,CLA可降低肥胖大鼠的高胰岛素、高糖血症,低、中、高剂量组胰岛素水平分别为（6．99±1．77）μU／ml、（7．36±1．48）μU／ml、（7．85±1．60）μU／ml,血糖水平分别为（4．28±0．72）mmol／L、（4．18±0．55）mmol／L、（4．06±0．63）mmol／L,且高脂组大鼠骨骼肌GLUT4蛋白的表达水平较基础组降低,CLA可增加高脂组大鼠骨骼肌GLUT4蛋白的表达水平。结论CLA可通过增加胰岛素抵抗大鼠骨骼肌GLUT4蛋白的表达水平,改善胰岛素抵抗。     

Silymarin as an adjunct to glibenclamide therapy improves long-term and postprandial glycemic control and body mass index in type 2 diabetes

Oxidative stress is increased postprandially and during long-term hyperglycemia in type 2 diabetic patients who present with poor response to glibenclamide. This study was designed to evaluate the effects of the antioxidant flavonoid silymarin in improving long-term and postprandial glycemic and weight control in type 2 diabetic patients treated with glibenclamide. Using a randomized, double-blind, placebo-controlled design, 59 type 2 diabetic patients, previously maintained on 10 mg/day glibenclamide and diet control, with poor glycemic control, were randomized into three groups: the first two groups were treated with either 200 mg/day silymarin or placebo as adjuncts to glibenclamide, and the third group was maintained on glibenclamide alone for 120 days. Fasting and 4-hour postprandial plasma glucose, glycated hemoglobin (HbA(1c)), and body mass index (BMI) were evaluated at baseline and after 120 days. Compared with placebo, silymarin treatment significantly reduced both fasting and postprandial plasma glucose excursions, in addition to significantly reducing HbA(1c) levels and BMI after 120 days. No significantly different effects were observed for placebo compared to glibenclamide alone. In conclusion, adjunct use of silymarin with glibenclamide improves the glycemic control targeted by glibenclamide, during both fasting and postprandially, an effect that may be related to increased insulin sensitivity in peripheral tissues.     

Hypoglycaemia in severe falciparum malaria

The incidence of hypoglycaemia and the role of quinine in its causation was assessed in 46 patients with severe Plasmodium falciparum malaria. Plasma glucose and immunoreactive insulin were estimated before, during and after quinine therapy. In 5 patients the plasma glucose was in the hypoglycaemic range, the lowest value being 0.67 mmol/litre (12 mg/dl) in a pregnant patient. Most of the remaining patients showed a significant fall in plasma glucose (P less than 0.05), but not to the hypoglycaemic range, and an increase in plasma insulin after quinine (P less than 0.01). A good correlation was found between these changes (r = 0.79, P less than 0.01). Patients with severe P. falciparum malaria, particularly those on quinine therapy, should be watched carefully for developing hypoglycaemia.     

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.     

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.     

Insulin sensitivity in Chinese ovo-lactovegetarians compared with omnivores

AIM: To compare the insulin sensitivity indices between Chinese vegetarians and omnivores. METHODS: The study included 36 healthy volunteers (vegetarian, n=19; omnivore, n=17) who had normal fasting plasma glucose levels. Each participant completed an insulin suppression test. We compared steady-state plasma glucose (SSPG), fasting insulin, the homeostasis model assessment for insulin sensitivity (HOMA-IR and HOMA %S) and beta-cell function (HOMA %beta) between the groups. We also tested the correlation of SSPG with years on a vegetarian diet. RESULTS: The omnivore subjects were younger than the vegetarians (55.7+/-3.7 vs 58.6+/-3.6 year of age, P=0.022). There was no difference between the two groups in sex, blood pressure, renal function tests and lipid profiles. The omnivores had higher serum uric acid levels than vegetarians (5.25+/-0.84 vs 4.54+/-0.75 mg/dl, P=0.011). The results of the indices were different between omnivores and vegetarians (SSPG (mean+/-s.d.) 105.4+/-10.2 vs 80.3+/-11.3 mg/dl, P<0.001; fasting insulin, 4.06+/-0.77 vs 3.02+/-1.19 microU/ml, P=0.004; HOMA-IR, 6.75+/-1.31 vs 4.78+/-2.07, P=0.002; HOMA %S, 159.2+/-31.7 vs 264.3+/-171.7%, P=0.018) except insulin secretion index, HOMA %beta (65.6+/-18.0 vs 58.6+/-14.8%, P=0.208). We found a clear linear relation between years on a vegetarian diet and SSPG (r=-0.541, P=0.017). CONCLUSIONS: The vegetarians were more insulin sensitive than the omnivore counterparts. The degree of insulin sensitivity appeared to be correlated with years on a vegetarian diet.     

Sucrose-induced insulin resistance in the rat: modulation by exercise and diet

Isocaloric substitution of sucrose for starch results in hyperinsulinemia and deterioration of glucose tolerance, suggesting a loss of insulin sensitivity. In this study we have quantitated the insulin resistance which develops with sucrose feeding, and evaluated the ability of dietary fiber, or an increase in skeletal muscle activity, to inhibit, or even prevent, the detrimental effect of sucrose feeding on in vivo insulin action. Thus, 6-wk-old rats were fed one of the following regimens for three weeks: a 64% cornstarch diet (C), a 32% cornstarch + 32% sucrose diet (S), the (S) diet containing added wheat bran fiber (S/F), and the (S) diet given to rats running spontaneously in exercise wheel cages (S/ET). Insulin sensitivity was evaluated by comparing steady-state plasma glucose (SSPG) concentrations at constant plasma insulin levels approximately 70 microU/ml attained during the continuous infusion of epinephrine (0.08 micrograms/kg/min), propranolol (1.7 micrograms/kg/min), glucose (8 mg/kg/min), and insulin (2.5 mU/kg/min) to each experimental group. The results show that rats fed the S diet had a significant increase (p less than 0.01) in mean (+/- SEM) SSPG concentration compared with rats fed the C diet (255 +/- 14 versus 165 +/- 3 mg/dl). SSPG concentrations, although lower (p less than 0.05) in rats fed S/F (205 +/- 8 mg/dl), were still higher (p less than 0.05) than the C levels (165 +/- 3 mg/dl). However, S/ET completely inhibited the increase in SSPG concentration seen in rats fed S and the values were actually lower (p less than 0.05) than in rats fed C (100 +/- 10 versus 165 +/- 3 mg/dl). In conclusion 1) sucrose feeding results in a loss of insulin sensitivity in normal rats; 2) addition of fiber attenuates, but does not completely prevent, the loss of insulin sensitivity associated with feeding sucrose; 3) exercise training prevents the loss of insulin sensitivity seen in sucrose-fed rats, and actually improves glucose uptake beyond that seen in the control group. These results document the profound effect of environmental factors on in vivo insulin action.     

阿卡波糖联合二甲双胍对2型糖尿病的疗效及安全性评价

目的 探讨阿卡波糖联合二甲双胍对2型糖尿病的治疗效果及安全性.方法 选取2011年1月至2014年3月间入住我院接受诊断和治疗的2型糖尿病患者120例,随机分成对照组和观察组各60例.对照组给予二甲双胍治疗,观察组给予阿卡波糖联合二甲双胍治疗,分析两组患者治疗前后血糖变化情况以及不良反应发生情况.结果 治疗前,两组患者的空腹血糖和餐后2h血糖无显著差异（P＞0.05）;治疗后,两组患者的空腹血糖和餐后2h血糖均显著降低,观察组患者的空腹血糖和餐后2h血糖水平显著性低于对照组,差异具有统计学意义（P＜0.05）;两组患者均无严重不良反应发生,差异无统计学意义（P＞0.05）.结论 阿卡波糖联合二甲双胍可以有效治疗2型糖尿病,有效降低患者空腹血糖和餐后2h血糖水平,而且无严重并发症发生,值得在临床推广和应用.     

Plasma homocysteine levels in hyperinsulinemic patients

In order to evaluate the clinical characteristics of metabolic syndrome, a screening procedure was performed and in a cohort of middle-aged (40-60 years) hyperinsulinaemic (fasting plasma insulin > 15 microU/ml) and/or postprandial [120 min after 75 g glucose load] insulin > 45 microU/ml) subjects (n = 91; men/women: 38/53; age mean +/- SD 47.6 +/- 4.3 years; body mass index: 34.6 +/- 4.9 kg/m2; waist-hip ratio: 0.92 +/- 0.07; actual blood pressure 146 +/- 16/87 +/- 9 mmHg; fasting insulin: 24.2 +/- 11.3 microU/ml; postprandial insulin 125.5 +/- 103.8 microU/ml; serum LDL-cholesterol: 3.73 +/- 1.09 mmol/l; HDL-cholesterol: 1.12 +/- 0.30 mmol/l; triglycerides: 2.97 +/- 2.38 mmol/l; uric acid 279 +/- 79 mumol/l) plasma fasting homocysteine, vitamin B12 and folic acid levels were simultaneously determined. The values were separately evaluated according to the stages of glucose tolerance (normal glucose tolerance [n = 47]; impaired glucose tolerance [n = 24] and diabetes mellitus [n = 20]). Laboratory normal values were determined in 47 healthy subjects (control group, age: 45.0 +/- 7.8 years, men/women: 19/28). There was no significant difference between hyperinsulinaemic and control subjects regarding plasma homocysteine (9.28 +/- 3.81 mumol/l vs. 9.63 +/- 2.70 mumol/l), folic acid (8.5 +/- 5.9 ng/ml vs. 7.5 +/- 2.1 ng/ml) and vitamin B12 levels (423 +/- 141 pg/ml vs. 356 +/- 121 pg/ml). Plasma homocysteine levels were significantly (p < 0.001) higher in hyperinsulinaemic men than women (11.34 +/- 4.72 mumol/l [n = 38] vs. 7.86 +/- 2.13 mumol/l [n = 53]). There was no significant difference between subgroups classified according to the stages of glucose tolerance in hyperinsulinaemic groups. Plasma homocysteine values exceeding the upper limit of normal range (> 12.45 mumol/l) were detected at a similar prevalence rate in control (4/47 = 8.5%) and in hyperinsulinaemic subjects (10/91 = 10.9%). A weak but statistically significant correlation was found between plasma homocysteine values and age of subjects (r = 0.222; p < 0.05) whereas a stronger correlation was documented between plasma homocysteine and serum creatinine values (r = 0.658; p < 0.001) in hyperinsulinaemic groups (n = 91). Plasma homocysteine values independently from the stages of glucose tolerance are not elevated in hyperinsulinaemic subjects. Hyperhomocysteinaemia is not a characteristic feature of hyperinsulinism suggesting that plasma homocysteine levels are of no considerable importance in the complex pathomechanism of atherosclerosis at early stages of metabolic syndrome.