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1.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

2.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

3.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

4.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

5.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

6.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

7.
正Objective To study the relationship between serum uric acid and insulin resistance in type 2 diabetic patients.Methods A total of 728 middle-aged and elderly type 2 diabetic patients were recruited and the anthropometric,clinical and biochemical parameters and fasting  相似文献   

8.
改善胰岛素抵抗是预防和治疗2型糖尿病的关键.针对胰岛素抵抗进行治疗能在更早的阶段更好地预防2型糖尿病、防止β细胞功能衰退,同时延缓动脉粥样硬化的进展.
Abstract:
Improving insulin resistance is the key to prevention and treatment of type 2 diabetes.Treatment aimed at insulin resistance can prevent type 2 diabetes in an earlier stage with a better effect, prevent the deterioration of β-cell function, and decrease the rate of the progression to atherosclerosis.  相似文献   

9.
Glucagon-like peptide-1 (GLP-1) is an insulin secretagogue that secreted by intestinal L-cells. After binding with its receptor, GLP-1 stimulates glucose-dependent insulin secretion, β-cell prolifera-tion and differentiation as well as inhibits its apeptosis, decelerates gastric emptying, improves insulin sensi-tivity of periphery tissue. The long-acting GLP-1 analogues decrease hyperglycemia safely without weight gain and hypoglycemia and protect the function of pancreatic islet beta-cell. Using GLP-1 analogues at early stages of the disease,impaired beta-cell function and possibly beta-cell mass appear to be reversible. These agents axe, therefore, considered new therapeutic agents for the treatment of patients with type 2 diabetes.  相似文献   

10.
The main treatment of diabetes is oral antidiabetic drugs, but none of them can prevent β cell apoptosis. Diazoxide is a non-selective potassium channel opener (KCOs) ,which is first used in clinic. It can reduce autoantigen expression of type 1 diabetes,inhibit insulin secretion of pancreatic β-cell effectively, give a period of time for β-cell to rest, reduce excessive apoptosis of β cells, then restore β cell function. It can improve the sensitivity of insulin in peripheral tissues of type 2 diabetes meilitus ,as well as glucose-stim-ulated insulin secretion (GSIS), and can delay and block the process of diabetes and its complications.  相似文献   

11.
Beneficial effects of nateglinide on insulin resistance in type 2 diabetes   总被引:9,自引:0,他引:9  
Nateglinide, a rapid insulin secretagogue, is known to facilitate the early phase of insulin secretion and has been used for the treatment of type 2 diabetic patients with postprandial hyperglycemia. The aim of this study is to evaluate the effect of nateglinide on insulin resistance as well as insulin secretory defects in type 2 diabetic patients. Insulin secretion ability was evaluated by the hyperglycemic clamp test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp test, using an artificial pancreas. The hyperglycemic clamp test showed that a 7-day treatment with nateglinide significantly increased insulin secretion in response to high glucose. Interestingly, although nateglinide is known to facilitate insulin secretion, daily urinary C-peptide excretion was decreased after nateglinide treatment. Moreover, in the euglycemic hyperinsulinemic clamp test, glucose infusion rate was significantly increased by nateglinide treatment, indicating that nateglinide functions to decrease insulin resistance. Nateglinide ameliorates insulin resistance as well as insulin secretory defects in type 2 diabetic patients.  相似文献   

12.
The insulin secretory pattern as a phenotype of type 2 diabetes is an impairment in the rapid, pulsatile secretion of insulin in response to a rise in blood glucose after meal-intake. The restoration of endogenous rapid insulin secretion after oral glucose load was established for the first time by using nateglinide, which is a newly developed insulin secretagogue, in obese patients with type 2 diabetes mellitus. It was clearly demonstrated that with nateglinide, serum insulin levels were quickly raised, and glycemic response curves were almost normalized with the same amount of insulin secretion during 180 min. Therefore, the lack of rapid, pulsatile secretion of insulin in response to glycemic rise after oral glucose load, rather than insulin resistance, is responsible for postprandial glycemic response in obese type 2 diabetes patients.  相似文献   

13.
目的比较那格列奈和阿卡波糖对新诊断2刑糖尿病患者餐后血清游离脂肪酸(FFA)和甘油三酯(TG)的影响。方法16例新诊断2型糖尿病患者随机分为两组,进行为期9周的自身交叉对照研究。前4周两组分别给于阿卡波糖(50mg,日三次)和那格列奈(120mg,日三次),而后停药清洗药物1周。后4周两组交换药物。在第1周和第6周的第1天,所有患者进行标准餐试验,同时服用阿卡波糖50mg或那格列奈120mg,测定0、30、60、120min的血糖、胰岛素、FFA及TG。在第4周和第9周末,测定空腹血糖、胰岛素、FFA、TG。结果单剂景那格列奈和阿卡波糖降低标准餐后血糖的效果相似。与阿卡波糖相比,那格列奈可显著增加2型糖尿病患者标准餐后30min胰岛素分泌水平,降低餐后120min血清FFA水平,但对餐后血清TG水平兀明显影响。那格列奈或阿卡波糖治疗4周前后,空腹FFA和TG水平无显著改变。结论那格列奈在降低餐后血清FFA方而优于阿号波糖,这可能与其部分恢复早时相胰岛素分泌有关。  相似文献   

14.

Aims/Introduction

Dipeptidyl peptidase-4 inhibitors and glinides are effective in reducing postprandial hyperglycemia. However, little information is available on the comparative effects of the two drugs on the levels of postprandial glucose. The aim of the present study was to compare the effects of sitagliptin and nateglinide on meal tolerance tests in drug-naïve patients with type 2 diabetes mellitus.

Materials and Methods

The study participants were 19 patients with type 2 diabetes mellitus, which was inadequately controlled by diet and exercise. An open-label, prospective, cross-over trial was carried out to compare the effects of single-dose sitagliptin and nateglinide on the postprandial glucose level and its related hormones during meal tests.

Results

The change in area under the curve (AUC) of glucose from 0 to 180 min (AUC0–180 min) during the meal test by nateglinide was similar to that by sitagliptin. As expected, the change in active glucagon like peptide-1 was significantly higher after a single-dose of sitagliptin than nateglinide. Then, insulin secretion relative to glucose elevation (ISG) (ΔISG0–180 min: ΔAUC0–180 min insulin/AUC0–180 min glucose) was significantly enhanced by nateglinide compared with sitagliptin. Conversely, glucagon level (ΔAUC0–180 min glucagon) was increased by administration of nateglinide, whereas the glucagon level was reduced by administration of sitagliptin.

Conclusions

The effects of sitagliptin on postprandial glucose levels were similar to those of nateglinide in drug-naïve type 2 diabetes patients. However, the induced changes in insulin, active glucagon-like peptide-1 and glucagon during meal loading suggest that reduction of postprandial hyperglycemia was achieved by the unique effect of each drug.  相似文献   

15.
Nateglinide is a new, fast-onset, short-acting hypoglycemic agent, which increases early phase insulin secretion and the total amount of insulin secreted. However, it is not clear which of these effects contribute more to the decrease in postprandial plasma glucose (PG). To further clarify the pharmacologic actions of nateglinide, we investigated the changes in PG and insulin levels during meal tolerance tests with and without nateglinide. Subjects were 10 newly diagnosed and untreated inpatients with type 2 diabetes. After diet and exercise therapy for 1 week, nateglinide at 270 mg divided 3 times a day, was started. Meal tolerance tests were performed before (baseline) and after a single nateglinide administration (day 1), after 7 days of repeated administration (day 7), and after cessation of nateglinide on day 8. Mean fasting PG was 146 +/- 6 mg/dl (mean +/- SEM) at baseline and 130 +/- 6 mg/dL on day 7 (P =.0004). The 2-hour postprandial PG level was 226 +/- 10 mg/dL at baseline, 145 +/- 11 mg/dL on day 1 (P =.0008), and 190 +/- 15 mg/dL on day 8 (P =.08, baseline; P =.01, day 7). The mean fasting insulin level was 5.4 +/- 1.0 microU/mL at baseline and did not change significantly during the study. The 30-minute postprandial insulin level was 14.4 +/- 1.9 microU/mL at baseline, 39.5 +/- 4.5 microU/mL on day 1 (P =.0004), and 23.6 +/- 3.6 microU/mL on day 8 (P =.045, baseline; P =.010, day 7). The total insulin amount, in terms of area under the curve (AUC. IRI), was 3.99 +/- 0.7 x 10(3) microU/mL. min at baseline, 5.47 +/- 0.8 microU/mL. min on day 1 (P =.029), and 6.01 +/- 1.9 microU/mL. min on day 8 (P =.047 v baseline). The early phase of insulin secretion, based on the ratio of delta IRI to delta PG from fasting to 30 minutes after a meal was 0.15 +/- 0.13 at baseline, 1.44 +/- 0.26 on day 1 (P =.0009) and 0.26 +/- 0.06 on day 8 (P =.05 v day 1). After cessation of nateglinide, the postprandial PG level increased immediately. Although early phase insulin secretion returned nearly to the baseline level, total insulin secretion remained at a high level. These results suggested that early phase insulin secretion contributes more than total insulin secretion to the improvement of postprandial hyperglycemia in type 2 diabetes.  相似文献   

16.
AIMS: The new non-sulphonylurea oral hypoglycaemic agent nateglinide has been shown to enhance insulin secretion in animals and in healthy human volunteers and thus offers a potential advance in the treatment of Type 2 diabetes mellitus. This study examined whether nateglinide can enhance insulin secretion, and particularly the first phase insulin response, in patients with Type 2 diabetes. METHODS: A double-blind, placebo-controlled trial, examining the effects of a single oral dose of 60 mg nateglinide, given 20 min prior to an intravenous glucose tolerance test (IGTT), on insulin secretion in 10 otherwise healthy Caucasian men with recently diagnosed Type 2 diabetes (duration since diagnosis 0-44 months). RESULTS: Insulin secretion (both overall and first phase) was significantly increased by nateglinide (P < 0.001), as were C-peptide (P < 0.001) and proinsulin (P < 0.001) secretion. Overall glucose concentrations following glucose challenge were lower after nateglinide than after placebo (P = 0.05). CONCLUSIONS: Nateglinide significantly increases insulin secretion in Type 2 diabetic patients, in particular restoring the first phase insulin response. Further study is necessary to determine the effects of chronic administration on insulin secretion and blood glucose concentration.  相似文献   

17.
AIMS: This randomized crossover placebo-controlled study aimed to assess the efficacy of nateglinide, a phenylalanine-derived insulin secretagogue, on forearm endothelial function in diabetic subjects before and after an oral glucose load. METHODS: Forearm blood flow (FBF) was measured using strain-gauge plethysmography during reactive hyperaemia before and after an oral glucose load (75 g) with a prior use of placebo or nateglinide (90 mg) in 15 diet-treated Type 2 diabetic patients or age-matched controls with normal glucose tolerance. RESULTS: The peak FBF response and total reactive hyperaemic flow (flow debt repayment: FDR), indices of resistance artery endothelial function, were decreased after an oral glucose load in diabetic patients, but unchanged in controls. Nateglinide administered to diabetic patients accelerated insulin secretion and reduced post-challenge plasma glucose, and also abolished the post-challenge impairment of endothelial function. The peak FBF and FDR were well correlated with 120-min glucose levels and 30-min insulinogenic index. CONCLUSIONS: A single challenge of glucose was shown to impair endothelial function in diabetic patients, and the post-challenge endothelial dysfunction was improved by a prior use of nateglinide. Long-term effects of nateglinide on endothelial function in Type 2 diabetic patients need to be clarified in future studies.  相似文献   

18.
Every diabetes treatment contributes to the control of postprandial blood glucose, yet some agents more specifically target this goal. Alpha-glucosidase inhibitors, led by acarbose, mainly address postprandial glucose control. These agents inhibit intestinal disaccharidases through a competitive effect and can be used either as the sole treatment or in combination with other antidiabetic drugs. Other agents improve insulin secretion kinetics. This is the case for repaglinide et nateglinide, which are efficient in controlling postprandial blood glucose, and to a lesser degree, fasting blood glucose. These agents shortly and quickly stimulate insulin secretion and should be available soon. In oral therapy secondary failures, trials are currently being conducted to clarify the role of fast-acting insulin analogs, as monotherapy or in combination. Finally, insulin sensitizing agents are being investigated as a way to improve postprandial glucose efflux by potentiating insulin effects. The optimal strategy for the use of these different therapeutic agents remains to be established, as well as their long-term effects on diabetic complications.  相似文献   

19.
BACKGROUND: To study the acute effect of nateglinide, an insulinotropic agent, on the postprandial triglyceride and lipoprotein responses in subjects at risk for type 2 diabetes. METHODS: Six women and 10 men, with at least one first-degree relative with type 2 diabetes were included (Age: 48 +/- 7 years, BMI: 27.5 +/- 2.8 kg m(-2), P-triglycerides: 1.3 +/- 0.4 mmol L(-1), P-cholesterol: 5.4 +/- 0.6 mmol L(-1), B-glucose: 4.6 +/- 0.3 mmol L(-1)). They each had two 8-h meal tolerance tests with either nateglinide or placebo given 10 min prior to the meals in randomized order. Lipoprotein fractions were separated by density gradient ultracentrifugation. First-phase insulin secretion was assessed by an intravenous glucose tolerance test (300 mg kg(-1) body weight) and insulin sensitivity by a hyperinsulinaemic euglycaemic clamp (40 mU m(-2) min(-1)). RESULTS: The 1-h insulin levels during the meal tolerance test were significantly higher with nateglinide (577 +/- 81 vs 376 +/- 58 pmol L(-1), p < 0.001), as well as the response during the first two hours (IAUC: 41 243 +/- 5844 vs 29 956 +/- 4662 pmol L(-1) min, p < 0.01). Accordingly, nateglinide lowered the 8-h postprandial glucose response by around 60% compared to placebo (p < 0.001). In contrast, no significant lowering was seen in the excursion of postprandial triglycerides in total plasma or lipoprotein fractions. Consistently, the concentration of exogenous (apoB-48) and endogenous (apoB-100) lipoproteins was not reduced by nateglinide. CONCLUSIONS: Acute administration of nateglinide reduces, as expected, the postprandial glucose concentration, but no reduction in triglyceride or lipoprotein responses are seen in subjects at risk for type 2 diabetes.  相似文献   

20.
BACKGROUND AND AIM: Postprandial glycaemia and lipaemia are known risk factors for atherosclerosis in type 2 diabetes. Coagulation activation in the postprandial state also contributes to acceleration of atherosclerosis. Nateglinide is effective in reducing postprandial glycaemia. Its effect on glycaemia may also be beneficial in postprandial lipaemia and coagulation. The aim of this study was to examine the potential effect of a single dose of nateglinide on postprandial triglyceridaemia, coagulation, and fibrinolysis in patients with type 2 diabetes. METHODS AND RESULTS: Ten subjects with type 2 diabetes, treated with diet alone were recruited in a crossover randomized study. In the morning, after a 12- to 14-h fast, each subject received a standard mixed meal (total energy 783 kcal), preceded by one tablet of 120 mg nateglinide or placebo. Venous blood samples were drawn prior to meal consumption and 6h afterwards for the measurement of plasma glucose, insulin, and C-peptide, lipids, coagulation, and fibrinolysis factors. As expected, there was a significant reduction in postprandial glycaemia after nateglinide administration compared to placebo (P<0.001). Plasma insulin levels were significantly higher after nateglinide than after placebo (P=0.002). Nateglinide administration resulted in a lower overall postprandial reduction of tissue-plasminogen activator than placebo (-2.9+/-1.3 vs. -8.3+/-3.7 ng/ml h, P=0.003). In addition, a significant reduction of postprandial plasminogen activator inhibitor-1 was observed in comparison with the baseline values after nateglinide (P=0.001), although the overall response was not significantly different after nateglinide and placebo (P=0.31). Plasma concentrations of C-peptide, lipids and the remaining coagulation parameters studied were not different between nateglinide and placebo. CONCLUSIONS: Acute nateglinide administration improves postprandial glycaemia and fibrinolytic activity in patients with type 2 diabetes. This combined effect, if confirmed by a long-treatment study, might reduce cardiovascular risk in type 2 diabetes.  相似文献   

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