Glucose Tolerance In Rats Research Articles

Calcium Channel Blockers Inhibit the Hyperglycemic Effect of Calcitonin

We studied the effect of Russian preparation of porcine calcitonin (calcitrin, 1 U/100 g) and blockers of Ca(2+) channels nifedipine (1 mg/kg, blocker of chemosensitive Ca(2+) channels) and isoptin (5 mg/kg, blocker of voltage-dependent Ca(2+) channels) on glucose metabolism. Calcitonin produced a pronounced hyperglycemic effect in rats. A close negative correlation was found between glucose level and total calcium content. Injection of calcitonin reduced glucose tolerance in rats. Isoptin and nifedipine reduced plasma calcium level and did not affect significantly the blood glucose levels, did not change the pattern of alimentary hyperglycemia in response to glucose load, completely abolished the hyperglycemic effect of calcitonin, and prevented calcitonin-induced impairment of glucose tolerance.

When GLP-1 hits the liver: a novel approach for insulin resistance and NASH

nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to steatohepatitis (NASH), increasing fibrosis and eventually, cirrhosis ([22][1]). Importantly, NASH accompanied by fibrosis and severe inflammation is the most relevant predictor for disease progression

Enhanced insulin secretion and glucose tolerance in rats exhibiting low plasma free fatty acid levels and hypertriglyceridaemia due to congenital albumin deficiency

Congenitally analbuminaemic individuals and rats (NARs) exhibit several metabolic abnormalities, including hypertriglyceridaemia and plasma free fatty acid deficiency. Our aim was to study glucose homeostasis and insulin secretion in NARs. Plasma concentrations of lipids, glucose and insulin and secretion of insulin from the pancreatic islets were measured in female NARs and control animals (Sprague-Dawley rats; SDRs). Glucose homeostasis tests were also performed. Plasma glucose levels were similar between NARs and SDRs, irrespective of feeding status. However, fed insulinaemia was ∼37% higher (P 0.05) in NARs than in SDRs. The NARs displayed a markedly increased glucose tolerance, i.e. the integrated glycaemic response was one-third that of the control animals. Enhanced glucose tolerance was associated with threefold higher insulinaemia at peak glycaemia after a glucose load than in the control animals. Similar peripheral insulin sensitivity was observed between groups. Isolated pancreatic islets from NARs secreted significantly more insulin than islets from SDRs in response to a wide range of glucose concentrations (2.8-33.3 mm). Despite having similar liver glycogen contents in the fully fed state, NARs had ∼40% (P 0.05) lower glycogen contents than SDRs after 6 h fasting. The injection of a gluconeogenic substrate, pyruvate, elicited a faster rise in glycaemia in NARs compared with SDRs. Overall, NARs displayed enhanced glucose tolerance, insulin secretion and gluconeogenic flux. The higher glucose tolerance in NARs compared with SDRs is attributed to enhanced islet responsiveness to secretagogues, while peripheral insulin sensitivity seems not to be involved in this alteration. We propose that the enhanced glucose metabolism is a chronic compensatory adaptation to decreased free fatty acid availability in NARs.

Assessment of Bridelia ferruginea benth for its therapeutic potential in pregnancy-induced impaired glucose tolerance in rats

Background : Pregnancy induced diabetes also known as gestational diabetes develops during pregnancy. Pregnancy is an insulin resistant state that may induce impaired glucose tolerance and often gestational diabetes in susceptible women. Gestational diabetes causes serious problems to the mother and the baby. Therefore, the use of herbal remedies such as Bridelia ferruginea with the potential ability to improve glucose tolerance during pregnancy will definitely improve pregnancy outcome in gestational diabetes. Aim : This paper presents an evaluation of possible therapeutic potential of B. ferruginea in gestational diabetes by assessing the anti-glycaemic effects of the plant’s aqueous extracts on pregnancy-induced glucose intolerance in rats. Materials and Methods : Adult virgin, timed-pregnant and non-pregnant rats were subjected to brief ether anaesthesia after 18-hour overnight fasting period to allow for oro-gastric administration of glucose load at 3.0g/kg body weight as 30% solution. The oral glucose load was given at an administration volume of 1.0ml/100g bw. Results : Oral glucose tolerance test showed that pregnancy induced glucose intolerance in the rats. However, B. ferruginea caused a reduction in glycaemic response to glucose challenge and an increased glucose tolerance in rats that had pregnancy-induced glucose intolerance. Thus, diabetogenic effect of pregnancy was ameliorated by oral administration of aqueous extracts of B. ferruginea to pregnant albino rats. Keywords : Gestational diabetes, pregnancy-induced diabetes, hypoglycaemic, glycaemic response, glucose tolerance.

GLP-1, exendin-4 and C-peptide regulate pancreatic islet microcirculation, insulin secretion and glucose tolerance in rats

GLP-1 (glucagon-like peptide 1) and its mimetic exendin-4 are used against Type2 diabetes. C-peptide has also proven promising to enhance insulin action. Since insulin secretion in vivo can be rapidly tuned by changes in islet microcirculation, we evaluated the influence of GLP-1, exendin-4 and C-peptide on pancreatic IBF (islet blood flow), and dynamic changes in insulin secretion and glycaemia in the rat. Adult male Wistar rats were divided into four groups given intravenous saline, GLP-1, exendin-4 or C-peptide respectively and administered either saline or 30% glucose. Furthermore, we investigated the effect of intravenous infusion of different doses of exendin-4 into either the femoral vein or the portal vein on islet microcirculation. A non-radioactive microsphere technique was adopted to measure the regional blood flow. Both GLP-1 and exendin-4 prevented the glucose-induced PBF (pancreatic blood flow) redistribution into the islets. Infusion of exendin-4 into the portal vein did not alter pancreatic islet microcirculation, while infusion of exendin-4 into femoral vein significantly decreased basal IBF. C-peptide increased basal IBF and the proportion of IBF out of total PBF, but did not affect the islet microcirculation after glucose administration. GLP-1, exendin-4 and C-peptide stimulated insulin secretion and significantly decreased glycaemia. Blocking NO formation did not prevent the decreased IBF and post-load glycaemia evoked by exendin-4, but further decreased IBF and KBF (kidney blood flow) and increased basal glycaemia. Blocking the vagus nerve enhanced pancreatic IBF and further decreased post-load glycaemia and KBF and increased basal glycaemia. The vascular modulatory effect on pancreatic islet microcirculation described herein, with subsequent effects on in vivo insulin secretion and glycaemia, might be one of the mechanisms underlying the anti-diabetic actions of GLP-1 and its long acting mimetic exendin-4, as well as that of C-peptide.

Clofibrate‐Induced Reduction of Plasma Branched‐Chain Amino Acid Concentrations Impairs Glucose Tolerance in Rats

It has been reported that branched-chain amino acid (BCAA) administration stimulates glucose uptake into muscles and whole body glucose oxidation in rats. The authors examined the effect of decreased plasma BCAA concentrations induced by clofibrate treatment on glucose tolerance in rats. Since clofibrate, a drug for hyperlipidemia (high serum triglyceride concentration), is a potent inhibitor of the branched-chain α-keto acid dehydrogenase kinase, clofibrate treatment (0.2 g/kg body weight) activated the hepatic branched-chain α-keto acid dehydrogenase complex, resulting in decreased plasma BCAA concentrations by 30% to 50% from the normal level. An intraperitoneal glucose tolerance test was conducted after clofibrate administration, and the results showed that peak plasma glucose concentration and the area under the curve of glucose concentration during the intraperitoneal glucose tolerance test were significantly higher in clofibrate-treated rats than in control rats. This impaired glucose tolerance in the clofibrate-treated rats was ameliorated by administration of BCAAs (0.45 g/kg body weight, leucine:isoleucine:valine = 2:1:1), which kept plasma BCAA concentrations at normal levels during the intraperitoneal glucose tolerance test. These results suggest that plasma BCAAs play an important role in maintaining normal glucose tolerance in rats.

Glucose Tolerance Evaluation in Graves Patients Treated with Methimazole and Radioiodine

The manuscript, “Evaluation of Glucose Tolerance in Methimazole and Radioiodine Treated Graves’ Patients,” by Kiani J et al. (1) compared glucose tolerance in Graves’ disease patients treated with methimazole to those treated with radioiodine. The results indicated that radioiodine therapy had no adverse effects on glucose tolerance or insulin resistance. This study has an impact on whether particular attention should be paid to diabetes mellitus in patients after radioiodine therapy. The conclusion is reasonable, but the design of this study raises several questions concerning glucose tolerance, beyond simply damage to the pancreas caused by radioiodine. First, not only the present state of thyroid function but also its functional changes throughout each treatment for Graves' disease may affect glucose tolerance. Without knowing the patient’s glucose tolerance before receiving radioiodine, the exact change is difficult to evaluate in each individual. Second, the level of sodium iodide symporter (NIS) expression in the pancreas remains controversial. One report demonstrated strong NIS immunoreactivity in pancreatic islet cells (2). Another report, however, did not find any evidence of NIS immunoreactivity in the pancreas (3). This discrepancy may be caused by the anti-NIS antibodies used in each study. Regardless, in both studies, the NIS expression level in the pancreas was quite low compared to the level in the thyroid gland. Given that TSH stimulates radioiodine uptake in thyroid tissue but not in extrathyroidal tissue because of the absence of TSH receptors, radioiodine accumulation in the pancreas is inhibited in the presence of the thyroid gland. To decrease this interference with radioiodine uptake, more efficient radioiodine accumulation in the pancreas may be one way to administer high doses of radioiodine as pointed out by the authors. Alternatively, thyroid-cancer patients who undergo a total thyroidectomy followed by remnant ablation may be good candidates for evaluation of glucose tolerance in patients after radioiodine therapy (1). In this situation, physiological accumulation of radioiodine can be identified by scintigraphy, and, when present, suggests possible subsequent damage in the tissues. Although it is rare to detect clear radioiodine accumulation in the pancreas of thyroid-cancer patients after radioiodine therapy or development Copyright c 2011 Kowsar M. P. Co. All rights reserved.

Platyconic acid, a saponin from Platycodi radix, improves glucose homeostasis by enhancing insulin sensitivity in vitro and in vivo

Previous research demonstrated that the crude saponins of Platycodi radix improve glucose metabolism by enhancing insulin sensitivity in type 2 diabetic animals; however, which individual saponins are the most potent insulin sensitizers is unknown. This study investigated which saponin(s) have anti-diabetic action in vitro and in vivo. The insulin-stimulated glucose uptake and PPAR-γ agonistic actions of six saponins from Platycodi radix were investigated in 3T3-L1 adipocytes, and glucose-stimulated insulin secretion was determined in Min6 cells. Four individual saponins (20 mg/kg body weight) were orally administered to low-dose streptozotocin-injected diabetic mice fed a high-fat diet for 8 weeks to evaluate glucose tolerance by oral glucose tolerance testing (OGTT), insulin sensitivity by insulin tolerance testing, and insulin signaling in the liver and adipose tissues. Platyconic acid (PA) most effectively increased insulin-stimulated glucose uptake in 3T3-L1 adipocytes, possibly in part by working as a peroxisome proliferator-activated receptors (PPAR)-γ activator; however, none of the saponins improved glucose-stimulated insulin secretion in insulinoma cells. PA-treated diabetic mice exhibited the lowest peak serum glucose levels and highest serum insulin levels during the first part of OGTT. PA also improved insulin sensitivity: PA increased glycogen accumulation and decreased triacylglycerol storage in liver, which was associated with enhanced hepatic insulin signaling, while PA potentiated the expression of adiponectin and PPAR-γ in adipose tissue, and improved insulin signaling and increased GLUT4 translocation into the membranes. PA improves glucose homeostasis in type 2 diabetic mice, partly by enhancing hepatic and adipocyte insulin sensitivity, possibly by activating PPAR-γ.

Removal of intra-abdominal visceral adipose tissue improves glucose tolerance in rats: Role of hepatic triglyceride storage

Epidemiological studies have demonstrated a strong link between increased visceral fat and metabolic syndrome. In rodents, removal of intra-abdominal but non-visceral fat improves insulin sensitivity and glucose homeostasis, though previous studies make an imprecise comparison to human physiology because actual visceral fat was not removed. We hypothesize that nutrient release from visceral adipose tissue may have greater consequences on metabolic regulation than nutrient release from non-visceral adipose depots since the latter drains into systemic but not portal circulation. To assess this we surgically decreased visceral white adipose tissue (~0.5g VWATx) and compared the effects to removal of non-visceral epididymal fat (~4g; EWATx), combination removal of visceral and non-visceral fat (~4.5g; EWATx/VWATx) and sham-operated controls, in chow-fed rats. At 8weeks after surgery, only the groups with visceral fat removed had a significantly improved glucose tolerance, although 8 times more fat was removed in EWATx compared with VWATx. This suggests that mechanisms controlling glucose metabolism are relatively more sensitive to reductions in visceral adipose tissue mass. Groups with visceral fat removed also had significantly decreased hepatic lipoprotein lipase (LPL) and triglyceride content compared with controls, while carnitine palmitoyltransferase (CPT-1A) was decreased in all fat-removal groups. In a preliminary experiment, we assessed the opposite hypothesis; i.e., we transplanted excess visceral fat from a donor rat to the visceral cavity (omentum and mesentery), which drains into the hepatic portal vein, of a recipient rat but observed no major metabolic effect. Overall, our results indicate surgical removal of intra-abdominal fat improves glucose tolerance through mechanism that may be mediated by reductions in liver triglyceride.

Dietary‐resistant starch improves maternal glycemic control in Goto–Kakizaki rat

Dietary prebiotics show potential in anti-diabetes. Dietary resistant starch (RS) has a favorable impact on gut hormone profiles, including glucagon-like peptide-1 (GLP-1) consistently released, a potent anti-diabetic incretin. Also RS reduced body fat and improved glucose tolerance in rats and mice. In the current project, we hypothesize that dietary-resistant starch can improve insulin sensitivity and pancreatic β cell mass in a type 2 diabetic rat model. Altered gut fermentation and microbiota are the initial mechanisms, and enhancement in serum GLP-1 is the secondary mechanism. In this study, GK rats were fed an RS diet with 30% RS and an energy control diet. After 10 wk, these rats were mated and went through pregnancy and lactation. At the end of the study, pancreatic β cell mass, insulin sensitivity, pancreatic insulin content, total GLP-1 levels, cecal short-chain fatty acid concentrations and butyrate producing bacteria in cecal contents were greatly improved by RS feeding. The offspring of RS-fed dams showed improved fasting glucose levels and normal growth curves. Dietary RS is potentially of great therapeutic importance in the treatment of diabetes and improvement in outcomes of pregnancy complicated by diabetes.

Effect Of an Amino Acid Supplement on Glucose Tolerance in Healthy Overweight Adults

It is estimated that two-thirds of the adult population and a growing number of children in US are overweight or obese. Overweight is considered the single strongest predictor of type 2 diabetes, which is primarily characterized by insulin resistance and hyperglycemia. Amino acids, such as leucine and isoleucine, have been shown to improve blood glucose tolerance in rats. PURPOSE: To determine whether an amino acid mixture could improve the blood glucose clearance of healthy overweight men and women following an oral glucose tolerance test (OGTT). METHODS: Twenty-two overweight healthy subjects (31±2 yrs, BMI 34.6±1.1 kg/m2) completed two OGTT after consuming two different test beverages. The amino acid beverage (CHO/AA) contained 12.395g amino acid mixture consisting of isoleucine, leucine, cystine 2HCl, methionine and valine in a 12 oz solution. The control beverage (CHO) consisted of a 12 oz placebo drink. Both beverages were mixed with a 10 oz orange-flavored drink containing 100g dextrose to make a drink totaling 22 oz. Venous blood samples were drawn 10min before the drinks, and 15, 30, 60, 120 and 180min after the drinks. RESULTS: During the OGTT, the plasma glucose response for the CHO/AA treatment was significantly lower than that of the CHO treatment, which was supported by the finding that the glucose AUC for the CHO/AA treatment was significantly lower than that for the CHO treatment (806.9±31.4 vs. 942.6±40.6 mmol/L/3h, p<0.05). The plasma glucose levels were significantly lower during the CHO/AA treatment than the CHO treatment at 30, 60, 120, and 180 min post supplementation (5.4±0.2 vs. 6.3±0.2, 4.7±0.3 vs. 5.6±0.4, 4.2±0.2 vs. 4.9±0.3, 3.9±0.2 vs. 4.4±0.2 mmol/L, respectively, p<0.05). However, there were no significant differences in plasma insulin (p=0.343) and c-peptide (p=0.079) responses between treatments. A significant treatment effect was found in plasma glucagon (p<0.05). The amino acid mixture had no significant effects on plasma FFA, triglyceride, and lactate. CONCLUSION: An amino acid mixture, composed of 5 amino acids, lowers the glucose response to an OGTT in healthy overweight subjects in an insulin-independent manner. Supported by Abbott Laboratories.

Identification of insulin secretory defects and insulin resistance during oral glucose tolerance test in a cohort of cystic fibrosis patients

Cystic fibrosis (CF)-related diabetes is a leading complication of CF and is associated with pulmonary and nutritional deterioration, years before an evident hyperglycemia, possibly because of insulin deficiency and resistance. To evaluate glucose tolerance, insulin secretion, and insulin sensitivity by a widely applicable method suitable for accurate and prospective measurements in a CF population. A total of 165 CF subjects (80 females) aged 17±5 years and 18 age- and sex-matched healthy controls (CON) received an oral glucose tolerance test with glucose, insulin and C-peptide determinations. Insulin sensitivity was defined on the basis of glucose and insulin concentrations using the oral glucose insulin sensitivity index, whereas β-cell function was determined on the basis of a model relating insulin secretion (C-peptide profile) to glucose concentration. Fifteen percent of CF patients had glucose intolerance and 6% had diabetes without fasting hyperglycemia and 3% had diabetes with fasting hyperglycemia. β-cell function was reduced in CF patients compared with CON (70.0±4.1 vs 117.9±11.6 pmol/min per m(2) per mM, P<0.001) and decreased significantly with age by -2.7 pmol/min per m(2) per mM per year (confidence interval (CI) -4.5 to -0.82), i.e. almost 4% yearly. The early insulin secretion index was also reduced. Insulin sensitivity was similar to CON. CF patients who attained glucose tolerance comparable to CON had lower β-cell function and higher insulin sensitivity. The major alteration in insulin secretion and insulin sensitivity of CF patients is slowly declining β-cell function, consisting of delayed and reduced responsiveness to hyperglycemia, that in CF patients with normal glucose tolerance may be compensated by an increased insulin sensitivity.

The effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats

In previous study, heat treatment and AMPK activation by exercise improved glucose tolerance in rat.PURPOSETo determine the effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats.METHODSOtsuka Long‐Evans Tokushima Fatty rat (OLETF: n=16, 305.3±11.4g), an accurate animal model for human type 2 diabetes, and their counter parts (LETO: n=8, 226.7±14.1g) were used. Sixteen OLETF rats were divided into two groups; Control (n=8: CON) and Heat treatment (n=8: HT). HT received a lower‐body heat treatment (41 °C for 20 min) using water bath under anesthesia once a week for twelve weeks. An intraperitoneal glucose tolerance test was performed for each group in week‐11. In week‐12, the soleus muscles were removed 48 h after the last heat treatment. Phospho‐AMPK and total‐AMPK in the muscle was determined by Western blot analysis.RESULTSAt 120 min after glucose injection, blood glucose levels of CON and HT were significantly higher than LETO, whereas blood glucose level of HT was lower than CON. AMPK phosphorylation ratio in the soleus muscle of CON was significantly lower than LETO. However, heat treatment significantly increased AMPK phosphorylation ratio in HT compared with CON, and there was no significant difference between LETO and HT.CONCLUSIONOur results indicate that weekly heat treatment for twelve weeks could increase AMPK activation in skeletal muscle in type 2 diabetic rats.

Electroacupuncture improves glucose tolerance through cholinergic nerve and nitric oxide synthase effects in rats

The purpose of this investigation was to evaluate the effect and mechanisms of electroacupuncture (EA) at the bilateral Zusanli acupoints (ST-36) on glucose tolerance in normal rats. Intravenous glucose tolerance test (IVGTT) was performed to examine the effects of electroacupuncture (EA) on glucose tolerance in rats. The EA group underwent EA at the ST-36, with settings of 15 Hz, 10 mA, and 60 min; the control group underwent the same treatments, but without EA. Atropine, hemicholinium-3 (HC-3) or NG-nitro- l-arginine methyl ester ( l-NAME) were injected into the rats alone or simultaneously and EA was performed to investigate differences in plasma glucose levels compared to the control group. Plasma samples were obtained for assaying plasma glucose and free fatty acid (FFA) levels. Western blot was done to determine the insulin signal protein and nNOS to exam the correlation between EA and improvement in glucose tolerance. The EA group had significantly lower plasma glucose levels compared to the control group. Plasma glucose levels differed significantly between the EA and control groups after the administration of l-NAME, atropine, or HC-3 treatments alone, but there were no significant differences in plasma glucose with combined treatment of l-NAME and atropine or l-NAME and HC-3. EA decreased FFA levels and enhanced insulin signal protein (IRS1) and nNOS activities in skeletal muscle during IVGTT. In summary, EA stimulated cholinergic nerves and nitric oxide synthase for lowering plasma FFA levels to improve glucose tolerance.

Gastric Emptying of Orally Administered Glucose Solutions and Incretin Hormone Responses Are Unaffected by Laparoscopic Adjustable Gastric Banding

Laparoscopic adjustable gastric banding (LAGB) provides weight loss in obese individuals and is associated with improved glucose homeostasis and resolution of type 2 diabetes. However, in most available reports, potentially inappropriate methodology has been applied when measuring the impact of LAGB on glucose intolerance. In order to clarify the applicability of the diagnostic 75 g-oral glucose tolerance test (OGTT) to measure the effect of LAGB on glucose metabolism, we investigated the effect of LAGB on gastric emptying for liquids as well as pancreatic and incretin hormone responses. Eight obese patients (three with normal glucose tolerance, three with impaired glucose tolerance, and two with type 2 diabetes; age 47.5 ± 1.1 years (mean±SEM); body mass index 44 ± 1 kg/m²; HbA(1)c 6.2 ± 0.4%) underwent a 75 g-oral glucose tolerance test with 1 g acetaminophen before and ~6 weeks after LAGB. A small weight reduction was seen after LAGB (125 ± 8 vs. 121 ± 8 kg, P = 0.014). No differences in determinants of gastric emptying were observed before and after LAGB (area under the serum acetaminophen curve 10.1 ± 0.6 vs. 9.8 ± 0.5 mM x 4 h, P = 0.8; peak acetaminophen concentration 62 ± 3 vs. 61 ± 3 μM, P = 0.8; acetaminophen peak time 98 ± 6 vs. 100 ± 6 min, P = 0.9). No differences in plasma glucose, insulin, C-peptide, glucagon, glucose-dependent insulinotropic polypeptide, or glucagon-like peptide-1 responses to the OGTT were observed before as compared to after LAGB. OGTT can be used to evaluate glucose tolerance in obese patients before and after LAGB without bias from changes in gastric emptying. LAGB has no direct impact on incretin hormone secretion.

The effect of nitric oxide inhibitors and Snitroso-Nacetylpenicillamine on glucose concentration in an animal model.

Background:Nitric oxide (NO) is becoming an increasingly important signaling molecule implicated in a growing number of physiological and pathophysiological processes. Research on the effect of NO donors on glucose metabolism in peripheral tissues have grown rapidly in the last decade. This study examined the effects of NGmethyl-L-arginine acetate (L-NMMA) and NGmethyl-L-arginine ester (L-NAME) on fasting and postprandial blood glucose concentrations. The study also investigated if L-NMMA and L-NAME decrease the hyperglycemic effect caused by the NO donor S-nitrosoN-acetylpenicillamine (SNAP) in normoglycemic rats.Results:L-NAME and L-NMMA significantly lowered the postprandial blood glucose concentrations. Mean postprandial blood glucose concentrations in rats treated with L-NAME were 5.04 ± 0.07 mmol/L at 120 min, 4.62 ± 0.19 mmol/L at 150 min and 4.36 ± 0.17 mmol/L at 180 min time points compared with 5.46 ± 0.14 (P = 0.029), 5.20 ± 0.17 mmol/L (P = 0.036), and 4.89 ± 0.14 mmol/L (P = 0.015) at the same time points respectively for saline control. Mean blood glucose concentrations in rats treated with L-NMMA were 4.35 ± 0.23 mmol/L (P = 0.0018) at 120 min, 4.60 ± 0.14 mmol/L (P = 0.090) at 150 min and 3.88 ± 0.16 mmol/L (P 0.001) at 180 min. There were significant differences in mean postprandial blood glucose concentrations in rats treated with SNAP, compared with those treated with L-NAME and SNAP at 90 min (P = 0.012), 180 min (P = 0.013) and 210 min (P < 0.0001). In addition, there were significant differences in mean postprandial blood glucose concentrations in rats treated with SNAP compared with those treated with L-NMMA and SNAP at 90 min (P = 0.0011), 180 min (P = 0.015) and 210 min (P = 0.0077).Conclusion:The nitric oxide synthase [NOS] inhibitors were effective in reducing postprandial blood glucose concentration in rats treated with SNAP. This suggests that although SNAP is an effective antihypertensive agent it decreases glucose tolerance which can be improved by the use of NOS inhibitors such as L-NMMA or L-NAME. These drugs could be beneficial in controlling blood glucose tolerance in rats administered with SNAP, and possibly in humans.

Gum Guar fiber associated with fructose reduces serum triacylglycerol but did not improve the glucose tolerance in rats

IntroductionThe increased intake of dietary fructose can be associated with alterations on energy homeostasis and lipid/carbohydrate metabolism, such as insulin resistance and dislipidemia. On the other hand, the ingestion of soluble fiber gum guar could improve benefic mechanism on glucose tolerance and lipids profile.ObjectiveThe aim of the present study were to investigate the effects of the supplemental feeding partially hydrolyzed gum guar on glucose and lipid homeostasis, in rats fed with fructose solution.MethodsThe study was performed on thirty day-old male Wistar rats randomly assigned into four groups: control(C) or treated with fructose (F-20%), fiber (FB-5%), or fructose plus fiber (F-20% + FB-5% = FF) solution for 30 days on glucose tolerance (OGTT), triacylglycerol concentration in the liver by chloroform/methanol method, glucose, triacylglycerol and total cholesterol serum concentration by assayed by enzymatic colorimetric method, insulin receptor (IR) concentration in the liver by Western Blotting.ResultsThe total body weight gain was not different between groups; in regards of total caloric intake, in the F group was significantly higher and in the FB group was lower than other groups. The triacylglycerol concentration in the liver of FF group was significantly higher than F group, the triacylglycerol concentration in the serum was higher the F group compared with other groups. The OGTT reveal impaired on glucose tolerance in the F, FB, FF compared with C. The IR concentration in the liver was lower in the F, FB, FF compared with C, no significant difference was observed between groups for IR concentration in the gastrocnemius muscle. No significant difference was observed between groups for carcass fat content and serum total cholesterol.ConclusionFructose induced important alterations on glucose tolerance and lipid metabolism, despite of fiber showed reversion of part this alterations. The association fructose plus fiber to seem decrease insulin receptor concentration in the liver, with consequent impair on glucose tolerance.

Characteristics and risk factors for hyperglycemia in Chinese female patients with systemic lupus erythematosus

The aim of the study was to investigate the characteristics and risk factors for hyperglycemia in Chinese female patients with systemic lupus erythematosus (SLE). One hundred and forty-six female SLE patients without a history of diabetes underwent a 75 g oral glucose tolerance test to evaluate glucose tolerance, insulin sensitivity and pancreatic beta cell function. According to the 1999 World Health Organization criteria, all patients were divided into three groups: normal glucose regulation, impaired glucose tolerance and diabetes mellitus. Glucocorticoid doses, insulin sensitivity and pancreatic beta cell function were compared among these groups. Risk factors for hyperglycemia were analyzed by univariate and multi-variate regression analysis. Our results showed that 46 of the 146 female SLE patients (31.5 %) were hyperglycemic, including 21 (14.4%) diabetes mellitus patients and 25 (17.1%) impaired glucose tolerance patients. These female SLE patients with hyperglycemia were characterized by insulin resistance and reduced pancreatic beta cell function, and they were relatively young. Age ≥35 years and high glucocorticoid doses were risk factors for hyperglycemia in Chinese female SLE patients. The prevalence of diabetes mellitus and impaired glucose tolerance are quite high in Chinese female SLE patients. It is suggested that plasma glucose concentration should be monitored regularly and oral glucose tolerance test should be recommended for SLE patients who have risk factors for hyperglycemia.

Systemic hemodynamics in relation to glucose tolerance: the Health 2000 Survey

The influence of impaired glucose metabolism—that is, impaired fasting glucose, impaired glucose tolerance (IGT), and type 2 diabetes mellitus diabetes (DM2)—on systemic hemodynamics is largely unknown. Therefore, we investigated the associations of glucose metabolism disturbances with stroke index (SI), cardiac index, systemic vascular resistance index (SVRI), arterial pulse wave velocity (PWV), and heart rate among Finnish adults (N = 389; mean age, 58.3 ± 7.9 years) participating in the Health 2000 Survey. Systemic hemodynamic parameters were measured using the whole-body impedance cardiography device, and an oral glucose tolerance test (OGTT) was performed to evaluate glucose tolerance status. We found a decreasing trend for SI and increasing trends for SVRI and PWV according to the worsening of glucose tolerance ( P for trend < .003 for all). In pairwise comparisons, SI was lower in the impaired fasting glucose group ( P = .041) and the IGT group ( P < .001) as compared with the normal glucose tolerance (NGT) group. Systemic vascular resistance index was higher in the IGT group ( P = .045) and the DM2 group ( P = .043) than in the NGT group. Subjects with IGT or DM2 had higher arterial PWV (10.7 ± 0.2 m/s, P < .001 and 11.7 ± 0.5 m/s, P = .001, respectively) than subjects with NGT (9.5 ± 0.1 m/s). Moreover, 2-hour glucose in OGTT was an independent determinant of SVRI and PWV ( P < .001 and P = .005, respectively) in multivariable linear regression models. In conclusion, the present study demonstrates that glucose intolerance, even without DM2, associates with several adverse changes in systemic hemodynamics and that 2-hour glucose in OGTT is an independent determinant of SVRI and PWV. These findings support the systematic evaluation of glucose tolerance status in the estimation of cardiovascular risk among the middle-aged population.

The concentrations of branched‐chain amino acids affect glucose tolerance in rats

It has been reported that branched‐chain amino acid (BCAA) administration stimulates glucose uptake into muscles and body glucose oxidation. We examined the effect of plasma BCAA concentrations decreased by the clofibrate treatment on glucose tolerance in rats. Since clofibrate, a drug for hyperlipidemia (high serum triglyceride concentration) is a potent inhibitor of branchedchain alpha‐keto acid dehydrogenase (BCKDH) kinase, the clofibrate treatment activates the BCKDH complex, resulting in promotion of the BCAA catobolism. Male Sprague‐Dawley rats (8weeks of age) were divided into two groups: vehicle and clofibrate (0.2 g/kg BW) treatments 3 h before an intraperitoneal glucose tolerance test (IPGTT). Each group of rats was subdivided into saline and BCAA (0.45 g/kg BW, Val: Leu: Ile = 1:2:1) administration 2 h before IPGTT. Results of IPGTT showed that clofibrate treatment impaired glucose tolerance and that BCAA administration in this group of rats recovered glucose tolerance to the level in the control rats, suggesting that plasma BCAA concentrations play an important role in sustaining the normal glucose tolerance. Activities of hepatic BCKDH complex in each group of rats will be also presented.