Non-insulin-dependent Diabetes Mellitus Rats Research Articles

Effect of SKF96365 on Myocardial Fibrosis in Type-II Diabetic Rats.

Diabetes mellitus type 2 is a risk factor for developing heart failure and myocardial fibrosis, but there is no specific therapy for diabetic heart disease. 1-[2-(4-methoxyphenyl)]-2-[3-(4-methoxyphenyl) propoxy]ethyl-1H-imidazole (SKF96365) is regarded as an inhibitor of receptor-mediated calcium ion (Ca2+) entry. This study aimed to explore the effects of SKF96365 on diabetic myocardial fibrosis. A type 2 diabetic rat model induced by a high-sugar and high-fat diet combined with streptozotocin was established. Thirty specific pathogen-free male Wistar rats were divided randomly into three groups: group A (the blank control group), group B (the diabetes group) and group C (the diabetes + transient receptor potential canonical channel [TRPC] blocker intervention group). Group C was given 0.74-µmol/kg SKF96365 by intraperitoneal injection, and groups A and B were given the same amount of normal saline by intraperitoneal injection. The weight and blood sugar of the rats were monitored. After 12 weeks, the weight of the whole heart and the left ventricle was measured, and the heart and the left ventricular weight ratios were calculated. Haematoxylin-eosin (HE) staining was used to observe pathological changes in the myocardial tissue and the distribution of nuclei. Masson staining was used to identify collagen and muscle fibres, and the myocardial collagen volume fraction (CVF) was calculated. Semi-quantitative reverse transcription-polymerase chain reaction was used to detect the messenger ribonucleic acid (mRNA) expression of SKF96365 target genes. A value of p < 0.05 indicated that the difference between the groups was statistically significant. Compared with the weight of the rats in group A, the weight of those in groups B and C decreased, while blood sugar, whole heart weight and left ventricular weight increased (p < 0.05). There was no significant difference in body weight between the rats in groups B and C (p > 0.05). The HE staining results showed that the arrangement of cardiomyocytes in groups B and C was irregular, and focal necrosis was seen in severe cases. The degree of diabetic cardiomyopathy (DCM) in group C was less severe than that in group B. Masson staining showed that the CVF increased in groups B and C, with group B > group C (p < 0.05); the mRNA expressions of TRPC3 and TRPC6 were upregulated in groups A, B and C, and the mRNA expressions of TRPC3 and TRPC6 in group C were downregulated compared with those in group B (p < 0.05). Compared with the expression levels of SKF96365 target genes (STIM1, Orai1 and Homer1) in group A, those in group B were lower, while the administration of SKF96365 in group C did not affect the expression levels of those genes. SKF96365 can effectively improve myocardial fibrosis in type-II diabetic rats.

Ischemic-Postconditioning Improves Myocardial Injury and Fibrosis Following Ischemia/Reperfusion Injury in Diabetic Rats Pretreated with Alpha-Lipoic Acid

Background: Myocardial ischemia/reperfusion (I/R) injury is one of the pre-eminent causes of death. Prevention of I/R injury in diabetic patients is full of ups and downs. This study has investigated the effect of co-administration of alpha-lipoic acid (ALA) preconditioning and ischemic-postconditioning (Post) on myocardial injury and fibrosis in type-II diabetic rats suffering from I/R injury. Methods: Chronic diabetes was induced by a high-fat supplemented diet and low-dose streptozotocin within 3 months. Diabetic rats received ALA (100 mg/kg/d, orally) for 5 weeks before I/R induction. The myocardium underwent 35 minutes of ischemia through left anterior descending (LAD) coronary artery ligation and 60 minutes of reperfusion. Post was consisted of six cycles of 10/10 seconds algorithm and applied in the early stage of reperfusion. The release of creatine kinase (CK) as the injury enzyme was measured with ELISA. The protein expression of fibrosis markers was evaluated with western blotting and tissue fibrosis was scored through Masson’s trichrome staining. Results: Post alone had no considerable effect on cardiac injury marker CK, while ALA had somehow a positive impact. However, the application of Post in ALA-pretreated rats significantly reduced the injury marker in comparison with the untreated I/R group. In addition, this combination therapy decreased Smad3 and transforming growth factor-β (TGF-β) expression and improved tissue fibrosis as compared with the untreated group. Conclusion: Combination of ALA pretreatment and Post evoked a cardio-protective effect by improving myocardial injury and attenuating fibrosis induced by diabetes. This combined treatment can be recommended as a useful strategy to restore cardio-protection in hearts with diabetic comorbidity.

Proteomic analysis of Substantia nigra proteins in STZ-induced Type-II diabetic rats: A possible link with Parkinson’s disease

Proteomic analysis of Substantia nigra proteins in STZ-induced Type-II diabetic rats: A possible link with Parkinson’s disease

Dehydrozingerone promotes healing of diabetic foot ulcers: a molecular insight.

One of the most common problems of diabetes are diabetic foot ulcers (DFUs). According to National Institute for Health, initial management of DFUs can decrease the complication of limb amputations and can improve the patient's quality of life. DFU treatment can be optimized with the help of multidisciplinary approach. Based on many studies, control of glucose levels in blood, antioxidant activity, reduction in cytokine levels, re-epithelialization, collagen formation, migration of fibroblasts are major phases involved in managing DFU. Dehydrozingerone (DHZ), has been known for its anti-inflammatory, antioxidant and wound healing properties. Three months high-fat dietand low dose of streptozotocin-induced type-II diabetic foot ulcer model was used to evaluate the effectiveness of dehydrozingerone. DHZ was given orally to rats for 15days post wounding. TNF-α, IL-1β and antioxidant parameters like lipid peroxidation, glutathione reductase were estimated. Immunoblotting was done to investigate the effect of DHZ on the expression of ERK, JNK, HSP-27, P38, SIRT-1, NFκB, SMA, VEGF andMMP-9 in skin tissue. Histopathology was performed for analyzing DHZ effect on migration of fibroblasts, formation of epithelium, granulation tissue formation, angiogenesis and collagen formation. DHZ decreased the levels of malondialdehyde, TNF-α, IL-1β and increased glutathione levels in wound tissue. Western blotting results suggested that DHZ activated ERK1/2/JNK/p38 signaling, increased expression of HSP-27, SIRT-1, VEGF, SMA thus facilitating the migration and proliferation of fibroblasts, angiogenesis and decreased inflammation. Masson Trichrome & histopathology showedan increase in collagen, epithelial and granulation tissue formation. DHZ significantly accelerates the healing of diabetic foot ulcers in high fat diet fed pluslow dose streptozotocin induced type-II diabetic Wistar rats.

Alpha-lipoic acid potentiates the anti-arrhythmic effects of ischemic postconditioning in the setting of cardiac ischemia/reperfusion injury in diabetic rats.

Prevention of lethal ventricular arrhythmias induced by myocardial ischemia/reperfusion (I/R) in diabetic patients is the major goal of cardioprotective strategies. Here, we aimed to examine the anti-arrhythmic effect of ischemic postconditioning (IPostC) and alpha-lipoic acid (ALA) in myocardial I/R injury of type-II diabetic rats, focusing on the involvement of connexin-43 and nitric oxide (NO) in this context. Diabetes (duration of 12weeks) was induced by high-fat diet and low dose of streptozotocin in thirty male Wistar rats (12weeks old, 200-250g). After mounting the hearts on the Langendorff apparatus, I/R was induced by the ligation of left anterior descending coronary artery for 35min, and reperfusion for 60min. ALA (100mg/kg/day) was administered orally in diabetic rats for five weeks before I/R. IPostC was applied immediately at early reperfusion. The arrhythmias were evaluated according to the Lambeth convention. Connexin-43 expression and NO levels were assessed by western blotting and Griess calorimetric method, respectively. IPostC could not significantly decrease the number, duration, and incidence of premature ventricular contraction, ventricular tachycardia, and ventricular fibrillation, also the severity of arrhythmias in diabetic hearts. However, IPostC in combination with ALA-preconditioning significantly decreased the above mentioned parameters compared with untreated or monotherapies-received diabetic rats (P < 0.05 to P < 0.001). Furthermore, this combination therapy significantly increased connexin-43 expression and NO levels, compared with untreated diabetic rats (P < 0.01). Preconditioning with ALA restored anti-arrhythmic effect of IPostC in diabetic hearts. Increased connexin-43 expression and NO levels may be the key players in this cardioprotection.

Alpha-lipoic acid preconditioning plus ischemic postconditioning provides additional protection against myocardial reperfusion injury of diabetic rats: modulation of autophagy and mitochondrial function.

Investigating the interaction of diabetes with ischemic postconditioning (IPostC)-associated cardioprotection in myocardial ischemia/reperfusion (I/R) damage is of great clinical importance. The present work was designed to determine the possible synergistic effects of alpha-lipoic acid (LA) preconditioning and IPostC on myocardial I/R damage in type-II diabetic rats through modulating autophagy, and the involvement of mitochondrial function. High-fat diet/low dose of streptozotocin-induced type-II diabetic model with duration of 12 weeks was used in this study. LA (100mg/kg/day) was administered orally in diabetic rats for 5 weeks before I/R. Myocardial I/R was established on Langendorff apparatus through the ligation of left anterior descending coronary artery for 35min, then reperfusion for 60min. IPostC was carried out immediately at the beginning of the reperfusion. At the end of the experiment, myocardial infarct size (IS), autophagy markers at both gene and protein levels, and mitochondrial ROS production and membrane potential were assessed. Combined conditioning with LA and ischemia significantly decreased the IS of diabetic hearts (P < 0.05), however, single therapies had no significant effects. LA in combination with IPostC more significantly decreased LC3 and p62 mRNA levels (P < 0.01), and LC3II/LC3I and p62 protein levels (P < 0.01). Also, this combined therapy decreased mitochondrial ROS generation and membrane depolarization (P < 0.01). Pretreatment with LA in diabetic rats notably restored cardioprotection by IPostC via modulating autophagy and restoring mitochondrial function. This combined conditioning might be an effective strategy to diminish I/R damage in diabetic hearts.

Flexible Ultrasonic Patch for Accelerating Chronic Wound Healing.

Ultrasound treatment is an effective method for accelerating chronic wound healing. However, it is not widely used because traditional ultrasonic probes cannot be conformal to the wound surface, which leads to limitations of use and unstable treatment effects. In addition, the use of liquid coupling agent increases the chance of wound infection. A strategy is proposed to design and fabricate a flexible ultrasonic patch for treating chronic wounds effectively. The piezoelectric ceramic in the patch is discretized into several linearly arranged units, which are integrated on a flexible circuit substrate. A thin hydrogel patch is used as both encapsulation and coupling layer to avoid wound infection and ensure the penetration of ultrasound. The ultrasonic patch is soft, light, and can completely conform to the treatment area. Bending of the patch focuses the sound beams on the center of the bending circle, which achieves control of the target treatment area. Ultrasound treatment experiments are carried out on some type-II diabetic rats. Immunohistochemical (IHC) results indicate that ultrasound accelerates wound healing by activating Rac1 in both dermal and epidermal layers. Treatment results show that wound treated with the ultrasound heals faster than wounds without. The healing time is shortened by ≈40%.

Preparation of Nanocomposite Peptide and Its Inhibitory Effect on Myocardial Injury in Type-II Diabetic Rats.

Complications of diabetes are the main cause of death and disability in diabetic patients. Cardiovascular diseases, especially diabetic cardiomyopathy, are one of the major complications and causes of death in type 2 diabetes. Peptide drugs have a better effect on improving cellular oxidative damage, reducing tissue inflammation and inhibiting intracellular calcium overload. The application of nanotechnology to the preparation of peptide drugs and myocardial injury can effectively improve myocardial stun, arrhythmia and myocardial systolic dysfunction in patients with type 2 diabetes. The use of nanotechnology to develop more stable Glucagon-like peptide 1 analogues or sustained-release preparations, improve patient compliance and improve the efficacy of diabetes, is of great significance for the prevention and treatment of diabetic cardiomyopathy. Therefore, this study used nanotechnology to prepare PLGA-GLP-1 nanoparticles using polyglycolic acid glycolic acid as a drug carrier, which achieved long-acting drug and its morphology by transmission electron microscopy. At the same time, this study explored the anti-cardiomyocyte injury and anti-myocardial damage of PLGA-GLP-1 nanocomposite peptide and its molecular mechanism by using animal models and cell models. Experimental studies have shown that PLGA-GLP-1 nanocomposite peptide has a protective effect on myocardial injury in diabetic rats. Its mechanism is related to the PLGA-GLP-1 nanocomposite peptide enhancing the body's antioxidant capacity, anti-cardiomyocyte apoptosis, and promoting mitochondrial DNA repair in cardiomyocytes.

Antihyperglicemic and Antioxidant Potential of Aloe vera Juice Supplementation in the Type-II Diabetic Rats Model

To evaluate the potential effects of Aloe vera supplementation on blood glucose and antioxidant enzymes (Glutathione peroxidase, GPx; Superoxide dismutase, SOD) as well as lipid peroxides (Malondialdehyde, MDA) in the kidneys of experimental type-II Diabetic rats model. This was an experimental study with post-test only control group study design. Type-II diabetes rats were induced by streptozotocin (60 mg/kg, ip) and nicotinamide (230 mg/kg, ip) to Wistar rats. The diabetic rats were randomized into three groups, as follows: (i) Diabetic control rats (received CMC-Na 1 % vehicle only); (ii). Diabetic rats received glibenclamide 0,18 mg/200g orally once daily; (iii) diabetic rats group received glibenclamide (0,18 mg/200g body weight) as well as Aloe vera juice supplementation (3,6 mL/200 g body weight) orally once daily for 30 days. Rats fasted over night and the blood was withdrawn by retro-orbital puncture under light ether anesthesia on the pre-induction and 1st, 7th, 14th and 28th post induction to determine blood glucose. The kidney tissues of rats were taken under anesthesia at the end of 30 days. In the third group showed the decrease of blood glucose level significantly (p

Abstract TMP32: Ischemic Stroke Causes Vascular Regression in Type-II Diabetic Male Rats: Potential Role of Regulated Cell Death Mechanisms

Diabetes not only increases the risk of stroke, it also worsens recovery after stroke. We previously showed that ischemic stroke causes cerebral vasoregression that is associated with poor outcomes in a lean model of diabetes. Current experiments were designed to 1) study the effect of ischemic stroke on cerebral vasculature in male and female rats using a diet-induced model of diabetes, and 2) identify mechanisms involved in vascular regression. Methods: Diabetes was induced in male and female Wistar rats using high fat diet and low dose of streptozotocin. After 8 weeks of diabetes animals were subjected to embolic stroke or sham surgeries. After 14 days of stroke, vascular indices (vascular volume, surface area and branch density) were measured in cortex and striatum of both hemispheres using confocal images of FITC filled brain sections. Regulated cell death markers (necroptosis and ferroptosis) were tested in brain sections by immunohistochemistry. Results: In male animals, diabetes alone promoted pathological vascularization. There was an interaction such that stroke increased vascular volume and branch density in control rats while decreasing it in diabetes in both ipsilateral and contralateral side. However, in females, diabetes did not impact vascularization with the exception that branch density was decreased in ipsilateral cortex. Cell death markers of necroptosis (TLR-4) and ferroptosis (IREB2, citrate synthase) were upregulated in male diabetic animals. Conclusions: Ischemic stroke impairs cerebral vasculature in diabetic male animals and it was associated with upregulation of newly described regulated cell death pathways.

Evaluation of 4-methyl-2-[(2-methylbenzyl) amino]-1,3-thiazole-5-carboxylic acid against hyperglycemia, insulin sensitivity, and oxidative stress-induced inflammatory responses and β-cell damage in the pancreas of streptozotocin-induced diabetic rats.

4-Methyl-2-[(2-methylbenzyl) amino]-1,3-thiazole-5-carboxylic acid (bioactive compound (BAC)), a novel thiazole derivative, is a xanthine oxidase inhibitor and free radical scavenging agent. Effects of BAC on hyperglycemia, insulin sensitivity, oxidative stress, and inflammatory mediators were evaluated in streptozotocin (STZ)-induced neonatal models of non-insulin-dependent diabetes mellitus (NIDDM) rats where NIDDM was induced in neonatal pups with single intraperitoneal injection of STZ (100 mg/kg). The effect of BAC (10 and 20 mg/kg, p.o.) for 3 weeks was evaluated by the determination of blood glucose, oral glucose tolerance test (OGTT), HbA1c level, insulin level, insulin sensitivity, and insulin resistance (IR). Furthermore, inflammatory mediators (tumor necrosis factor-alpha and interleukin-6) and oxidative stress were estimated in serum and pancreatic tissue, respectively. Significant alteration in the level of blood glucose, OGTT, HbA1c, insulin level, insulin sensitivity, in addition variation in the antioxidant status and inflammatory mediators, and alteration in histoarchitecture of pancreatic tissue confirmed the potential of BAC in STZ-induced neonatal models of NIDDM rats. Pretreatment with BAC restored the level of glucose by decreasing the IR and increasing the insulin sensitivity. Furthermore, BAC balanced the antioxidant status and preserved the inflammatory mediators. Histological studies of pancreatic tissues showed normal architecture after BAC administration to diabetic rats. Altogether, our results suggest that BAC successfully reduces the blood glucose level and possesses antioxidant as well as anti-inflammatory activities. This leads to decreased histological damage in diabetic pancreatic tissues, suggesting the possibility of future diabetes treatments.

Potential invivo antidiabetic activity of “aavari kudineerformulation” (akf) in normal and streptozotocin Induced type-ii diabetic rats

The present study demonstrates that “Aavarai Kudineer formulation” (AKF) exhibits promising antidiabetic activity and help to maintain good glycemic and metabolic control. The herbal formulation, AKF elicit hypo-glycaemic and antidiabetic effects in both normal and Streptozotocin (STZ) induced type- II hyperglycemic rats. The herbal formulation under acute toxicity studies shows, it is non toxic upto 2000mg/kg/BW. It is possible that the herbal formulation may act through both, pancreatic and extrapancreatic mechanism(s). This Aavarai Kudineer formulation elicited a significant antidiabetic effect in Streptozotocin induced diabetic rats as reflected by its ability to inhibit lipid peroxidation and to elevate the enzymatic antioxidants in pancreatic tissue. This extract showed improvement in parameters like body weight, food consumption, organ weight and biochemical parameters and might be of great valuable in diabetic treatment. The histopathological studies during 28 days long term treatment have shown to ameliorate the Streptozotocin induced histological damage of Islets of Langerhans. Moreover the inhibitory effects on biochemical and histological parameters induced by herbal formulation at a dose of 500mg/kg were almost comparable to that of standard drug, Glibenclamide (5mg/kg).

In vitro and in silico PTP-1B inhibition and in vivo antidiabetic activity of semisynthetic moronic acid derivatives

Six derivatives (1–6) of moronic acid were semi-synthesized and their in vitro protein tyrosine phosphatase 1B (PTP-1B) inhibition activity assessed. Derivatives 2 (IC50=10.8±0.5μM) and 6 (IC50=7.5±0.1μM) displayed the most potent inhibitory activity. Therefore, they (50mg/Kg) were tested for their antidiabetic effect in vivo using a non-insulin dependent diabetes mellitus rat model. The results indicated that they decrease plasma glucose levels during all the experiment (p <0.05). Docking analysis of 2 and 6 with PTP-1B orthosteric site A and allosteric site B, showed that 2 had polar and Van der Waals interactions in both sites with Val49, Gln262, Met258, Phe182, Ala217, Ile219 and Gly259, displaying more affinity for site A. Compound 6 showed polar interaction with Gln262 and Van der Waals with Val49, Ile219, Gly259, Arg254, Ala27, Phe52, Met258, Asp48 and Phe182, suggesting that the potential binding site is localized in site B, close to the catalytic site A. Therefore, derivatives 2 and 6 have potential for the development of antidiabetic agents.

P162Sitagliptin reduces fatty-acids uptake in detriment of glucose in experimental type-II diabetic hearts

Objective: To study the effect of sitagliptin on glucose and fatty-acids uptake in the myocardium of type-II diabetic rats. Background: The energy source in the heart shifts from fatty-acids to glucose after damage. However, fatty-acids are used as the only substrate available in the diabetic myocardium. Sitagliptin improves hyperglycemia and insulin resistance, but it is unknown whether it could influence the cellular transporters for both glucose and fatty-acids. Methods: Non-obese, non-hypertensive type-II diabetic rats (Goto-Kakizaki; GK) were treated with sitagliptin (10 mg/kg/day) or vehicle. A group of wistar rats were used as control. (N=10 rats, each). After 20 weeks, cardiac structure and function were measured by Echo-Doppler, and glucose uptake was examined by positron emission tomography (PET). Then, hearts were isolated and processed for protein and RNA extracts. Plasmas were used to evaluate metabolic parameters. Results: GK rats developed hyperglycemia (452 vs. 208 mg/dl, for GK and wistar, respectively. p<0.01), cardiac hypertrophy (0.22 vs. 0.19 mm left ventricular posterior wall thickness, for GK and wistar, respectively. p<0.05), and diastolic dysfunction (36.16 vs. 33.72 ms decceleration time, and 1.05 vs. 1.39 E/A ratio. p<0.05). GK exhibited also a reduction in the left ventricular diastolic diameter (LVDD; 0.61 vs. 0.8 mm. p<0.05), and left ventricular systolic diameter (LVSD; 0.28 vs. 0.53 mm. p<0.05), without significant changes in ejection fraction. In addition, GK rats showed a reduced myocardial glucose uptake (~30%) mainly in basal and middle regions of the heart, and the expression and translocation of Glut4 (a glucose transporter), in favor of FAT/CD36 (a fatty-acid transporter). Interestingly, sitagliptin treatment attenuated hyperglycemia (382 mg/dl), increased LVDD (0.73 mm) and LVSD (0.43 mm), reduced the decceleration time (31.1 ms), and elevated E/A ratio (1.2). Furthermore, sitagliptin increased glucose uptake and Glut4 translocation to the sarcolema (p<0.05). Conclusions: Sitagliptin could improve cardiac function in type-II diabetes by increased glucose uptake and reduced fatty-acids uptake, and their respective cellular receptors.

Recombinant keratinocyte growth factor 1 in tobacco potentially promotes wound healing in diabetic rats.

Keratinocyte growth factor 1 (KGF1) is a growth factor that promotes epidermal cell proliferation, migration, differentiation, and wound repair. It is expressed at low levels in a form of inclusion body in E. coli. In order to increase its expression and activity, we produced tobacco plants expressing KGF1 via Agrobacterium-mediated transformation using a potato virus X (PVX)-based vector (pgR107). The vector contained the sequence encoding the KGF1 gene fused with a green florescence protein. The recombinant plasmid was introduced into leaf cells of Nicotiana benthamiana (a wild Australian tobacco) via Agrobacterium-mediated agroinfiltration. As determined by fluorescence and Western blot of leaf extracts, the KGF1 gene was correctly translated into the tobacco plants. The recombinant KGF1 was purified from plant tissues by heparin affinity chromatography, and cell proliferation in NIH/3T3 cells was stimulated by the purified KGF1. The purified KGF1 was also applied to the wounds of type-II diabetic rats. KGF1 had accumulated to levels as high as 530 μg/g fresh weight in the leaves of agroinfected plants. We show that plant-derived KGF1 can promote the proliferation of NIH/3T3 cells and have significant effects on the type-II diabetic rat. The present findings indicated that KGF1 from tobacco maintains its biological activity, implying prospective industrial production in a plant bioreactor.

Study of the Hypoglycemic Effect of Tamarindus indica Linn. Seeds on Non-Diabetic and Diabetic Model Rats

Aim: The present study was undertaken to evaluate the antidiabetic effects of the Tamarindus indica Linn seed in normal (non-diabetic), type-I and type-II model rats and to investigate their effect on gastrointestinal motility and intestinal glucose absorption. Methodology: T. indica seed powder was used at a dose of 1.25g/kg bw/10 ml water. Male Long-Evans rats (160-210g body weight) were used for the experiment. Experiments were done in non-diabetic and streptozotocin-induced diabetic model rats with a single feeding in different prandial states and blood was collected. An intestinal perfusion technique was used to study the effects of T. indica seed powder on intestinal glucose absorption in normal and type-II model rats. Gut motility was evaluated using barium sulfate milk. Glucose was measured by Glucose oxidase-peroxidase (GOD-POD) method. Result: The screening results showed that T. indica seed powder had no effect on fasting or postprandial serum glucose level of normal and type-I diabetic rat. The seed powder also showed no hypoglycemic effect in the fasting state and no antihyperglycemic effect in type-II model rats when fed simultaneously with oral glucose load, but it exhibited significant antihyperglycemic effect when the seed powder was fed 30 minutes prior to the glucose load at 105 minutes (p&lt;0.03). Glibenclamide significantly lowered postprandial serum glucose levels of non-diabetic and type-II diabetic model rats (p&lt;0.02-0.001). T. indica exerted inhibition on glucose absorption in type-II rats during the whole perfusion period when compared with control. On the other hand, T. indica seed powder significantly inhibited the gastrointestinal motility in type-II rats. Conclusion: The present data suggest that T. indica possesses antihyperglycemic properties in type-II rats which are at least partly due to its inhibitory effect on intestinal glucose absorption. This effect cannot be attributed to the acceleration of intestinal transit.

Effects of Shaddock (Citrus maxima) Fruit Juice on Glucose Tolerance and Lipid Profile in Type-II Diabetic Rats

Cirus maxima commonly known as Shaddock has been proved for hypoglycaemic effects. The objective of the present study was to evaluate the effects of Shaddock (C.maxima) fruit juice on glucose tolerance and lipid profile in streptozotocin (STZ) induced type-II diabetic rat. Two days old neonatal pups (7-10 g) were used and they were made diabetic by intraperitoneally (i.p.) injection of 90 mg/kg STZ in citrate buffer solution. Different groups of animals were treated by 25% and 50% Shaddock fruit juice (SFJ) for 8 weeks. After 8 weeks treatment biochemical parameters from blood serum were analyzed. The significant differences of glucose, cholesterol, HDL, LDL, triglyceride, in 50% SFJ treated group compare to diabetic group were found. Therefore we conclude from this present study that Shaddock fruit juice has beneficial effects on glucose tolerance and lipid profile in streptozotocin-induced type-II diabetic rat.

Antidiabetic activity of Pseudarthria viscida aqueous root extract in neonatal streptozotocin-induced NIDDM rats

The antidiabetic activity of the aqueous root extract of Pseudarthria viscida (L.) Wight & Arn., Fabaceae, was investigated in normal and neonatal streptozotocin (n2-STZ)-induced non insulin-dependent diabetes mellitus (NIDDM) rats and compared with glibenclamide as a reference standard. Two different doses (250 and 500 mg/kg) of the extract were administered to normal and experimental diabetic rats for 21 days. Fasting blood glucose levels, serum lipid profiles and changes in body weight were evaluated in normal and diabetic rats while serum insulin, glycated hemoglobin, urea, creatinine, magnesium, protein, albumin and glycogen, glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate dehydrogenase (LDH) levels in kidney and liver were evaluated additionally in diabetic rats. Treatment with extract at both dose levels was found to exhibit antidiabetic activity, with the higher dose showing more significant activity.

Protective effect of Luffa acutangula extracts on gastric ulceration in NIDDM rats: Role of gastric mucosal glycoproteins and antioxidants

ObjectiveTo study the comparative gastroprotective effect of Luffa acutangula methanolic extract (LAM) and aqueous extract (LAW) on type II diabetes rats. MethodsStreptozotocin (65 mg/kg, i.p.) along with nicotinamide (120 mg/kg, i.p.) was used to induce non insulin dependent diabetes mellitus (NIDDM) in rats. A daily oral dose of aspirin (200 mg/kg, i.p.) was administered for initial seven days to induce gastric ulcerations in the diabetic rats. LAM and LAW were administered orally in the doses of 100, 200 and 400 mg/kg once daily for 21 days. Glibenclamide and ranitidine were used as standards for comparing the antidiabetic and antiulcer effect respectively. ResultsLAM significantly (P<0.01) increased mucosal glycoprotein and antioxidant enzyme level in gastric mucosa of diabetic rats than LAW (P <0.05). LAM was efficient in reversing the delayed healing of gastric ulcer in diabetic rats close to the normal level. LAM exhibited better ulcer healing effect than glibenclamide and LAW, because of its both antihyperglycemic and mucosal defensive actions. ConclusionsThus, LAM is proved to be a better alternative for treating gastric ulcers co-occurring with diabetes.

Carioprotective Effects of Lisinopril in Streptozotocin Induced Type-II Diabetic Rats

Carioprotective Effects of Lisinopril in Streptozotocin Induced Type-II Diabetic Rats