Effect Of Experimental Diabetes Research Articles

Demonstration of antidiabetic effect of Asiatic Acid in streptozotocin induced diabetic rat

Diabetes mellitus is one of most prominent disorder among others spreading at an alarming rate across the globe. The quest to obtain a potential active ingredient for antidiabetic activity is on. The present study was designed to examine the antidiabetic effect of asiatic acid (AA) in streptozotocin (STZ) induced diabetic rats. Diabetes was induced in male Wistar rats by a single intraperitoneal injection of STZ (40 mg/kg body weight). Diabetic rats show increased plasma glucose, total cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low-density lipoprotein and decreased insulin and high-density lipoprotein in diabetic rats. The antidiabetic effect of AA was compared with glibenclamide, a well-known antihyperglycemic drug. In conclusion, this study indicates that AA showed antidiabetic effect in experimental diabetes.

The effect of experimental diabetes and membrane occlusiveness on guided bone regeneration: A proof of principle study.

To evaluate the effect of membrane occlusiveness and experimental diabetes on early and late healing following guided bone regeneration. A total of 30 Wistar rats were randomly allocated to three groups: healthy (H), uncontrolled diabetic (UD) and controlled diabetic (CD). A critical size calvarial defect (CSD) was created at the mid-portion of one parietal bone, and it was treated with a double layer of e-PTFE membrane presenting 0.5mm perforations. The animals were killed at 7 and 30days of healing, and qualitative and quantitative histological evaluations were performed. Data were compared with the ones previously obtained from other 30 animals (10H, 10UD, 10 CD), where two CSDs were randomly treated with a double-layer e-PTFE occlusive membrane or left empty. Following application of cell occlusive or cell permeable membranes, significant regeneration can be observed. However, at 30days in the H group occlusive compared to cell permeable membranes promoted enhanced bone regeneration (83.9 ± 7.3% vs. 52.5 ± 8.6%), while no significant differences were observed within the CD and UD groups. UD led to reduced regeneration compared to H when an occlusive barrier was applied, whereas comparable outcomes to H and CD were observed when placing perforated membranes. The application of cell permeable membranes may have masked the potentially adverse effect of experimental UD on bone regeneration. Membrane porosity might contribute to modulate the bone regenerative response in UD conditions. Future studies are needed to establish the degree of porosity associated with the best regenerative outcomesas well as the underlying molecular mechanisms.

Retraction: The Role of Allograft Inflammatory Factor-1 in the Effects of Experimental Diabetes on B Cell Functions in the Heart.

[This retracts the article DOI: 10.3389/fcvm.2018.00126.].

Mitochondrial Antioxidant SkQ1 Has a Beneficial Effect in Experimental Diabetes as Based on the Analysis of Expression of microRNAs and mRNAs for the Oxidative Metabolism Regulators.

Diabetes mellitus and related complications are among the most important problems of the world-leading healthcare systems. Despite their priority, molecular and genetic aspects of diabetes pathogenesis are poorly understood; however, the involvement of oxidative stress in this process is undoubted. Rats with experimental diabetes induced by the intraperitoneal injection of alloxan were subjected to the antioxidant pre-therapy with a series of mitochondria-targeted 10-(6’-plastoquinonyl)decyltriphenylphosphonium (SkQ1) injections and analyzed for the expression of mRNAs and microRNAs by real-time quantitative polymerase chain reaction to identify potential predictors of diabetes. Animals that received SkQ1 before diabetes induction demonstrated lower blood glucose levels compared to the diabetic animals not subjected to the therapy. SkQ1 caused changes in the mRNA levels of genes involved in the cellular defense against free radicals, which indicates a beneficial effect of the pre-therapy. Moreover, similar changes were observed on the epigenetic level, as the microRNA expression patterns not only proved the SkQ1 efficacy but also correlated with the expression levels of their mRNA targets. Oxidative stress and macromolecule damage by free radicals are determining factors in diabetes, which suggests that strategies aimed at restoring the antioxidant status of the cell can be beneficial. Mitochondria-targeted antioxidant SkQ1 demonstrates positive effects on several levels, from the normalization of the blood glucose content to genetic and epigenetic changes. Our results can serve as a basis for the development of novel therapeutic and diagnostic strategies.

Can melatonin correct the negative effect of experimental diabetes created during the maternal period on fetal rat development and puppies cognitive functions?

Can melatonin correct the negative effect of experimental diabetes created during the maternal period on fetal rat development and puppies cognitive functions?

Dipeptidyl peptidase IV Inhibitory activity of Terminalia arjuna attributes to its cardioprotective effects in experimental diabetes: In silico, in vitro and in vivo analyses

BackgroundThe marketed synthetic (Dipeptidyl peptidase-IV) DPP-IV Inhibitors are expensive antidiabetic drugs and have been reported to cause unacceptable adverse effects such as pancreatitis, angioedema, thyroid and pancreatic cancers. In this scenario research to develop novel DPP-IV Inhibitors from alternative sources is the need of the hour. Hypothesis/purposeTerminalia arjuna, a medicinal herb with antidiabetic and cardioprotective activities may represent a natural DPP-IV Inhibitor, the DPP-IV Inhibitory activity of which may translate into demonstrable therapeutic benefits in setting of diabetes with cardiovascular co-morbidities. Study designThe study type used for the present study was an experimental (In vitro, In vivo and In silico) design. MethodThe DPP-IV Inhibitory, antidiabetic and cardioprotective effects of Terminalia arjuna was evaluated in the experimental model of myocardial infarction co-existing with diabetes. To determine the active principle of Terminalia arjuna responsible for DPP-IV Inhibitory activity, the crystal structure of DPP-IV was considered as receptor which was docked against Arjunetin, Arjungenin, Arjunic acid, Arjunone, Ellagic acid, Gallic acid, Sitagliptin and Vildagliptin. The binding sites as well as affinity of various active ingredients of Terminalia arjuna for DPP- IV enzyme was elucidated using in silico studies and compared to Vildagliptin. ResultsTerminalia arjuna demonstrated significant DPP-IV Inhibitory, antidiabetic (significant reduction in HbA1C) and cardioprotective effects (restoration of myocardial CPK-MB) in the experimental model of myocardial infarction co-existing with diabetes. The cardioprotective efficacy correlated to its DPP-IV Inhibitory activity. The active ingredients of Terminalia arjuna (Arjunetin, Arjungenin, Arjunic Acid Arjunone, Ellagic acid and Gallic acid) demonstrated significant inhibition of DPP-IV enzyme. Arjunic acid and Arjunone prefers the active site pocket of DPP-IV enzyme. Compounds like Arjunetin and Vildagliptin prefers to bind near the interface region of the DPP-IV as their biological active forms are homodimer. Sitagliptin binds near the α/β hydrolase domain. ConclusionThe DPP-IV Inhibitory activity of Terminalia arjuna was found to be comparable to Vildagliptin. The DPP-IV Inhibitory activity translated into significant cardioprotective effects in the setting of diabetes. The active ingredient of Terminalia arjuna; Arjunetin, Arjungenin, Ellagic acid and Arjunic acid showed superior DPP-IV Inhibitory activity as compared to synthetic DPP-IV inhibitors (Sitagliptin and Vildagliptin) based on results of docking studies.

The Role of Allograft Inflammatory Factor-1 in the Effects of Experimental Diabetes on B Cell Functions in the Heart.

Diabetes mellitus (DM) often causes chronic inflammation, hypertrophy, apoptosis and fibrosis in the heart and subsequently leads to myocardial remodeling, deteriorated cardiac function and heart failure. However, the etiology of the cardiac disease is unknown. Therefore, we assessed the gene expression in the left ventricle of diabetic and non-diabetic mice using Affymetrix microarray analysis. Allograft inflammatory factor-1 (AIF-1), one of the top downregulated B cell inflammatory genes, is associated with B cell functions in inflammatory responses. Real-time reverse transcriptase-polymerase chain reaction confirmed the Affymetrix data. The expression of CD19 and AIF-1 were downregulated in diabetic hearts as compared to control hearts. Using in vitro migration assay, we showed for the first time that AIF-1 is responsible for B cell migration as B cells migrated to GFP-AIF-1-transfected H9C2 cells compared to empty vector-transfected cells. Interestingly, overexpression of AIF-1 in diabetic mice prevented streptozotocin-induced cardiac dysfunction, inflammation and promoted B cell homing into the heart. Our results suggest that AIF-1 downregulation inhibited B cell homing into diabetic hearts, thus promoting inflammation that leads to the development of diabetic cardiomyopathy, and that overexpression of AIF-1 could be a novel treatment for this condition.

Calcitonin and Omega–3 Fatty Acids Exhibit Antagonistic and Non-Additive Effects in Experimental Diabetes

Because optimising therapy for the management of diabetes mellitus remains challenging, the study investigated the effects of salmon calcitonin (Sct) and/or omega-3 fatty acids (N-3 – eicosapentaenoic acid and docosahexaenoic acid-3:2), compared to metformin, on selected biochemical parameters in male Wistar rats, in an experimental model of diabetes. Forty rats were used for this study. They were divided into eight groups of five rats each, which included: Normal control; Diabetic (D) control; D + N-3; D + low dose Sct (Sct. Lw); D + high dose Sct (Sct. Hi); D + N-3 + Sct.Lw; D + N-3 + Sct.Hi; and D + metformin. Diabetes was induced in overnight fasted rats by the administration of streptozotocin (65 mg/kg b.w., i.p.), 15 min after the administration of nicotinamide (110 mg/kg b.w., i.p.). Nine days later, Sct was administered at 2.5 and 5.0 IU/kg b.w./day (i.m.), while N-3 and metformin were administered at 200 and 180 mg/kg b.w./day (p.o.) respectively, for four weeks. Sct, N-3, and metformin significantly reduced total cholesterol, LDL-C, cortisol, c-telopeptide of type 1 collagen, and collagen type 2 alpha-1. The combined administration of Sct and N-3 had more favorable effects on triglyceride and HDL-C than either monotherapy. Unlike metformin and Sct. Hi, N-3 significantly reduced alkaline phosphatase activity. Moreover, N-3 significantly suppressed the hypocalcaemic, hyperglycaemic, and insulin resistance provoking actions of Sct. Furthermore, N-3 contradicted the hepatic glycogen depletion and inhibition of nitric oxide synthesis brought about by Sct. In conclusion, N-3 demonstrated antagonistic and non-additive actions with Sct. Moreover, the effects of the combined administration of Sct and N-3 were comparable to that of metformin; therefore, they might be considered as therapeutic alternatives in diabetes.

Rosemary (Rosmarinus officinalis) essential oil components exhibit anti-hyperglycemic, anti-hyperlipidemic and antioxidant effects in experimental diabetes

IntroductionThe present study aims to investigate the protective effects of Rosemary (Rosmarinus officinalis L.) essential oils (ROEO) against alloxan-induced diabetes and oxidative stress in rats. MethodsThe animals were divided into four groups: Healthy Control (HC); Diabetic Control (DC); Healthy+ROEO (H+ROEO) and Diabetic+ROEO (D+ROEO). ResultsThe use of GC/MS technique has allowed us to identify fifteen compounds in ROEO. We have found that alloxan administration induced hyperglycaemia, lipid metabolic parameters deregulation as well as liver and kidney dysfunctions. Alloxan administration has also induced an oxidative stress status as assessed by malondialdehyde (MDA) content increase, thiol groups (−SH) level decrease and antioxidant enzyme activities depletion such as catalase (CAT), total superoxide dismutase (SOD), Cu/Zn-SOD, Mn-SOD and Fe-SOD in both liver and kidney tissues. More importantly subacute (15days) ROEO administration has significantly corrected all biochemical alterations induced by alloxan intoxication. ConclusionsWe propose that Rosmarinus officinalis essential oils exhibit protective effects in alloxan-induced hyperglycaemia as well as protecting against liver and kidney oxidative stress in rats, reflecting its antioxidant properties.

Obestatin as a key regulator of metabolism and cardiovascular function with emerging therapeutic potential for diabetes.

Obestatin is a 23-amino acid C-terminally amidated gastrointestinal peptide derived from preproghrelin and which forms an α helix. Although obestatin has a short biological half-life and is rapidly degraded, it is proposed to exert wide-ranging pathophysiological actions. Whilst the precise nature of many of its effects is unclear, accumulating evidence supports positive actions on both metabolism and cardiovascular function. For example, obestatin has been reported to inhibit food and water intake, body weight gain and gastrointestinal motility and also to mediate promotion of cell survival and prevention of apoptosis. Obestatin-induced increases in beta cell mass, enhanced adipogenesis and improved lipid metabolism have been noted along with up-regulation of genes associated with beta cell regeneration, insulin production and adipogenesis. Furthermore, human circulating obestatin levels generally demonstrate an inverse association with obesity and diabetes, whilst the peptide has been shown to confer protective metabolic effects in experimental diabetes, suggesting that it may hold therapeutic potential in this setting. Obestatin also appears to be involved in blood pressure regulation and to exert beneficial effects on endothelial function, with experimental studies indicating that it may also promote cardioprotective actions against, for example, ischaemia-reperfusion injury. This review will present a critical appraisal of the expanding obestatin research area and discuss the emerging therapeutic potential of this peptide for both metabolic and cardiovascular complications of diabetes.

The effect of reamberin and alpha-lipoic acid on the tolerance to acute cerebral ischemia in experimental diabetes mellitus

To study an effect of reamberin and α-lipoic acid (α-LA) on the tolerance of mice with experimental diabetes mellitus (DM) to acute cerebrovascular accident (ACVA) in mice experiments. The authors studied mice with alloxan diabetes and subtotal and total brain ischemia. In additional experimental series, an effect of reamberin and α-lipoic acid on the tolerance to acute hypoxic hypoxia and intensity of hyperglycemia in experimental DM was studied. The increased vulnerability of animals to ACVA due to hyperglycemia and increased sensitivity to acute hypoxic hypoxia was established. Reamberin and α-lipoic acid administered for 14 days in doses, which are equivalent to therapeutic range in humans, enhance the tolerance to ACVA and acute hypoxic hypoxia in mice with alloxan diabetes. These medications also decrease the intensity of hyperglycemia during concurrent insulin replacement therapy. The increased tolerance to ACVA in mice with alloxan diabetes caused by reamberin and alpha-lipoic acid is associated with an antihypoxic effect of these medications and does not depend on their effect on the intensity of hyperglycemia. Reamberin outperformed α-lipoic acid in the antihypoxic activity, protection against ACVA and the rate of onset of glucose reducing effect in experimental diabetes mellitus.

Effect of experimental diabetes and insulin replacement on intestinal metabolism and excretion of 4-nitrophenol in rats.

Luminal appearance of 4-nitrophenol (PNP) metabolites (4-nitrophenol-β-glucuronide (PNP-G) and 4-nitrophenol-sulfate (PNP-S)) and activity of the related metabolic enzymes have been investigated in control and experimental diabetic rats. Experimental diabetes was induced by administration of streptozotocin (65 mg/kg i.v.). PNP (500 μmol/L) was luminally perfused in the small intestine and the metabolites were determined in the perfusion solution. Effect of insulin replacement was also investigated in the diabetic rats. It was found that experimental diabetes increased the luminal appearance of PNP-G, which could be completely compensated by rapid-acting insulin administration (1 U/kg i.v.). Activities of the enzymes involved in PNP-G production (UDP-glucuronyltransferase and β-glucuronidase) were also elevated; however, these changes were only partially compensated by insulin. Luminal appearance of PNP-S was not significantly changed by administration of streptozotocin and insulin. Activities of the enzymes of PNP-S production (sulfotransferases and arylsulfatases) did not change in the diabetic rats. The results indicate that experimental diabetes can provoke changes in intestinal drug metabolism. It increased intestinal glucuronidation of PNP but did not influence sulfate conjugation. No direct correlation was found between the changes of metabolic enzyme activities and the luminal appearance of the metabolites.

The effects of fish oil emulsion supplementation on synaptosomal membrane enzyme activities in diabetic rats: Protective effect on K+‐paranitrophenylphosphatase activity only in non‐diabetic rats but no significant influence on Na+/K+‐ATPase activity

This study evaluated the effect of fish oil emulsion supplementation (rich in ω‐3 fatty acids) on synaptosomal Na+,K+‐ATPase and K+‐dependent‐paranitrophenyl phosphatase (K+‐pNPPase) activities in diabetic rats. Diabetes mellitus was induced in 36 rats by injection of streptozotocin (STZ) via the tail vein at a dose of 45 mg/kg of body weight. After 7 days, animals were randomly divided into six groups according to the administration and doses of the fish oil emulsion: (1) control rats, (2) untreated diabetic rats, (3) control rats treated with the 45% fish oil emulsion at a dose of 160 mg/kg/day, (4) control rats treated with a dose of 800 mg/kg/day, (5) diabetic rats treated with the fish oil emulsion at a dose of 160 mg/kg/day, and (6) diabetic rats treated with a dose of 800 mg/kg/day. The composition of fish oil emulsion was: 8.1% eicosapenthaenoic acid (EPA, 20:5, ω‐3), 5.9% DHA (22:6, ω‐3). We found a non‐significant 26% reduction of Na+,K+‐ATPase activity (0.724 nkat/mg vs. 0.974 nkat/mg proteins) and no change in K+‐pNPPase activity in diabetic synaptosomes vs. control group. 7‐wk fish oil supplementation indicated a non‐significant restoration of Na+,K+‐ATPase activity in diabetic synaptosomes compared to untreated diabetic group. In addition, a significantly protective effect of supplementation with the fish oil emulsion on the K+‐pNPPase activity only in non‐diabetic animals was observed. However, there was no effect of the fish oil emulsion supplementation on the enzyme activity in diabetic animals. The findings with different effects of experimental diabetes and the fish oil emulsion supplementation on Na+,K+‐ATPase and K+‐pNPPase activities may support the possibility of additional function of K+‐pNPPase outside the ATPase complex. Another possibility is that ROS or products of oxidative damage to macromolecules might influence these two enzyme activities by a different mechanism.The fish oil riched in ω‐3 fatty acids may have made the brain more susceptible to lipid peroxidation but also to the antioxidant enzymes. The effect of fish oil emulsion on membrane enzyme activities is more preferable to investigate under the physiological conditions than in diabetes mellitus.

Antidiabetic and antihyperlipidemic activity of asiatic acid in diabetic rats, role of HMG CoA: In vivo and in silico approaches

Hyperlipidemia is an associated complication of diabetes and also a major risk factor for cardiovascular diseases. The present study was designed to examine the antihyperlipidemic effect of asiatic acid (AA) in streptozotocin (STZ) induced diabetic rats. Diabetes was induced in male Wistar rats by a single intraperitoneal injection of STZ (40mg/kg b.w.). Diabetic rats show increased plasma glucose, total cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density liprotein, atherogenic index and decreased insulin and high density lipoprotein in diabetic rats. The activity of 3-hydroxy 3-methylglutaryl coenzyme A (HMG CoA) reductase increased significantly in contrast to the activities of lipoprotein lipase and lecithin cholesterol acyltransferase. In addition, the molecular docking of AA against HMG CoA reductase involved in cholesterol biosynthesis using Argus software. Diabetic rats were treated with AA shifted all these parameters towards normalcy. AA has shown best ligand binding energy 11.8122kcal/mol. The antihyperlipidemic effect of AA was compared with glibenclamide; a well-known antihyperglycemic drug. In conclusion, this study indicates that AA showed an antihyperlipidemic effect in addition to its antidiabetic effect in experimental diabetes.

Effects of Experimental Diabetes on C/EBP Proteins in Rat Hippocampus, Sciatic Nerve and Ganglia

Neurodegeneration is one of the most important complications of diabetes mellitus (DM). The exact mechanisms underlying neurodegeneration related to diabetic complications such as cognitive deficits and peripheral neuropathy are not clarified yet. Due to the fact that CCAAT/enhancer binding proteins (C/EBPs) have roles in cognitive functions, memory, synaptic plasticity, inflammation, lipid storage, and response to neurotrophic factors, it is possible to suggest that these transcription factors could have roles in neurodegeneration. Hence, in this study, the effects of experimental diabetes on C/EBPs in the hippocampus, sciatic nerve, and ganglia tissues were examined. After experimentally induced diabetes, immunoreactivity of related proteins was measured by western blotting. C/EBPα immunoreactivity in the hippocampus was not altered at 4-weeks but significantly decreased at 12-weeks of diabetes. C/EBPβ immunoreactivity was not altered at 4-weeks whereas significantly increased at 12-weeks of diabetes. In the ganglion, C/EBPα immunoreactivity was significantly decreased in diabetes, but C/EBPβ immunoreactivity was not affected. In the sciatic nerve, C/EBPα and β immunoreactivities were significantly decreased in diabetic rats. Furthermore, insulin therapy prevented diabetes-induced alterations in C/EBPα and β immunoreactivities. This study indicated, for the first time, that DM altered the immunoreactivity of C/EBPs in the nervous system. C/EBPs might be one of the important molecular targets which are responsible for neurodegeneration seen in diabetes.

Syringic acid, a novel natural phenolic acid, normalizes hyperglycemia with special reference to glycoprotein components in experimental diabetic rats

ObjectiveTo evaluate the antidiabetic effect of syringic acid, a natural phenolic compound on the levels of glycoprotein components in plasma and tissues of alloxan induced diabetic rats. MethodsDiabetes was induced in male Wistar rats by a single intraperitoneal injection of alloxan (150 mg/kg b.w). Syringic acid (50 mg/kg b.w) was administered orally for 30 d. The effects of syringic acid on plasma glucose, insulin, C-peptide, plasma and tissue glycoproteins were studied. ResultsOral administration of syringic acid (50 mg/kg b.w) for 30 d positively modulates the glycemic status in alloxan induced diabetic rats. The levels of plasma glucose were decreased with significant increase of plasma insulin and C-peptide level. The altered levels of plasma and tissue glycoprotein components were restored to near normal. No significant changes were noticed in normal rats treated with syringic acid. ConclusionsThe present findings suggest that syringic acid can potentially ameliorate glycoprotein components abnormalities in addition to its antidiabetic effect in experimental diabetes, further clinical studies are required to evaluate the use of syringic acid as an effective therapeutic agent for the treatment of diabetes mellitus.

Antihyperglycemic effect of carvone: Effect on the levels of glycoprotein components in streptozotocin-induced diabetic rats

ObjectiveTo investigate the effect of carvone on dearrangement in glycoprotein levels in the streptozotocin(STZ)-induced diabetic model. MethodsDiabetes was induced in male Wistar rats by a single intraperitoneal injection of STZ (40 mg/kg b.w). The levels of glycoproteins were altered in experimental diabetes mellitus. Carvone were administered to diabetic rats intragastrically at 25, 50, 100 mg/kg bw for 30 d. The effects of carvone on plasma glucose, insulin, plasma and tissue glycoproteins were studied. ResultsOral administration of carvone (50 mg/kg b.w) for 30 d, dose dependently improved the glycemic status in STZ-induced diabetic rats. The levels of plasma glucose were decreased with significant increase of plasma insulin level. The altered levels of plasma and tissue glycoprotein components were restored to near normal. ConclusionsThe present findings suggest that carvone can potentially ameliorate glycoprotein components abnormalities in addition to its antihyperglycemic effect in experimental diabetes. In light of these advantageous results, it is advisable to broaden the scale of use of carvone in a trial to alleviate the adverse effects of diabetes.

Protective role of 20-OH ecdysone on lipid profile and tissue fatty acid changes in streptozotocin induced diabetic rats

Hyperlipidemia is an associated complication of diabetes mellitus. The association of hyperglycemia with an alteration of lipid parameters presents a major risk for cardiovascular complications in diabetes. The present study was designed to examine the antihyperlipidemic effect of 20-OH ecdysone on lipid profile and tissue fatty acid changes in streptozotocin induced diabetic rats. The levels of blood glucose, cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density lipoprotein, high density lipoprotein, lipoprotein lipase, lecithin cholesterol acyl transferase, 3-hydroxy 3-methylglutaryl coenzyme A reductase and fatty acid composition were estimated in plasma, liver and kidneys of control and experimental groups of rats. Oral administration of 20-OH ecdysone at a dose of 5mg/kg bodyweight per day to STZ-induced diabetic rats for a period of 30 days resulted in a significant reduction in fasting blood glucose, cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density lipoprotein, 3-hydroxy 3-methylglutaryl coenzyme A reductase and elevation of high density lipoprotein, lipoprotein lipase and lecithin cholesterol acyl transferasein comparison with diabetic untreated rats. Moreover, administration of 20-OH ecdysone to diabetic rats also decreased the concentrations of fatty acids, viz., palmitic, stearic (16:1) and oleic acid (18:1), whereas linolenic (18:3) and arachidonic acid (20:4) were elevated. The antihyperlipidemic effect of 20-OH ecdysone was compared with glibenclamide a well-known antihyperglycemic drug. The result of the present study indicates that 20-OH ecdysone showed an antihyperlipidemic effect in addition to its antidiabetic effect in experimental diabetes.

Protective Effects of d‐Limonene on Lipid Peroxidation and Antioxidant Enzymes in Streptozotocin‐Induced Diabetic Rats

The aim of this study was to evaluate the protective effects of D-limonene on the levels of lipid peroxidation by-products and antioxidant defence systems in the plasma and tissues of normal and streptozotocin (STZ)-induced diabetes rats. The experimental diabetes was induced in rats by a single dose of STZ (40 mg/kg i.p.) injection, and treatment with D-limonene was continued for 45 days. After the treatment period, oxidative stress parameters such as lipid peroxidation by-products; enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase; non-enzymic antioxidants including reduced glutathione, Vitamins C and E were measured in the plasma and tissues of experimental rats. An increase in the levels of lipid peroxidation by-products and significant decrease in antioxidant enzymes were observed in untreated diabetic rats. Administration of D-limonene to diabetic rats for 45 days caused a significant reduction in the levels of lipid peroxidation by-products and an increase in the activities of antioxidant enzymes, when compared with the untreated diabetic group. There was no significant difference in normal treated groups, when compared with normal rats. Biochemical observations were substantiated with the help of histopathological examinations through its antioxidant properties and thereby conferred protection against STZ-induced diabetic rats. The result of this study indicates that D-limonene has antioxidant potential in addition to its antidiabetic effect in experimental diabetes.

Neural stem cells in the diabetic brain.

Experimental diabetes in rodents rapidly affects the neurogenic niches of the adult brain. Moreover, behavioral disorders suggest that a similar dysfunction of the neurogenic niches most likely affects diabetic and prediabetic patients. Here, we review our present knowledge about adult neural stem cells, the methods used for their study in diabetic models, and the effects of experimental diabetes. Variations in diet and even a short hyperglycemia profoundly change the structure and the proliferative dynamics of the neurogenic niches. Moreover, alterations of diabetic neurogenic niches appear to be associated with diabetic cognitive disorders. Available evidence supports the hypothesis that, in the adult, early changes of the neurogenic niches might enhance development of the diabetic disease.