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At least 685 records · Page 38Linked to original sources
PubMed2004

Antidiabetic activity of Caesalpinia bonducella F. in chronic type 2 diabetic model in Long-Evans rats and evaluation of insulin secretagogue property of its fractions on isolated islets.

Caesalpinia bonducella F., is a shrub widely distributed throughout the coastal region of India and is ethnically used by the tribal people of Andaman and Nicober Island as a remedy of symptoms of diabetes mellitus. This ethnic report prompted the detail investigation of hypoglycemic activity of Caesalpinia bonducella seeds, initially on physiological hyperglycemic model and then on type 1 and type 2 sub-acute diabetic animal models which has already been reported. Evaluation of different extracts from Caesalpinia bonducella in chronic type 2 diabetic model alongwith insulin secretagogue activity of five fractions isolated from the Caesalpinia bonducella seed kernel are presented in this paper. Both the aqueous and ethanolic extracts showed potent hypoglycemic activity in chronic type 2 diabetic model. Two fractions BM 169 and BM 170 B could increase secretion of insulin from isolated islets.

Animals↗
PubMed2005

Hypoglycemic and antidiabetic effect of ethanolic extract of leaves of Annona squamosa L. in experimental animals.

The ethanolic extract of Annona squamosa L. (Annonaceae) leaves was administered orally at different doses to normal as well as streptozotocin (STZ)-induced diabetic rats and alloxan-induced diabetic rabbits. The dose of 350 mg/kg body weight (bw) reduced the fasting blood glucose (FBG) level by 6.0% within 1 h, whereas, the peak blood glucose at 1 h during glucose tolerance test (GTT) was reduced by 17.1% in normal rats. The same dose of ethanolic extract reduced FBG by 26.8% and improved glucose tolerance by 38.5 and 40.6% at 1 and 2 h, respectively, during GTT in alloxan-induced diabetic rabbits. In STZ-diabetic rats, a fall of 13.0% in FBG and an improvement in glucose tolerance by 37.2 and 60.6% at 1 and 2 h, respectively, was observed during GTT. The dose of 350 mg/kg bw of ethanolic extract in 10-day treatment of a group of STZ-diabetic rats produced 73.3% fall in FBG level and no sugar was observed in fasting urine. Treatment of severely-diabetic rabbits for 15 days with a dose of 350 mg/kg of extract reduce FBG by 52.7% and urine sugar by 75%. It brought about fall in the level of total cholesterol (TC) by 49.3% with increase of 30.3% in high-density lipoprotein (HDL) and decrease of 71.9 and 28.7% in low-density lipoprotein (LDL) and triglycerides (TG) levels, respectively.

Animals↗
PubMed2005

Antidiabetic activity and toxicity of Zizyphus spina-christi leaves.

The effect of the butanol extract of Zizyphus spina-christi (L.), Willd (Rhamnaceae) leaves and its major saponin glycoside, christinin-A, on the serum glucose and insulin levels was studied in non-diabetic control, type-I (insulin-dependent) and type-II (non-insulin-dependent) diabetic rats. Pretreatment either with 100 mg/kg butanol extract or christinin-A potentiated glucose-induced insulin release in non-diabetic control rats. In type-II but not in type-I diabetic rats pretreatment with the butanol extract or christinin-A improved the oral glucose tolerance and potentiated glucose-induced insulin release. Treatment either with 100 mg/kg butanol extract or christinin-A reduced the serum glucose level and increased the serum insulin level of non-diabetic control and type-II diabetic rats but not of type-I diabetic rats. Effects of the butanol extract and christinin-A were similar. Pretreatment of non-diabetic control and type-II diabetic rats either with 100 mg/kg butanol extract or christinin-A enhanced the glucose lowering and insulinotropic effects of 5 g/kg glibenclamide. The hyperglycemic and hypoinsulinemic effects of 30 mg/kg diazoxide in non-diabetic control and type-II diabetic rats were inhibited and antagonized, respectively by pretreatment with the butanol extract or christinin-A. The relaxant effects of different concentrations of diazoxide on the isolated norepinephrine-contracted aortic strips were inhibited by 100 micromol/l christinin-A or 10 micromol/l glibenclamide. The combination of glibenclamide and christinin-A led to complete inhibition of the relaxant effects of different concentrations of diazoxide. At a dose level much higher than that required to produce satisfactory insulinotropic and hypoglycemic effects, the butanol extract of Zizyphus spina-christi leaves produced a depressant effect on the central nervous system in rats. Treatment of rats with 100mg/kg butanol extract for 3 months produced no functional or structural disturbances in liver and kidney and no haematological changes. In addition, the oral LD50 of the butanol extract in mice was 3820 mg/kg, while that of glibenclamide was 3160 mg/kg. Thus, Zizyphusspina-christi leaves appears to be a safe alternative to lower blood glucose. The safe insulinotropic and subsequent hypoglycemic effects of Zizyphus spina-christi leaves may be due to a sulfonylurea-like activity.

Animals↗
PubMed2006

In-vivo assessment of antidiabetic and antioxidant activities of grapevine leaves (Vitis vinifera) in diabetic rats.

The acute and the subacute (15 days) hypoglycaemic and antihyperglycaemic effect of the two different doses (250, 500 mg/kg) of the aqueous extract from the leaves of Vitis vinifera L. were evaluated in this study. The aqueous extract was further fractionated through successive solvent extractions and the acute effect of different doses of its subfractions, 25 mg/kg for ethylacetate fraction, 80 mg/kg for n-butanol fraction and 375 mg/kg for remaining aqueous fraction were investigated using normal, glucose-hyperglycaemic and streptozotocin-induced diabetic rats. Blood glucose levels were measured according to the glucose oxidase method. Tolbutamide was used as a reference drug at a dose of 100 mg/kg. The antioxidant activity of the test samples was studied in the liver, kidney and heart tissues of diabetic rats by measuring malondialdehyde (MDA) and glutathion (GSH) levels. All results were compared to the diabetic control groups. The results showed that EtOAc Fr. was rich in polyphenolics and possessed a significant antihyperglycaemic and antioxidant activity equipotent with the reference hypoglycaemic agent (tolbutamide), when evaluated in diabetic rats.

Animals↗
PubMed2006

In vivo antidiabetic and antioxidant potential of Helichrysum plicatum ssp. plicatum capitulums in streptozotocin-induced-diabetic rats.

Helichrysum species (Asteraceae) are widely found in Anatolia. Decoction prepared from the capitulums of Helichrysum plicatum ssp. plicatum is used to alleviate the symptoms of diabetes mellitus in folk medicine. In the present study, the hypoglycaemic and antioxidant potential of Helichrysum plicatum ssp. plicatum was evaluated by using in vivo methods in normal and streptozotocin-induced-diabetic rats. After the oral administration of water and ethanolic extracts at doses of 500mg/kg body weight prepared from the capitulums of plant, blood glucose levels were monitored at specific intervals. Tolbutamide was used as a reference drug at a dose of 100mg/kg. The experimental data indicated that water and ethanol extracts of capitulums demonstrate significant antihyperglycaemic and antioxidant activity in streptozotocin-induced rats which confirmed the folkloric utilization. In order to assess the role of polyphenolic components in the relevant activity, phenolic and flavonoid contents of each extract were also determined in terms of total phenols: 113.5+/-8.6mg (gallic acid equivalent/1g extract) and total flavanoids 50.5+/-1.9mg (quercetin equivalent/1g extract) for ethanol extract, total phenols: 75.9+/-3.7, flavonoids: 31.5+/-2.3 for water extract using Folin-Ciocalteu reagent.

Animals↗
PubMed2004

Antidiabetic effect of Pycnogenol French maritime pine bark extract in patients with diabetes type II.

A double-blind, placebo-controlled, randomized, multi-center study was performed with 77 diabetes type II patients to investigate anti-diabetic effects of the French maritime pine bark extract, Pynogenol. Supplementation with 100 mg Pycnogenol for 12 weeks, during which a standard anti-diabetic treatment was continued, significantly lowered plasma glucose levels as compared to placebo. HbA1(c) was also lowered; however, the difference as compared to placebo was statistically significant only for the first month. In the Pycnogenol-group endothelin-1 was significantly decreased, while 6-ketoprostaglandin F(1a) in plasma was elevated compared to placebo. Nitric oxide levels in plasma increased during treatment in both groups, but, differences did not reach statistical significance. Pycnogenol was well-tolerated with ECG, electrolytes, creatinine and blood urea nitrogen remaining unchanged in both groups. Mild and transient unwanted effects were reported for both groups without significant differences. Supplementation of Pycnogenol to conventional diabetes treatment lowers glucose levels and improves endothelial function.

6-Ketoprostaglandin F1 alpha↗
PubMed2004

Insulin-secretagogue activity and cytoprotective role of the traditional antidiabetic plant Scoparia dulcis (Sweet Broomweed).

Scoparia dulcis (Sweet Broomweed) has been documented as a traditional treatment of diabetes. The administration of an aqueous extract of Scoparia dulcis at a dose of 200 mg/kg body weight significantly decreased the blood glucose with significant increase in plasma insulin level in streptozotocin diabetic rats at the end of 15 days treatment. The insulin secretagogue action of Scoparia dulcis plant extract (SPEt) was further investigated using isolated pancreatic islets from mice. SPEt at a dose of 10 microg/ml evoked 6.0 fold stimulation of insulin secretion from isolated islets indicating its insulin secretagogue activity. In addition the effect of SPEt on streptozotocin induced cell death and nitric oxide (NO) in terms of nitrite production were also examined. SPEt protected against streptozotocin- mediated cytotoxicity (88%) and NO production in rat insulinoma cell line (RINm5F). Above results suggest the glucose lowering effect of SPEt to be associated with potentiation of insulin release from pancreatic islets. Our results revealed the possible therapeutic value of Scoparia dulcis for the better control, management and prevention of diabetes mellitus progression.

Animals↗
PubMed2004

Oral antidiabetic agents: 2004.

The appropriate management of patients with type 2 diabetes presents many challenges to health care providers. The first several years of type 2 diabetes are likely to be unrecognized and untreated. The pathophysiology of type 2 diabetes dictates that treatment of insulin resistance should be an early and central focus for every therapeutic program. The pharmacologic tools currently available are capable of allowing most patients with type 2 diabetes to achieve good metabolic control. Implementation of early combination therapy is essential if glycemic targets are to be met.

Administration, Oral↗
PubMed2004

Antidiabetic and adipogenic properties in a newly synthesized thiazolidine derivative, FPFS-410.

We report here a newly synthesized cyanoimino-oxothiazolidine derivative, FPFS-410, which has properties to ameliorate both hyperglycemia and dyslipidemia. Treatment of genetically obese-diabetic db/db mice with FPFS-410 markedly ameliorates severe hyperglycemia and hypertriglyceridemia. Although the oxothiazolidine ring of FPFS-410 shares a structural similarity with other thiazolidinedione derivatives, reporter assays showed that FPFS-410 was much less potent to activate peroxisome proliferators-activated receptor gamma (PPAR gamma) as compared with pioglitazone. When 3T3-L1 preadipocytes were treated with FPFS-410, intracellular accumulation of lipids was facilitated in a similar fashion to pioglitazone. Moreover, treatment with FPFS-410 throughout the differentiation course resulted in a significant increase in glucose transport. These results suggest that FPFS-410 may provide a useful therapeutic candidate for diabetes mellitus and dyslipidemia.

3T3-L1 Cells↗
PubMed2006

Antidiabetic effect of probiotic dahi containing Lactobacillus acidophilus and Lactobacillus casei in high fructose fed rats.

OBJECTIVE: We investigated the effect of low-fat (2.5%) dahi containing probiotic Lactobacillus acidophilus and Lactobacillus casei on progression of high fructose-induced type 2 diabetes in rats. METHODS: Diabetes was induced in male albino Wistar rats by feeding 21% fructose in water. The body weight, food and water intakes, fasting blood glucose, glycosylated hemoglobin, oral glucose tolerance test, plasma insulin, liver glycogen content, and blood lipid profile were recorded. The oxidative status in terms of thiobarbituric acid-reactive substances and reduced glutathione contents in liver and pancreatic tissues were also measured. RESULTS: Values for blood glucose, glycosylated hemoglobin, glucose intolerance, plasma insulin, liver glycogen, plasma total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and blood free fatty acids were increased significantly after 8 wk of high fructose feeding; however, the dahi-supplemented diet restricted the elevation of these parameters in comparison with the high fructose-fed control group. In contrast, high-density lipoprotein cholesterol decreased slightly and was retained in the dahi-fed group. The dahi-fed group also exhibited lower values of thiobarbituric acid-reactive substances and higher values of reduced glutathione in liver and pancreatic tissues compared with the high fructose-fed control group. CONCLUSION: The probiotic dahi-supplemented diet significantly delayed the onset of glucose intolerance, hyperglycemia, hyperinsulinemia, dyslipidemia, and oxidative stress in high fructose-induced diabetic rats, indicating a lower risk of diabetes and its complications.

Animals↗
PubMed2006

Pituitary adenylate cyclase-activating peptide (PACAP): assessment of dipeptidyl peptidase IV degradation, insulin-releasing activity and antidiabetic potential.

Pituitary adenylate cyclase-activating peptide (PACAP) is a member of the glucagon family of peptides. Like other members, most notably glucagon-like peptide-1 (GLP-1), PACAP is rapidly degraded by dipeptidylpeptidase IV (DPP IV). This study investigated how degradation by DPP IV affected the insulinotropic activity of PACAP, and whether PACAP exerted acute antihyperglycemic properties in normal or ob/ob mice. DPP IV degradation of PACAP(1-27) over 18 h led to the formation of PACAP(3-27), PACAP(5-27) and ultimately PACAP(6-27). In contrast to 1.4-1.8-fold concentration-dependent stimulation of insulin secretion by PACAP(1-27), these peptide fragments lacked insulinotropic activity. While PACAP(1-27) and PACAP(1-38) generated significant insulin responses when given alone or together with glucose in ob/ob and normal mice, they also elevated plasma glucose. These actions were eliminated following degradation of the peptide by incubation with DPP IV. The hyperglycemic effects may be explained at least partly by a potent glucagon-releasing action in ob/ob and normal mice. In conclusion, PACAP is inactivated by DPP IV and despite insulin-releasing effects, its actions on glucagon secretion and glucose homeostasis do not make it a good therapeutic tool for the treatment of type 2 diabetes.

Amino Acid Sequence↗
PubMed2005

Dipeptidyl peptidase IV inhibitors: how do they work as new antidiabetic agents?

A number of new approaches to diabetes therapy are currently undergoing clinical trials, including those involving stimulation of the pancreatic beta-cell with the gut-derived insulinotropic hormones (incretins), GIP and GLP-1. The current review focuses on an approach based on the inhibition of dipeptidyl peptidase IV (DP IV), the major enzyme responsible for degrading the incretins in vivo. The rationale for this approach was that blockade of incretin degradation would increase their physiological actions, including the stimulation of insulin secretion and inhibition of gastric emptying. It is now clear that both GIP and GLP-1 also have powerful effects on beta-cell differentation, mitogenesis and survival. By potentiating these pleiotropic actions of the incretins, DP IV inhibition can therefore preserve beta-cell mass and improve secretory function in diabetics.

Diabetes Mellitus, Type 2↗
PubMed2003

Antidiabetic and antimalarial biguanide drugs are metal-interactive antiproteolytic agents.

Various biguanide derivatives are used as antihyperglycemic and antimalarial drugs (e.g., 1,1-dimethyl biguanide (metformin), phenylethyl biguanide (phenformin), N-(4-chlorophenyl)-N'-(isopropyl)-imidodicarbonimidic diamide (proguanil)); however, no common mechanism has been suggested in these controversial therapeutic actions. Biguanides bind endogenous metals that inhibit cysteine proteases independently, e.g., Zn(2+), Cu(2+), Fe(3+). Here, various biguanide derivatives are reported to be metal-interactive inhibitors of cathepsin B from mammals and falcipain-2 from Plasmodium falciparum. Structural homologies were identified among the Phe-Arg protease substrate motif and the metal complexes of phenformin and proguanil. Molecular modeling revealed that the position of the scissile amide substrate bond corresponds to the biguanide-complexed inhibitory metal when the phenyl groups are homologously aligned. Binding of the phenformin-metal complex within the active site of human cathepsin B was modeled with computational docking. A major binding mode involved binding of the drug phenyl group at the protease S2 subsite, and the complexed inhibitory metal shared between the drug and the protease Cys29-His199 catalytic pair. Cysteine protease inhibition was assayed with carbobenzyloxy-PHE-ARG-7-aminomethylcoumarin substrate. In the absence of metal ions, phenformin was a weakly competitive protease inhibitor (apparent K(i) several microM); however, metformin was noninhibitory. In contrast, the metal complexes of both metformin and phenformin were protease inhibitors with potency at therapeutic concentrations. Biguanide-metal complexes were more potent cysteine protease inhibitors than either the biguanide or metal ions alone, i.e., synergistic. Similar to chloroquine, therapeutic extracellular concentrations of metformin, phenformin, and proguanil caused metal-interactive inhibition of lysosomal protein degradation as bioassayed in primary tissue using perfused myocardium. The biguanide moiety is identified as a past and future structural scaffold for synthesis of many protease inhibitors. Results are discussed in relation to Zn(2+)-interactive inhibition of insulin degradation in hormone target tissues, and Fe(3+)-interactive inhibition of hemoglobin degradation in parasite food vacuoles. Previous studies on insulin hypercatabolism and insulin resistance are speculatively reviewed in light of present findings.

Animals↗
PubMed1999

Insulin resistance and antidiabetic drugs.

Insulin resistance describes an impaired biological response to insulin, which underpins the development of type 2 (non-insulin-dependent) diabetes mellitus (T2DM). Initially, insulin resistance causes a compensatory hyperinsulinaemia, which gives way to pancreatic beta-cell failure. Insulin resistance and hyperinsulinaemia conspire together in the development of a diverse collection of risk factors for coronary heart disease, namely obesity, T2DM, dyslipidaemia, hypertension, atherosclerosis, and a pro-coagulant state. This collection of factors is commonly found in T2DM patients, and is recognised as the Insulin Resistance Syndrome or Syndrome X. By targeting insulin resistance as a treatment strategy for T2DM, it should be possible to broaden the potential benefits, so that improved glycaemic control is complemented with improvements to other components of Syndrome X. At present, metformin and thiazolidinediones are the only therapies for T2DM that directly address aspects of insulin resistance. Increasing awareness of the clinical implications of insulin resistance, and increasing knowledge of the cellular basis of insulin resistance, provide the rationale and a means for developing an anti-insulin resistance approach to the treatment of T2DM.

Arteriosclerosis↗