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At least 343 records · Page 19Linked to original sources
PubMed1995

Identification of 3-hydroxy-3-methylglutaric acid (HMG) as a hypoglycemic principle of Spanish moss (Tillandsia usneoides).

Bioactivity-directed fractionation, using brine shrimp lethality and murine hypoglycemia, of an ethanol extract prepared from Tillandsia usneoides, led to the isolation of four apparently bioactive compounds from the water-soluble fraction. The compounds were identified as citric acid, succinic acid, 3-hydroxy-3-methylglutaric acid (HMG), and 3,6,3',5'-tetramethoxy-5,7,4'-trihydroxyflavone-7-O-beta-D-g lucoside. The brine shrimp lethality of the acids was simply due to acidity; however, HMG elicited significant hypoglycemic responses in fasting normal mice. Ethyl and methyl esters of citric acid were prepared and tested in the murine hypoglycemic assay. Five of the predominant sugars were identified by tlc. Free thymidine was also isolated. Further evaluation of HMG and other potential inhibitors of HMG CoA lyase, in the treatment of symptoms of diabetes mellitus, is suggested.

Animals↗
PubMed1999

Patient education to users of oral hypoglycemic agents: the perspective of Dutch community pharmacists.

The purpose of this study was to indicate which patient education activities directed at users of oral hypoglycemic agents are desirable in Dutch community pharmacies and to explore which preconditions should be considered when implementing the desired activities. A qualitative study was conducted with a panel composed of seven pharmacists and seven technicians with considerable experience in giving advice to people with diabetes mellitus type 2. A consensus method was used, which consisted of a written questionnaire and a feedback discussion, to determine which activities were considered desirable and to identify which other health care providers should be involved. The way these activities should be implemented was explored by a focus-group discussion. The following goals of patient education activities were studied: 1) adherence to the dosage regimen, 2) adherence to lifestyle advices, 3) gaining awareness of effects and 4) self-monitoring. According to the members of the panel, patient education activities should be directed primarily at stimulating adherence to the dosage regimen, increasing awareness of side effects and improving the correct technical use of blood glucose meters. Activities directed at lifestyle advice seemed to be less desirable to the pharmacy staff. Preconditions that should be considered when implementing these activities were structural cooperation with GPs and diabetic nurses and specialization of tasks of pharmacy technicians. Our results indicate that deepening of existing tasks, such as stimulating adherence to the dosage regimen is desirable in developing patient education activities at users of oral hypoglycemic agents.

Administration, Oral↗
PubMed2002

Oral hypoglycemic agents and the pregnant diabetic: "from bench to bedside".

Today, the criteria for diagnosis and treatment have evolved into an evidence-based medicine approach. The need for evidence-based information is especially critical in the management of gestational diabetes, in general, and especially in the use of oral hypoglycemic agents. These agents have been categorically contraindicated for decades in the United States based on anecdotal and/or weak evidence for these recommendations. In this article, the similarities between gestational and type 2 diabetes are described and the rationale for the use of oral hypoglycemic agents for the treatment of both are discussed. The author will show how research from basic sciences (placental transfers) to clinical studies (perinatal outcome) can lead to significant evidence on which to base management recommendations.

Diabetes Mellitus, Type 2↗
PubMed1996

Intensive insulin therapy with insulin lispro in patients with type 1 diabetes reduces the frequency of hypoglycemic episodes.

In a randomized, open-label, controlled cross-over trial, 107 patients with type 1 diabetes were treated with either regular human insulin or insulin lispro, a rapid-acting insulin analogue. After a lead-in period of 2 to 4 weeks, the patients were randomized to receive intensified insulin treatment with one of the insulins. NPH-human insulin was used for basal substitution in both groups. The crossover took place after 3 months of treatment. Efficacy and safety of the drugs were established by the assessment of hemoglobin A1c, pretest blood glucose, 1 and 2-hour postprandial glucose excursions, number of hypoglycemic episodes, daily insulin doses, body weight, insulin antibodies, and the number and severity of adverse events. A questionnaire comprised of four primary domains was used to measure some quality of life aspects of the patients. Both treatment regimens were well tolerated. While no differences were seen in the hemoglobin A1c values, there was a trend for a decrease in the pretest blood glucose levels and significant decreases of the 1 and 2-hour postprandial glucose excursions in the patients treated with insulin lispro. The number of hypoglycemic episodes was also significantly lower in the insulin lispro treatment period. The evaluation of the quality of life questionnaire revealed an improvement in the patients treatment satisfaction for the insulin lispro group. During treatment with insulin lispro, the basal insulin doses increased slightly. However, the total daily insulin doses decreased to a greater extent with insulin lispro as compared to regular human insulin. Human insulin-specific antibody binding values at endpoint were not different for the two treatments. In conclusion, intensive insulin treatment with insulin lispro therapy results in improved postprandial glycemic control and HbA1c levels at least equal to the treatment with regular human insulin but with less hypoglycemia and more treatment satisfaction for the patient.

Adult↗
PubMed1991

Hypoglycemic effects of sesquiterpene glycosides and polyhydroxylated triterpenoids of Eriobotrya japonica.

The effects of the constituent sesquiterpene glycosides 1-3 and polyhydroxylated triterpenoids 5-6 isolated by MeOH extraction of Eriobotrya japonica were studied in genetically diabetic mice (C57BL/KS-db/db/Ola) and normoglycemic rats. The sesquiterpene glycoside 3 and the polyhydroxylated triterpenoids 5 and 6 produced a marked inhibition of glycosuria. Furthermore, 5 and 6 were able to reduce blood glucose levels in normoglycemic rats. While there are already some data reported on hypoglycemic activity of polyhydroxylated triterpenoids, there are no previous data showing hypoglycemic activity of sesquiterpene glycosides.

Animals↗
PubMed1989

Postreceptor regulation of insulin action in primary cultures of rat hepatocytes by oral hypoglycemic agents: effects of linogliride and chlorpropamide.

We have previously demonstrated the ability of the sulfonylurea tolazamide to potentiate insulin action in primary cultures of hepatocytes prepared from normal and streptozotocin-diabetic rats. To determine whether the pirogliride derivative linogliride, a non-sulfonylurea orally effective hypoglycemic agent, can potentiate insulin action, we evaluated the ability of linogliride to affect insulin-stimulated lipogenesis in primary cultures of hepatocytes prepared from normal rats. In addition, we also evaluated the ability of the sulfonylurea chlorpropamide to affect insulin-stimulated lipogenesis in the same in vitro system. The exposure of hepatocytes for 18 h to either linogliride (100 ug/ml) or chlorpropamide (175 ug/ml) resulted in dose-dependent (0.1 to 100 nM insulin) increases in insulin-stimulated lipogenesis, although the effects of chlorpropamide are approximately two times those of linogliride. This increase in insulin responsiveness was not associated with any change in insulin sensitivity (ED50) or insulin binding. The results provide evidence for an extra-pancreatic effect of linogliride and chlorpropamide in the liver and indicate that these structurally unrelated oral hypoglycemic agents enhance insulin responsiveness through postbinding mechanisms.

Animals↗
PubMed1995

Stimulation of insulin release by non-sulfonylurea hypoglycemic agents: the meglitinide family.

Several new non-sulfonylurea hypoglycemic agents such as A-4166, KAD-1229 and repaglinide are structurally related to meglitinide, previously known as the non-sulfonylurea moiety of glibenclamide, or its analog S 3075. There is no parallelism between the ionophoretic and insulinotropic efficiency of these compounds. They are all able, however, to decrease K+ conductance in islet cells as documented by a decrease in 86Rb outlfow from prelabelled pancreatic islets. In terms of concentrations of equal insulinotropic capacity, a difference of at least two orders of magnitude is observed between the weakest (meglitinide) and most potent (S 3075) compound. All these agents exert little effect upon insulin release in nutrient-deprived islets, but markedly augment glucose-stimulated insulin release. The hexose can be replaced, however, by a non-glucidic nutrient such as the methyl ester of succinic acid to support the insulinotropic action of the meglitinide analogs. The question is raised as to the potential advantage of these non-sulfonylurea insulinotropic agents over hypoglycemic sulfonylureas.

Animals↗
PubMed2002

When diet fails: insulin and oral hypoglycemic agents as alternatives for the management of gestational diabetes mellitus.

The principal approach for attaining glycemic control in gestational diabetes mellitus is diet, with the addition of insulin or oral hypoglycemic agents when needed. The purpose of this review is to provide an overview for the understanding of management guidelines that have been validated by appropriately conducted research trials. The similarity between gestational diabetes mellitus and type 2 diabetes is highlighted. Criteria for insulin initiation as well as the role of a hypoglycemic agent as a potential alternative to insulin are discussed.

Administration, Oral↗
PubMed2007

Effect of a hypoglycemic agent on ischemic preconditioning in patients with type 2 diabetes and stable angina pectoris.

OBJECTIVE: Ischemic preconditioning is an increased tolerance to myocardial ischemia during the second of two consecutive exercise tests. ATP-sensitive K(+) channel blockers, such as glinides and sulfonylurea drugs, can induce loss of ischemic preconditioning. This study aimed to investigate the effects of repaglinide, a hypoglycemic agent with an affinity for myocardial ATP-sensitive K (+)channels, on the results of consecutive exercise tests in patients with diabetes and multivessel coronary artery disease. METHODS: Forty-two patients with type 2 diabetes and chronic stable angina pectoris, and two-vessel or three-vessel disease participated in this study. The patients underwent two consecutive treadmill exercise tests (phase 1). On the day after these exercise tests, 2 mg of oral repaglinide was given to the patients. One week later, two exercise tests were repeated consecutively (phase 2). RESULTS: All patients achieved 1.0-mm ST-segment depression during the four exercise tests (T1, T2, T3, and T4). In phase 2, seven patients improved in time to onset of 1.0-mm ST-segment depression. The worsening of the time to onset of 1.0-mm ST-segment depression in phase 2 demonstrated ischemic preconditioning block in 83.3% of patients (P=0.0001). Even the postexercise electrocardiographic parameters (ST-segment depression morphology and magnitude and arrhythmias) were significantly different between the groups with and without pharmacologic ischemic preconditioning block (P=0.031). CONCLUSIONS: Repaglinide, an oral hypoglycemic agent with ATP-sensitive K(+) channel-blocker activity, eliminated the myocardial ischemic preconditioning in patients with coronary disease and diabetes.

Angina Pectoris↗
PubMed1985

Insulin secretion and immuno-genetic markers in diabetics with 'secondary failure' of oral hypoglycemic agents.

'Secondary failure' of oral hypoglycemics, in non-insulin dependent diabetics, has been attributed to dietary non-compliance, inadequate drug dosage, metabolic stress, or true drug failure. Progressive loss of beta cell function is a suggested mechanism for true drug failure but on the basis of little documented evidence. In view of this, we have measured basal and glucagon-stimulated C-peptide levels, human leukocyte antigen (HLA) types, and islet cell antibodies in 20 non-insulin dependent diabetics with 'secondary failure' of oral agents. There were 16 females and four males with a mean ideal body weight of 1.30 units and mean duration of diabetes of 9.5 years. Fasting insulin (mean +/- SD: 15.1 +/- 10.6 mU/l) and fasting C-peptide (2.3 +/- 1.2 micrograms/l) were normal or slightly elevated in all but one patient. Mean C-peptide increased from 2.3 +/- 1.2 micrograms/l to 3.5 +/- 2.2 micrograms/l (152% over basal) 6 minutes after 1 mg i.v. glucagon. In 15 patients the C-peptide response was greater than 130% of basal. Islet cell cytoplasmic antibodies were detected in only two patients. The distribution of HLA types was not significantly different from a control population, with no increase in DR3 or DR4. Thus, absolute insulin deficiency is uncommon in non-insulin dependent diabetics with 'secondary failure' of oral hypoglycemic agents and such patients do not exhibit the immuno-genetic markers of insulin-dependent diabetes.

Administration, Oral↗
PubMed1984

Effects of the oral hypoglycemic agent methyl palmoxirate on exercise capacity of rats.

The effect of the oral hypoglycemic agent methyl palmoxirate (methyl 2-tetradecylglycidate, McN-3716), a selective inhibitor of long chain fatty acid oxidation, on the exercise capacity of normal rats was evaluated. Daily administration of 2.5 mg/kg for 7 days, or of a single dose of 10 mg/kg, of methyl palmoxirate did not affect the ability of rats to perform strenuous exercise of an intensity that caused exhaustion in less than 30 min. The ability to perform prolonged, moderately strenuous exercise of an intensity that could be maintained for more than 60 min was decreased slightly (17%) in the methyl palmoxirate treated rats. This effect appeared to be mediated by a significant reduction in initial liver glycogen content in the methyl palmoxirate treated rats. As a consequence, the methyl palmoxirate treated rats became hypoglycemic during prolonged exercise. Inhibition of fatty acid oxidation in skeletal muscle was minimal. Treatment with methyl palmoxirate protected against the development of exercise-induced ketosis. It appears that the liver is the major site of action of methyl palmoxirate when given in low dosage.

Administration, Oral↗
PubMed1994

A novel D-phenylalanine-derivative hypoglycemic agent A-4166 increases cytosolic free Ca2+ in rat pancreatic beta-cells by stimulating Ca2+ influx.

It has recently been shown that N-[(trans-4-isopropylcyclohexyl)-carbonyl]D-phenylalanine (A-4166), a new nonsulfonylurea oral hypoglycemic agent, reduces blood glucose levels in nondiabetic and diabetic animals in a quicker and shorter lasting manner than sulfonylureas, and that the hypoglycemic effect of A-4166 is due to the stimulation of insulin release. However, the mechanism by which A-4166 stimulates insulin release is still unknown. In the present study, we investigated the effect of A-4166 on the cytosolic free Ca2+ concentration ([Ca2+]i) in pancreatic beta-cells from normal rats by dual wavelength fura-2 microfluorometry. In the presence of 2.8 mM glucose, A-4166 produced a rapid increase in [Ca2+]i in a concentration-dependent manner over the range of 3-30 microM. The increase in [Ca2+]i was transient, oscillatory, or sustained. A-4166 did not evoke any decrease in [Ca2+]i, whereas a high concentration of glucose (16.7 mM), a metabolized secretagogue, produced an initial decrease and a subsequent increase in [Ca2+]i. In the presence of 16.7 mM glucose, low concentrations (0.03-1 microM) of A-4166 produced an increase in [Ca2+]i in some of the beta-cells tested. The [Ca2+]i response to A-4166 was completely and reversibly inhibited under Ca(2+)-free conditions as well as by nitrendipine, a blocker of the L-type Ca2+ channel. Nitrendipine also inhibited insulin release from perfused rat pancreases stimulated by A-4166. Diazoxide, an opener of the ATP-sensitive K+ channel, blocked the [Ca2+]i response to A-4166. Sulfonylureas such as tolbutamide and glibenclamide increased [Ca2+]i in a manner similar to A-4166. These results indicate that at basal glucose concentrations, A-4166 increases [Ca2+]i in rat pancreatic beta-cells by stimulating Ca2+ influx through L-type Ca2+ channels, and that this effect is markedly augmented at elevated glucose concentrations. It appears that the increase in [Ca2+]i is related to the stimulation of insulin release by A-4166. Inhibition of ATP-sensitive potassium channels, but not stimulation of beta-cell metabolism, may be involved in the increase in [Ca2+]i by A-4166.

Animals↗
PubMed1996

Acute effects of the human amylin analog AC137 on basal and insulin-stimulated euglycemic and hypoglycemic fuel metabolism in patients with insulin-dependent diabetes mellitus.

Amylin has been reported to decrease glycogen storage in rodent skeletal muscles and produce insulin resistance in intact rats. To test the acute effect of a human amylin analog (AC137) on glucose metabolism in man, seven IDDM patients were infused in a randomized, double blind, cross-over study with AC137 (100 micrograms/h, n = 1; 50 micrograms/h, n = 6) or placebo for 330 min during a two-step euglycemic clamp (insulin infusion rates, 0.2 and 0.6 mU/kg.min; basal and hyperinsulinemic period, respectively) followed by a hyperinsulinemic hypoglycemic clamp (insulin infusion rate, 1.5 mU/kg.min; hypoglycemic period). During euglycemia, no differences were found in glucose disposal (step 1, 2.43 +/- 0.20 vs. 2.03 +/- 0.26; step 2, 4.28 +/- 0.54 vs. 4.11 +/- 0.45 mg/kg.min; AC137 vs. placebo, mean +/- SEM), arteriovenous substrate balances across the forearm, or hepatic glucose production. During hypoglycemia, glucose fluxes were also similar. However, lactate release from the forearm was more pronounced (P < 0.05) with the analog than with placebo (area under the curve, -11.2 +/- 4.6 vs. -1.4 +/- 2.2 mmol/min.L). Despite similar plasma glucose nadirs (2.7 +/- 0.0 vs. 2.6 +/- 0.1 mmol/L; AC137 vs. placebo), circulating cortisol and GH rose to significantly higher levels during hypoglycemia with the amylin analog (P < 0.05). In conclusion, acute administration of the amylin analog AC137 did not influence insulin-stimulated glucose metabolism during euglycemic conditions. During imposed hypoglycemia, lactate release from skeletal muscle was, however, enhanced, and the rise in cortisol and GH was augmented.

Adult↗
PubMed1995

Hypoglycemic effect of the rhizomes of ophiopogonis tuber in normal and diabetic mice.

The hypoglycemic effect of the rhizomes of Ophiopogonis Tuber (Liliaceae) was investigated in normal and streptozotocin-induced diabetic mice. The n-butanol extract of rhizomes of Ophiopogonis Tuber (BM) (100 mg/kg) reduced the blood glucose of normal mice from 201 +/- 13 to 151 +/- 7 mg/100 ml 4h after intraperitoneal administration (p < 0.054), and also significantly lowered the blood glucose of streptozotocin-induced diabetic mice from 590 +/- 28 to 470 +/- 37 mg/100 ml under similar conditions (p < 0.05). BM also tended to suppress epinephrine-induced hyperglycemia in mice. We concluded that the hypoglycemic effect of BM does not alter the insulin concentration.

Animals↗
PubMed1997

Hypoglycemic effect of the rhizomes of Smilax glabra in normal and diabetic mice.

The hypoglycemic effect of the rhizomes of Smilax glabra ROXBURGH (Liliaceae) was investigated in normal and KK-Ay mice, one of the animal models of non-insulin dependent diabetes mellitus (NIDDM) with hyperinsulinemia. The methanol extract of rhizomes of Smilax glabra ROXBURGH (SM, 100 mg/kg body weight) reduced the blood glucose of normal mice 4 h after intraperitoneal administration (p<0.05), and also significantly lowered the blood glucose of KK-Ay mice under similar conditions (p<0.001). However, SM did not affect the blood glucose in streptozotocin-induced diabetic mice, one of the animal models of insulin-dependent diabetes mellitus (IDDM) with hypoinsulinemia. SM also suppressed epinephrine-induced hyperglycemia in mice. SM-treated KK-Ay mice significantly decreased the blood glucose in an insulin tolerance test. We concluded that the hypoglycemic effect of SM raised insulin sensitivity.

Animals↗
PubMed2005

Antiallergic, antipyretic, hypoglycemic and hepatoprotective effects of aqueous extract of Coronopus didymus Linn.

The aqueous extract of whole plant of Coronopus didymus LINN (CD) [Family: Bracicacea] was screened for antiallergic, antipyretic and hepatoprotective effects in rats and hypoglycemic activity in mice. The extract showed significant antiallergic, antipyretic, hypoglycemic and hepatoprotective activity at 200 and 400 mg/kg doses on oral administration. Mechanistically, CD acts as an antioxidant as evidenced by its ability to scavenge DPPH and superoxide radicals. All the observed activities may be due to the presence of flavonoids, saponins and tannins as they are reported to possess a variety of biological activities.

Analgesics, Non-Narcotic↗
PubMed1990

Hypoglycemic effect of intestinally administered monosaccharide-modified insulin derivatives in rats.

The effect of the modification of insulin (INS) with p-succinylamidophenyl (SA)-alpha-D-glucopyranoside (SAPG), SA-alpha-D-mannopyranoside and SA-alpha-L-arabinopyranoside on the enzymatic degradation and the hypoglycemic effect in rats was studied. When SAPG-INS was administered intraintestinally in the absence of bile and pancreatic juice, blood glucose level decreased to 56% of initial value. Other monosaccharide derivatives were less effective than SAPG-INS. The digestion of monosaccharide derivatives by pepsin and chymotrypsin indicated that the resistance of insulin to enzymatic degradation was increased by its modification with monosaccharide. One possibility for the hypoglycemic effect of SAPG-INS could be the increased resistance of insulin to enzymatic degradation as a result of its modification with monosaccharide.

Animals↗
PubMed1993

Two new 2-arylbenzofuran derivatives from hypoglycemic activity-bearing fractions of Morus insignis.

Ethyl acetate- and n-butanol-soluble fractions of the leaves of Morus insignis showed a significant hypoglycemic activity on streptozotocin (STZ)-induced hyperglycemic rats. From these hypoglycemic activity-showing fractions, two new compounds, mulberrofuran U (2) and moracin M-3-O-beta-D-glucopyranoside (3) were isolated, along with six known compounds [beta-sitosterol, beta-sitosterol-3-O-beta-glucopyranoside, ursolic acid, moracin M (1), kaempferol-3-O-beta-glucopyranoside and quercetin-3-O-beta-glucopyranoside] and the structures of the new compounds were determined by spectroscopic and chemical methods.

Animals↗