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At least 505 records · Page 28Linked to original sources
PubMed1994

Glycemic thresholds for hypoglycemic responses in obese subjects.

The objective of this study was to compare glycemic thresholds for hypoglycemic responses in obese and control subjects. A modified glucose-clamp technique was used to produce a standardized fall in plasma glucose (0.5 mmol/l per 40 min) in nine morbidly obese and ten control subjects. The release of the counter-regulatory hormones was measured and a symptom questionnaire was filled out every 10 min. The hypoglycemic thresholds (taken as the plasma glucose level where the response exceeded the basal level +2 s.d.) were practically identical in the two groups both for the hormones and the symptoms (including hunger). Our results argue against the hypothesis that an increased sensitivity to a falling plasma glucose is of importance in the pathogenesis of obesity.

Adult↗
PubMed1993

Oral hypoglycemic agents in the treatment of type II diabetes.

The cornerstones of therapy for non-insulin-dependent diabetes mellitus are patient education, dietary modification with weight loss, and regular exercise. If diet and exercise fail to control hyperglycemia, pharmacologic intervention is warranted. The sulfonylureas are the only hypoglycemic agents approved for use in the United States. Their hypoglycemic effect is achieved through stimulation of insulin secretion and reduction of insulin resistance in the peripheral tissues. Two classes of sulfonylureas are available. First-generation drugs, such as tolbutamide and tolazamide, are less expensive and less powerful than second-generation drugs, such as glipizide and glyburide.

Administration, Oral↗
PubMed1993

[Hypoglycemic encephalopathy demonstrating generalized multiple cortical infarctions--sequential CT findings].

A fifty-nine-year-old alcoholic man with severe hypoglycemic encephalopathy was examined using sequential CT scans of the brain (CT). Twenty-seven hours after the attack, which resulted in a comatose state, CT disclosed multiple low density areas throughout the cerebral cortex which resembled multiple cortical infarctions. CT obtained four days after the ictus demonstrated more prominent low density areas in the cerebral cortex, diffuse cerebral edema and partial cortical enhancement after administration of contrast medium. Sixteen days after the ictus, the multiple low density areas in the cerebral cortex disappeared. Enhanced CT on day 23 demonstrated marked gyral enhancement throughout the cerebral cortex. Thereafter diffuse brain atrophy progressed rapidly as demonstrated by MRI on day 82 which showed extensive cortical and subcortical atrophy particularly in the frontoparietal and parieto-occipital regions bilaterally with dilated lateral ventricles. Hypoglycemia and anoxia have long been thought to give rise to similar types of brain damage based on neuropathological observations. But it has recently been shown that they are quite different based on neurochemical and neurophysiological findings. Numerous previously reported autopsy cases of hypoglycemia confirm these findings which are neuropathologically similar to the multiple infarction seen in the present case. We conclude that the acute cortical changes of the present case are specific for hypoglycemic encephalopathy. The findings indicate that the basic mechanisms operating in hypoglycemia and anoxia are different.

Atrophy↗
PubMed1996

Hypoglycemic hyperemia in retina of newborn pigs. Involvement of adenosine.

PURPOSE: To determine whether retinal blood flow increases in response to perinatal hypoglycemia and whether the vasodilator adenosine is involved in mediating the hyperemic response. METHODS: Retinal fluorescein videoangiography was undertaken in intact eyes of isoflurane-anesthetized piglets using intracarotid injections of sodium fluorescein. Angiograms were recorded to videotape and analyzed off-line by image analysis software to determine stimulus-induced changes in mean arteriovenous transit times, and arteriolar and venular diameters, from which retinal blood flow was calculated. Two groups of animals were rendered hypoglycemic (blood glucose = 19 +/- 1 mg/dl) by insulin (25 IU/kg, intravenously), and angiograms were obtained at 10-minute intervals for 0.5 hour of hypoglycemia. One group (n = 5) served as controls. In the other (n = 5), the nonspecific adenosine receptor antagonist 8-phenyltheophylline (8PT) was administered intravenously approximately 15 minutes before hypoglycemia to examine the role of adenosine in the hemodynamic response to hypoglycemia. RESULTS: Acute hypoglycemia was associated with an increase in mean retinal blood flow of 94 +/- 18% (P < 0.002). However, in animals pretreated with 8PT, this hyperemic response was severely attenuated, primarily by an effect on arteriovenous transit time. In these latter animals, mean retinal blood flow only increased 19 +/- 10% in response to hypoglycemia (P = 0.13 versus normoglycemic baseline; P = 0.007 versus untreated hypoglycemic animals). All other hemodynamic variables were similar between animal groups. CONCLUSIONS: Acute hypoglycemia causes a compensatory increase in retinal blood flow in the perinatal period. Because the adenosine receptor antagonist 8PT attenuated this hyperemic response, it is concluded that adenosine is involved in eliciting the increase in retinal blood flow that accompanies hypoglycemia.

Adenosine↗
PubMedDate not supplied

[Enzyme activity and level of GABA-shunt substrates in rat brain during repeated exposure to hypoglycemic doses of insulin].

The activity of glutamate decarboxylase, GABA-, aspartate-and alanine aminotransferases, the content of GABA, glutamate, aspartate and alanine were studied in the brain hemispheres and stem of rats that were undergoing the hypoglycemic coma as well as those rats had undergone 7-9 comas on the second day after the last coma. In hypoglycemia, the brain's content of glutamate, alanine and GABA decreased and content of aspartate increased; the activity of enzymes investigated did not change. On the second day after 7-9th hypoglycemic coma, the decrease of activity of glutamate decarboxylase in hemispheres and the decrease of GABA amount in brain stem were detected. This can be an evidence of decrease of GABA amount produced and secreted by nerve ends of the pathways leading from striata to substantia nigra. The detected changes result from multiple influence of hypoglycemia to the brain and may by important in the development of posthypoglycemic encephalopathy.

Amino Acids↗
PubMed2004

Antioxidant activity and hypoglycemic effect of ferulic acid in STZ-induced diabetic mice and KK-Ay mice.

Antioxidant activity and biological properties of ferulic acid (FA) are well recognized. This study was designed to estimate the potential utility of FA administered orally at low dosage for improvement of hyperglycemia in diabetes. With this aim we have evaluated the hypoglycemic effect of FA in two type diabetic animal models: (1) streptozotocin (STZ)-induced diabetic mice, a model of insulin-dependent diabetes mellitus (IDDM); (2) KK-Ay mice, a model of non-insulin dependent diabetes mellitus (NIDDM). In addition, we measured the production of thiobarbituric acid-reactive substances (TBARS) in brown adipose tissues of diabetic mice at the end of FA feeding experiment. FA at 0.01% and 0.1% of basal diet showed to suppress significantly blood glucose levels in STZ-induced diabetic mice. In KK-Ay mice 0.05% FA suppressed effectively blood glucose levels. In addition, FA inhibited the lipid peroxidation in brown adipose tissue of diabetic mice. Taken together, these findings suggest that dietary FA may be useful in alleviating oxidative stress and attenuating the hyperglycemic response associated with diabetes.

Animals↗
PubMed1996

Hypoglycemic effect and protein nutritive quality of soy and methionine-supplemented whole durum pasta products.

New low cost, high-protein and high-fiber pasta products processed from whole durum meal (WD) solely, WD supplemented with 7% or 12% defatted soy flour (SF), or 12% SF plus 0.3% methionine were evaluated in comparison with the regular pasta made of pure durum semolina (DS). Their protein nutritive quality was biologically evaluated by rat growth studies using diets containing 9% protein, through the parameters: food efficiency ratio (FER), protein efficiency ratio (PER), net protein utilization (NPU), digestibility coefficient (DC) and biological value (BV). The original products were administered to diabetic hypercholesterolemic albino rats, (injected with alloxane) to study their effects on the levels of blood glucose and plasma lipid fractions. The results indicate that diets based on pasta made of WD supplemented with SE or SF plus methionine had superior protein quality and succeeded in supporting normal growth of rats in contrast to the diets based on pasta made of unsupplemented WD or DS. These assays demonstrated that the values of FER, PER, NPU and BV of WD-pasta increased with increasing SF supplementation. However, high-fiber pasta made of unrefined WD solely or with SF had lower DC values compared to that of the regular DS-pasta. DC values decreased as the added SF increased. Adding methionine evidently affected FER, PER, BV and NPU values. Administration of high-protein and high-fiber pasta samples made of WD solely, supplemented with SF or SF plus methionine significantly reduced the elevated blood glucose as well as plasma cholesterol and plasma lipid fractions in hypercholesterolemic diabetic rats. Overall, considering nutritional evaluation, protein cost as well as hypoglycemic and hypocholesterolemic effects the pasta composed of 12% SF-WD and supplemented with 0.3% methionine represented the best high-fiber; high-protein and high-quality product.

Animals↗
PubMed1975

N-Substituted indanamines as potential hypoglycemic agents.

A number of indanamines substituted at the terminal amino nitrogen with various aliphatic, alicyclic, heterocyclic, and aromatic ring systems were synthesized and screened for hypoglycemic activity. None was found to possess significant activity compared to tolbutamide.

Amines↗
PubMed1982

Synthesis and hypoglycemic activity of benzamidophenyl-alkanoic acid derivates: new inhibitors of gluconeogenesis.

A series of omega-[2-(N-alkylbenzamido)-phenyl]-alkanoic acids was synthesized and tested for its effects on blood glucose concentration in fasted rats and on gluconeogenesis from lactate and pyruvate in isolated perfused rat livers. The compounds led to a dose-dependent and reversible inhibition of gluconeogenesis, with 4-[2-(N-methyl-3-trifluoromethylbenzamido)-phenyl]-butanoic acid leading to a 50% inhibition at 0.02 mM. The compounds lowered blood glucose in fasted rats. No correlation between hypoglycemic effect and inhibition of gluconeogenesis could be detected, however.

Animals↗
PubMed2003

HPLC fingerprinting and estimation of the bioactive components of Clutia richardiana L. as a potential hypoglycemic herbal tea.

Clutia richardiana L. is a traditional medicinal herb with demonstrated hypoglycemic effects. An HPLC method (Luna((R)) C(18) column, gradient elution, UV detection at 220 nm) has been utilized to determine the levels of the major diterpenes of C. richardiana in extracts obtained by using three different solvents. Extraction with the organic solvents methanol and acetonitrile was more efficient than aqueous extraction with hot water, but nine markers could be detected equally in all extracts. The aqueous extract was non-toxic against a number of human cell lines, which is a promising indication for its use as a safe and effective antidiabetic herbal preparation.

Chromatography, High Pressure Liquid↗
PubMed1994

Effects of the biguanide class of oral hypoglycemic agents on mouse embryogenesis.

The incidence of birth defects among offspring of mothers with non-insulin dependent diabetes mellitus (NIDDM) is 2-3-fold higher than among infants of non diabetics. Since mothers with NIDDM are frequently given oral hypoglycemic agents, including sulphonylureas and biguanides, to control their disease and since these agents have been associated with the occurrence of congenital malformations in humans and animals, the embryotoxic effects of the most commonly employed biguanides, metformin and phenformin, were evaluated in whole embryo culture. Neurulating mouse embryos were exposed to therapeutic concentrations (metformin 500-2,550 mg per day; phenformin 50-400 mg per day, respectively) of the compounds for 24-48 h. Concentrations of metformin in culture ranged from 0.15 to 1.8 mg/ml and phenformin from 2.5 x 10(-5) to 0.4 mg/ml. Cultures were terminated and scored for gross morphological alterations and total protein content. Metformin produced no alterations in embryonic growth and no major malformations. Approximately 10% of all embryos exposed to metformin regardless of dose, exhibited open cranial neuropores after 24 h of culture. However, this anomaly appeared to represent a delay in closure as opposed to an overt defect, since no embryos exposed to the highest concentration of the drug and cultured for 48 h showed open neural tubes. In contrast, phenformin produced dose dependent changes in incidence of malformations, protein content, and embryolethality. Malformations included neural tube closure defects, craniofacial hypoplasia, and reduction in size of the first and second visceral arches. Doses above 0.1 mg/ml produced embryolethality and all embryos were killed at the 0.4 mg/ml concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Metabolic, cationic and secretory effects of hypoglycemic sulfonylureas in pancreatic islets.

Tolbutamide, gliclazide and glibenclamide failed to stimulate glucose oxidation in rat pancreatic islets. Tolbutamide also failed to stimulate pyruvate and palmitate oxidation and decreased the islet content of NAD(P)H and ATP. Tolbutamide stimulated 45Ca net uptake, inhibited 86Rb net uptake and tended to increase 22Na net uptake by the islets. The effect of theophylline upon islet function differed from that of tolbutamide by the magnitude of its insulinotropic action as a function of the glucose concentration, by its stimulant action upon the utilization of endogenous nutrients in islets deprived of glucose and by the lack of gross alteration in 45Ca and 86Rb net uptake. It is concluded that the insulinotropic effect of hypoglycemic sulfonylureas cannot be merely equated to a facilitation of nutrient metabolism or inactivation of phosphodiesterase in the islet cells. The primary action of these drugs could be to affect cations transport across the B-cell membrane.

Animals↗
PubMed2000

Mechanisms of acute and chronic hypoglycemic action of gliclazide.

An extrapancreatic effect of sulfonylureas has been postulated. However, in vivo results have been disputed because the amelioration of insulin action that follows sulfonylurea may represent the relief from glucose toxicity rather than a direct effect of the drug. Therefore, we studied the hypoglycemic action of gliclazide acutely and after 2 months of therapy in seven type 2 diabetic patients. All patients received a 240-minute i.v. glucose infusion with [3-3H]glucose. In a random order, 160 mg gliclazide (study 1) or placebo (study 2) was given orally before glucose infusion. Finally, the effect of 160 mg gliclazide was reassessed after a two-month treatment with the same sulfonylurea (80 mg t.i.d.). Basal plasma glucose, insulin, C-peptide and endogenous glucose production (EGP) were similar before the two initial studies. During glucose infusion, EGP was more suppressed after gliclazide in spite of comparable increase in plasma insulin and C-peptide. After the two-month therapy, basal plasma glucose levels and HbA1c were lower while plasma insulin and C-peptide were higher with respect to baseline (p < 0.05). Gliclazide further reduced plasma glucose, the incremental area above baseline, and EGP during glucose infusion, while plasma insulin and C-peptide achieved higher plateaus (p < 0.05). When data were pooled, plasma glucose concentration and EGP correlated both in the basal state (r = 0.71) and during the last hour of glucose infusion (r = 0.84; both p < 0.05). These data suggest that gliclazide enhances the suppression of EGP induced by insulin and that this effect is greater with chronic treatment because of concomitant improvement of insulin secretion.

Acute Disease↗
PubMed2006

Hypoglycemic and hypocholesterolemic effects of Coptis chinensis franch inflorescence.

Hypocholesterolemic and hypoglycemic activities of Coptis chinensis franch inflorescence (Coptis inflorescence) were studied using animal models. Serum total and LDL cholesterol of rats fed a diet containing 1% cholesterol and 0.5% cholic acid increased, as compared with those of rats fed a normal diet. The level of total and LDL cholesterol were reduced markedly in a dose dependent manner, in rats given Coptis inflorescence extract orally at doses of 0.25, 0.5 g/kg.day for 4 weeks. In diabetic rats induced by alloxan, Coptis inflorescence extract showed a significant (p < 0.05) blood sugar lowering activity at all experimented doses (0.125, 0.25 and 0.5 g/kg.day). The highest reduction of blood sugar was about 58% when the rats were given Coptis inflorescence extract orally at a dose of 0.5 g/kg.day for 3 weeks. The 100 g dried water extract of Coptis inflorescence contained 8.11 g total alkaloid, 3.34 g berberin, 1.08 g palmatine and 0.66 g jatrorrhizine, which had long been identified as active compounds in Coptis chinensis franch root (Coptis root). Thus, the results suggest that Coptis inflorescence would be effective in the prevention and management of coronary artery disease by lowering serum cholesterol and blood sugar.

Animals↗
PubMed1994

Comparative placental transport of oral hypoglycemic agents in humans: a model of human placental drug transfer.

OBJECTIVE: This study compares the human placental transport of glyburide, glipizide, chlorpropamide, and tolbutamide. STUDY DESIGN: The recirculating single cotyledon human placenta model tested maternal-to-fetal transport in term placentas perfused immediately after delivery. Drug levels were measured by high-performance liquid chromatography and liquid scintillation spectrometry, and transport rates were calculated by comparing maternal and fetal concentrations. RESULTS: The transport of these substances differed significantly over a tenfold range (analysis of variance, p < 0.0008). A significant association exists by multiple linear regression between drug transfer and molecular weight, dissociation constant, and the octanol-water partition coefficient (R2 = 0.91, p < 0.0001). CONCLUSIONS: There is significant variability in human placental transfer rates of the oral hypoglycemics, which strongly correlates with molecular properties. These data suggest that less fetal exposure may occur with second-generation sulfonylureas and anticipate that regression models may be useful in selecting agents that minimize placental transport to the fetus.

Administration, Oral↗
PubMed1985

Effect of oral treatment with a new hypoglycemic agent, AS-6, on the metabolic activities of adipocytes in db/db mice: a comparative study.

The mechanism of a new hypoglycemic agent, AS-6, was comparatively studied using the adipocytes from AS-6 treated and untreated genetically obese diabetic mice, db/db. the db/db mice were treated for 1 week with a diet admixture of AS-6 (0.1%). The treatment resulted in the following alterations in metabolic activities; AS-6 treatment increased 125I-insulin binding by 1.4-3.3 fold over the insulin range of 1-1000 microU/ml, the treatment increased the basal activities in 2-deoxyglucose uptake, and in CO2 generation and lipogenesis from U-(14C)-glucose compared with the db/db controls, the treatment partially restored insulin responsiveness in 2-DG uptake and CO2 generation, and 1 mU/ml of insulin greatly stimulated lipogenesis by 5.6 fold above the basal in the control adipocytes while AS-6 treatment changed the lipogenic response less stimulative to the insulin. The results suggest that AS-6 treatment significantly increases insulin binding to the adipocytes associating with an enhancement in glucose metabolism under basal and physiological concentrations of insulin.

Adipose Tissue↗
PubMed1983

Studies on the mechanism of action of the hypoglycemic agent, 2-(3-methylcinnamylhydrazono)-propionate (BM 42.304).

A new hypoglycemic agent, 2-(3-methylcinnamylhydrazono)-propionate MCHP (BM 42.304) was shown to be an inhibitor of the transfer of long-chain fatty acids across the mitochondrial inner membrane. The following data support this conclusion: the drug, at already 5 microM, inhibited ketogenesis from oleate but not from octanoate in the perfused guinea-pig liver; likewise, ketogenesis from L-(-)-palmitoylcarnitine and palmitoyl-CoA + L-(-)-carnitine, but not from octanoate, was depressed in isolated guinea-pig liver mitochondria. Oxigraphic measurements of the oxygen uptake by isolated mitochondria showed that the drug impaired oxygen uptake with the long-chain fatty acid derivatives but not with octanoate. Finally, in vivo effects of the drug such as hypoketonemia and an increased concentration of free fatty acids in blood are in agreement with the above formulated mechanism of action. A comment is given on the relationships between fatty acid oxidation and gluconeogenesis in the guinea-pig liver.

Animals↗