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PubMed2002

Acute changes of bone turnover and PTH induced by insulin and glucose: euglycemic and hypoglycemic hyperinsulinemic clamp studies.

Bone turnover is acutely suppressed after feeding or oral glucose. Insulin infusion suppresses bone turnover and might mediate this effect, but this is confounded by a possible direct effect of hypoglycemia. We examined the effect of euglycemic hyperinsulinemia and hypoglycemic hyperinsulinemia on bone turnover using an insulin clamp. Sixteen men participated in this double-blind crossover study. Clamp induction involved infusion of insulin (80 mU/m(2).min) while maintaining euglycemia (5 mmol/liter) for 40 min with a variable rate dextrose infusion. Glucose was lowered to 2.5 mmol/liter (hypoglycemic clamp) or maintained at 5 mmol/liter (euglycemic clamp) for a further 105 min. Nine controls received a matched saline infusion. Measurements included serum C-terminal telopeptide of type I collagen, procollagen type I N-terminal propeptide, osteocalcin, and PTH. Induction of hyperinsulinemia resulted in a reduction in PTH (27% +/- 5; P < 0.01), but no significant change in bone turnover from baseline. Hypoglycemic clamp resulted in suppression of serum C-terminal telopeptide of type I collagen by 34% +/- 3, procollagen type I N-terminal propeptide by 15% +/- 1, osteocalcin by 5% +/- 1, and PTH by a further 12% +/- 5 (all P < 0.05). By contrast, there was no significant change in any marker of bone turnover during euglycemic clamp. Postprandial hyperinsulinemia is unlikely to explain the acute suppression of bone turnover with feeding. The reduction in bone turnover during hypoglycemia may be related to hypoglycemia itself, acute changes in PTH, or other hormones released in response to hypoglycemia.

Adult↗
PubMed1995

[Hypoglycemic activity and mechanisms of extracts from mulberry leaves (folium mori) and cortex mori radicis in streptozotocin-induced diabetic mice].

Averaged blood glucose levels were 400 mg/dl in nonfasted mice, and 250 mg/dl in fasted mice in 4 weeks after injection with streptozotocin (STZ, 150 mg/kg, i.v.). These mice were used for experiments. Hypoglycemic effects of hot water extracts (W) from Folium Mori (Mulberry leaves, Morus alba L., China and Japan) or Cortex Mori Radicis (Morus alba L., China) were observed in fasted and nonfasted STZ-induced diabetic mice at a single dose of 200 mg/kg (i.p.). The W from Folium Mori exhibited most potent hypoglycemic effects. The most potent fractions of Folium Mori and Cortex Mori Radicis were ethanol-insoluble extracts (A2). These A2 fractions demonstrated a fall in blood glucose levels of 24.6 +/- 6.0% and 60.5 +/- 9.1% at nonfasted STZ-mice, and 81.4 +/- 7.9% and 77.3 +/- 5.8% at fasted STZ-mice, respectively. The increase in glucose uptake was a mechanism of hypoglycemic actions by W and A2 of Folium Mori.

Animals↗
PubMed1992

[Hypoglycemic effects of Siamese Momordica charantia and Phyllanthus urinaria extracts in streptozotocin-induced diabetic rats (the 1st report)].

Hypoglycemic effects of the extracts of two Siamese plants, Momordica charantia (M.c.) and Phyllanthus urinaria (P.u.), were examined in streptozotocin-induced diabetic rats. Oral administration of a 50% methanol extract (30 mg/kg) of M.c. and P.u. decreased the blood glucose levels (BGL) by 25% and 24%, respectively, at 3 hr after administration. Among other fractions such as the ethyl ether or water soluble fractions, the 10 and 30 mg/kg n-butanol soluble fraction from M.c. extract was most effective in lowering BGL by 26% and 34%, respectively. Similarly with M.c., the n-butanol fraction from P.u. extract decreased BGL by 23% and 39% at the doses of 10 and 30 mg/kg, respectively. In the oral glucose tolerance test, n-butanol fractions from M.c. and P.u. (30 mg/kg, p.o.) both inhibited the initial increase in BGL to the same degree. In the intraperitoneal glucose tolerance test the n-butanol fraction of M.c. inhibited the increase of BGL prominently, but the n-butanol fraction of P.u. did not. These plants generally contain moderately non-polar hypoglycemic compound(s) soluble in n-butanol; and specifically, with regards to the hypoglycemic mechanism, the M.c. extract seems to act like insulin or via insulin secretion from the pancreas, like the action of sulfonyl ureas, and the P.u. extract may act via facilitation of glucose metabolism and/or the inhibition of glucose absorption in the gut like the action of biguanides.

Administration, Oral↗
PubMed1998

Hypoglycemic effect of water-soluble polysaccharide from Auricularia auricula-judae Quel. on genetically diabetic KK-Ay mice.

The hypoglycemic effect of water-soluble polysaccharide(FA) from fruiting bodies of Auricularia auricula-judae Quel. was investigated on genetically diabetic mice (KK-Ay) from 10 to 14 weeks of age. Male mice were divided into 3 groups, the control group and FA-fed group having free access to the control diet or FA diet (30 g of FA/kg of diet). The food-restricted group had restricted access to the control diet at the level of the diet consumed by the FA-fed group. Compared with the control group, FA supplementation had a significant effect in lowering plasma glucose, insulin, urinary glucose, and food intake. FA administration also increased the tolerance to intraperitoneal glucose loading and the hepatic glycogen content. In the food-restricted group, the reduced food intake slightly lowered the plasma and urinary glucose levels, but did not improve hyperinsulinemia and glucose tolerance. This study shows that FA had a hypoglycemic effect on KK-Ay mice, and the reduced food consumption was not a major factor which contributed to the hypoglycemic action of FA.

Agaricales↗
PubMed2001

Nateglinide: A structurally novel, short-acting, hypoglycemic agent.

Nateglinide is a short-acting, pancreatic, beta-cell-selective, K(ATP) potassium channel blocker that improves overall glycemic control in type 2 diabetes. Although nateglinide's mechanism of action is related to that of sulphonyl-ureas and repaglinide, important differences do exist. Nateglinide binds rapidly to the sulfonylurea SUR1 receptor with a relatively low affinity, and it dissociates from it extremely rapidly in a manner of seconds. This rapid association and dissociation gives nateglinide a unique "fast on-fast off" effect. Thus, nateglinide has a rapid onset and short duration of action stimulating insulin secretion in vivo and providing good control of postprandial hyperglycemia when taken immediately prior to meals. The rapid action of nateglinide on the beta cells stimulates and restores the normal physiological first and early phase of insulin secretion, consequently reducing postprandial hyperglycemia. This hypoglycemic effect of nateglinide leads to improved glycemic control, while the short duration avoids delayed hyperinsulinemia and hypoglycemia after meals. Nateglinide is not a sulfonylurea, but it shares the mechanism of action of commonly used oral hypoglycemic agents such as glibenclamide and glipizide. Like the recently introduced, short-acting agent, repaglinide, it does not incorporate a sulfonylurea moiety. However, nateglinide's effects on insulin secretion and glycemic control differ significantly from the sulfonylureas and repaglinide in that it preferentially stimulates acute phase insulin, better controls postprandial glucose excursions and spikes, and causes less hyperinsulinemia and hypoglycemia. Compounds with such a profile should not only achieve improved overall glucose control, but also reduce the risk of vascular complications which is the most important feature of nateglinide. Clinical studies with nateglinide have confirmed that it acts rapidly and both restores insulin release and attenuates the postprandial glucose spike. Nateglinide is both effective and well tolerated in the treatment of type 2 diabetes. The reported overall profile of adverse effects appears to be superior to that of other K(ATP) potassium channel blockers, the glucose modulator metformin and PPARgamma agonists such as troglitazone. Clinical comparisons of these agents have shown nateglinide to be more effective in attenuating postprandial glucose than any other oral hypoglycemic agent, and that treatment with both nateglinide and metformin provides additive effects that afford improved control of plasma glucose levels. The administration regimen for nateglinide, immediately prior to meals, also facilitates patient compliance. (c) 2001 Prous Science. All rights reserved.

Journal Article↗
PubMed2001

Hypoglycemic syncope induced by a combination of cibenzoline and angiotensin converting enzyme inhibitor.

A 65-year-old Japanese woman with dilated cardiomyopathy, hypothyroidism and refractory sustained ventricular tachycardia experienced a near-death hypoglycemic syncope. The attack seemed to be induced by a high level of serum insulin, probably due to cibenzoline and by concomitant use of an angiotensin converting enzyme inhibitor (ACEI). Additionally, decreased food intake because of a severe toothache may have contributed to the deterioration of her condition. This case warns cardiologists that a combined cibenzoline and ACEI therapy can provoke serious adverse effects such as hypoglycemic syncope in the elderly. Therefore, the possibility of a hypoglycemic attack associated with these drugs should be explained to patients who are in poor condition.

Aged↗
PubMed2003

The starch from Solanum lycocarpum St. Hill. fruit is not a hypoglycemic agent.

We have investigated the hypoglycemic effect induced by the starch obtained from the unripe fruits of Solanum lycocarpum (Solanaceae). Per os administration of the starch (1000 or 2000 mg/kg, twice daily for 7 days, N = 6) did not change glycemia levels of nondiabetic female Swiss mice weighing 25-30 g. In streptozotocin-induced diabetic mice, similar treatment with the starch did not change the elevated glycemia 3 h after the last dose (diabetic treated with saline = 288 17/309 18; starch 1000 mg/kg = 295 +/- 33; starch 2000 mg/kg = 258 +/- 37; N = 5). In animals fasted for 15 h, per os administration of glucose (600 mg/kg) significantly increased glycemia 1 h later. Previous (-30 min) treatment of the animals with the starch (1000 or 2000 mg/kg; N = 5) did not change the increase of glycemia. Per os administration of the starch (1000 or 2000 mg kg-1 day-1, twice daily for 7 days) did not induce body weight gain or loss. The chemical analysis of the starch indicated the presence of glycoalkaloids, a finding that represents a reason for concern since many of these substances are generally toxic. In interviews with 56 diabetic patients, 29 medicinal plants were reported as useful in their treatment of diabetes and S. lycocarpum was the sixth most frequently mentioned. All patients interviewed reported that they also used insulin or oral hypoglycemic drugs. The results of the present study do not provide evidence for a hypoglycemic effect associated with the polysaccharide fraction of S. lycocarpum in either normal or hyperglycemic mice. These data demonstrate the need for adequate pharmacological investigation of the natural products widely used in folk medicine.

Animals↗
PubMed2006

Metabolic sensors mediate hypoglycemic detection at the portal vein.

The current study sought to ascertain whether portal vein glucose sensing is mediated by a metabolic fuel sensor analogous to other metabolic sensors presumed to mediate hypoglycemic detection (e.g., hypothalamic metabosensors). We examined the impact of selectively elevating portal vein concentrations of lactate, pyruvate, or beta-hydroxybutyrate (BHB) on the sympathoadrenal response to insulin-induced hypoglycemia. Male Wistar rats (n = 36), chronically cannulated in the carotid artery (sampling), jugular vein (infusion), and portal vein (infusion), underwent hyperinsulinemic-hypoglycemic ( approximately 2.5 mmol/l) clamps with either portal or jugular vein infusions of lactate, pyruvate, or BHB. By design, arterial concentrations of glucose and the selected metabolite were matched between portal and jugular (NS). Portal vein concentrations were significantly elevated in portal versus jugular (P < 0.0001) for lactate (5.03 +/- 0.2 vs. 0.84 +/- 0.08 mmol/l), pyruvate (1.81 +/- 0.21 vs. 0.42 +/- 0.03 mmol/l), or BHB (2.02 +/- 0.1 vs. 0.16 +/- 0.03 mmol/l). Elevating portal lactate or pyruvate suppressed both the epinephrine (64% decrease; P < 0.01) and norepinephrine (75% decrease; P < 0.05) responses to hypoglycemia. In contrast, elevating portal BHB levels failed to impact epinephrine (P = 0.51) or norepinephrine (P = 0.47) levels during hypoglycemia. These findings indicate that hypoglycemic detection at the portal vein is mediated by a sensor responding to some metabolic event(s) subsequent to the uptake and oxidation of glucose.

Animals↗
PubMed1979

Effect of acetate on hypoglycemic seizures in mice.

In order to determine the effects of acetate on signs and symptoms of hypoglycemic seizures, Swiss Webster albino mice were injected intraperitoneally with solutions of NaCl, NaHCO3, NH4Cl, Na-acetate, or NH4-acetate, followed by subcutaneous injection of 7 U of insulin/kg body wt. Administration of Na- or NH4-acetate delayed and reduced the incidence of hypoglycemic reactions. Reinjection with Na-acetate or repeated injections with NH4-acetate caused a return to normal behavior patterns for 60 and 75%, respectively, of the affected hypoglycemic experimental animals. Injections of control animals with NaHCO3 or NH4Cl showed that the results were not due to alkalosis or acidosis. Acetate administration significantly increased plasma acetate and citrate, but not glucose, lactate, beta-hydroxybutyrate, or acetoacetate concentrations. The results indicate that intraperitoneal administration of acetate directly acted to prevent signs of hypoglycemia from occurring and reversed its manifestations when they were present. The protective effect of acetate suggests that it may serve as a fuel for the brain.

Acetates↗
PubMedDate not supplied

Hypoglycemic symptoms and decreased beta-adrenergic sensitivity in insulin-dependent diabetic patients.

Thirty-seven insulin-dependent diabetic patients were tested for symptoms of hypoglycemia, cardiac autonomic neuropathy (i.e., heart rate variation during deep breathing, Valsalva maneuver, immediate heart rate response to standing), and isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min: I25). Tests of cardiac autonomic neuropathy showed no relation to hypoglycemic symptoms. On the contrary, a clear relationship could be established between isoproterenol sensitivity and adrenergic symptoms of hypoglycemia. Diabetic patients with decreased response to isoproterenol had fewer adrenergic symptoms, perceived hypoglycemia at a lower blood glucose level, and had more hypoglycemic accidents. Symptoms most related to isoproterenol sensitivity were tremor, sweaty palms, and hunger. With the isoproterenol-sensitivity test a distinction could be made between the groups at high (I25 greater than 3 micrograms) and low (I25 less than 3 micrograms) risk for hypoglycemic accidents. We suggest that the isoproterenol-sensitivity test could be used to identify diabetic patients at increased risk for hypoglycemia.

Adult↗
PubMed1991

Hypoglycemic symptoms and frequency of severe hypoglycemia in patients treated with human and animal insulin preparations.

OBJECTIVES: To compare hypoglycemic warning symptoms (main objective) and incidence of severe hypoglycemia (secondary objective) between patients treated with animal and human insulin preparations. RESEARCH DESIGN AND METHODS: Two hundred forty-seven patients on treatment with animal insulin preparations and 276 patients on human insulins, matched for duration of diabetes (16 +/- 11 vs. 15 +/- 10 yr), were recruited for the study. Patients were interviewed with a standardized questionnaire. RESULTS: When asked which symptom usually occurs first during hypoglycemia, 19% of the animal insulin group and 22% of the human insulin group answered "sweating," 19 and 17%, respectively, answered "trembling," and 15 and 11%, respectively, answered "unrest." According to the patients' perception, in both groups, their most reliable hypoglycemic warning symptoms were "trembling" (26 and 22%) and "sweating" (15 and 18%). Six and eight percent of patients, respectively, reported hypoglycemia unawareness and 17 and 18%, respectively, impaired awareness of hypoglycemia. The incidence of severe hypoglycemia was 0.45 cases/patient-yr in patients treated with animal insulins and 0.46 cases/patient-yr in patients treated with human insulin preparations. The differences were not statistically significant. CONCLUSIONS: This study shows that hypoglycemic warning symptoms and the incidence of severe hypoglycemia are comparable between patients on treatment with human and animal insulin preparations.

Adult↗
PubMed1994

Accuracy of plasma glucose measurements in the hypoglycemic range.

OBJECTIVE: This study was designed to evaluate three different enzymatic methods for glucose measurement in plasma samples with special emphasis on glucose concentrations in the hypoglycemic range. RESEARCH DESIGN AND METHODS: Glucose dehydrogenase (Hemo-Cue analyzer), glucose oxidase (YSI analyzer), and hexokinase (Abbott analyzer) methods were used to measure plasma samples that were obtained during research studies. RESULTS: Mean glucose concentrations (n = 240) were 5.3 +/- 0.2, 5.4 +/- 0.2, and 5.6 +/- 0.2 mM (95.6 +/- 3.9, 96.7 +/- 3.9, and 101.6 +/- 4.0 mg/dl) using glucose dehydrogenase, glucose oxidase, and hexokinase, respectively (NS). In the hypoglycemic range, mean glucose concentrations with each method retained the same hierarchy of measurements: 2.7 +/- 0.05, 2.8 +/- 0.04, and 2.9 +/- 0.03 mM (48.4 +/- 0.9, 50.6 +/- 0.8, and 52.3 +/- 0.6 mg/dl) by glucose dehydrogenase, glucose oxidase, and hexokinase, respectively (P < 0.005). Individual glucose dehydrogenase measurements (n = 240) correlated well with glucose oxidase and hexokinase, r = 0.99, and were considerably easier to perform at the bedside. The differences between the glucose measurement methods were consistent and similar in low, normal, and high concentration ranges. CONCLUSIONS: We conclude that any interpretation or comparison of critical clinical and research measurements of glucose in different settings take into account methodological differences, particularly in the hypoglycemic range.

Analysis of Variance↗
PubMed1995

Reduced awareness of hypoglycemia in adults with IDDM. A prospective study of hypoglycemic frequency and associated symptoms.

OBJECTIVE: To prospectively evaluate the frequency and severity of hypoglycemic episodes in IDDM subjects who declare themselves to have reduced awareness of hypoglycemia, to validate their self-designations in their natural environment, and to determine objectively the presence or absence of autonomic and neuroglycopenic symptoms associated with their low blood glucose (BG) levels. RESEARCH DESIGN AND METHODS: A total of 78 insulin-dependent diabetes mellitus (IDDM) subjects (mean age 38.3 +/- 9.2 years; duration of diabetes 19.3 +/- 10.4 years) completed two sets of assessments separated by 6 months. The assessments included reports of frequency and severity of low BG, symptoms associated with low BG, and a BG symptom/estimation trial using a hand-held computer (HHC). Diaries of hypoglycemic episodes were kept for the intervening 6 months. HbA1 levels were determined at each assessment. RESULTS: Of the subjects, 39 declared themselves as having reduced awareness of hypoglycemia (reduced-awareness subjects). There were no differences between these reduced-awareness subjects and aware subjects with regard to age, sex, disease duration, insulin dose, or HbA1. During the HHC trials, reduced-awareness subjects were significantly less accurate in detecting BG < 3.9 mmol/l (33.2 +/- 47 vs. 47.6 +/- 50% detection, P = 0.001) and had significantly fewer autonomic (0.41 +/- 0.82 vs. 1.08 +/- 1.22, P = 0.006, reduced-awareness vs. aware) and neuroglycopenic (0.44 +/- 0.85 vs. 1.18 +/- 1.32, P = 0.004, reduced-awareness vs. aware) symptoms per subject. Prospective diary records revealed that reduced-awareness subjects experienced more moderate (351 vs. 238, P = 0.026) and severe (50 vs. 17, P = 0.0062) hypoglycemic events. The second assessment results were similar to the first and verified the reliability of the data. CONCLUSIONS: IDDM subjects who believe they have reduced awareness of hypoglycemia are generally correct. They have a history of more moderate and severe hypoglycemia, are less accurate at detecting BG < 3.9 mmol/l, and prospectively experience more moderate and severe hypoglycemia than do aware subjects. Neither disease duration nor level of glucose control explains their reduced awareness of hypoglycemia. Reduced-awareness individuals may benefit from interventions designed to teach them to recognize all of their potential early warning symptoms.

Adult↗
PubMedDate not supplied

Improved glycemic control with use of oral hypoglycemic therapy with or without insulin.

OBJECTIVE: To determine whether combination oral hypoglycemic therapy in insulin-using patients with non-insulin-dependent diabetes mellitus (NIDDM) can improve glycemic control for a prolonged period. METHODS: We expanded and extended an earlier study to include 130 patients with NIDDM for 10 to 30 years who had been using twice-daily mixed insulin for less than 10 years. Reduction and eventual elimination of the insulin therapy and substitution of metformin and a sulfonylurea were attempted. At follow-up visits, patients were weighed, random plasma glucose levels were determined, and glycosylated hemoglobin values were obtained. RESULTS: Of 130 C-peptide-positive patients with NIDDM receiving twice-daily mixed insulin, 100 were successfully transferred to combination oral hypoglycemic therapy with glyburide originally and later glimepiride and metformin--a primary failure rate of 23.1%. Secondary failure occurred in 20 patients after a mean duration of 6.4 months. Two patients with successful conversion to oral combination therapy resumed insulin treatment because of cost. Of the patients with primary failures, 6 had gastrointestinal side effects, 10 were successfully managed on combination oral therapy plus evening mixed insulin, and 14 ultimately received twice-daily insulin and metformin. Of the secondary failures, 13 were controlled on combination oral therapy plus evening insulin and 7 on twice-daily insulin in conjunction with metformin. No difference was found in the original C-peptide levels among these three groups. Glycosylated hemoglobin levels were significantly less on combined oral hypoglycemic therapy (9.8% versus 8.3%; P = 0.0001), on combination oral therapy plus evening insulin (11.2% versus 9.7%; P = 0.001), and on return to twice-daily mixed insulin with metformin (11.0% versus 9.9%; P = 0.04). Those eight patients who resumed twice-daily insulin therapy alone, however, had a nonsignificant increase in glycosylated hemoglobin (9.3% versus 9.9%). CONCLUSION: Improvement in glycosylated hemoglobin level in insulin-using patients with NIDDM can be obtained with combination oral therapy alone, combination oral therapy with once-daily evening insulin, or twice-daily mixed insulin with metformin in comparison with twice-daily insulin alone.

Journal Article↗
PubMed2000

Effect of succinylcholine on the neuromuscular junction of hypoglycemic rats.

The aim of the present study was to investigate the effect of neuromuscular blocking drugs on the neuromuscular junction in hypoglycemic rats. Three groups of 6 white adult Wistar albino rats were used. Group A consisted of the control animals with normal blood glucose levels ranging between 80-120 mg/dl. Groups B and C consisted of animals which were made hypoglycemic by intravenous injection of insulin at a dose of 1 iU/100 g b.w. In this way, their blood glucose levels were reduced to 50% of the blood glucose levels of the control animals. The test animals (groups B and C) were sacrificed 40 min after the injection of insulin and the preparations of the phrenic nerve-hemidiaphragm were placed into a 100 ml_bath containing Paradelis-Zaimis solution. The bath was aerized with O2/CO2:95/5%, it's temperature was maintained at 37 degrees C and it's pH at 7.2. After the stabilization of the system and the recording of neuromuscular activity, succinylcholine was administered (1.5 x 10(-8) M in groups A and B and 3.0 x 10(-8) M in group C). For the statistical analysis of the results, student's t-test was used. According to our results, there is a statistically significant difference (with p < 0.02 being considered significant) between the n.bl/t% (magnitude of final neuromuscular blockage) values of the animals of groups B and C and those of the animals of group A. We also observed a statistically significant difference (with p < 0.001 being considered significant) between the t (time required for complete blockage in groups A and C or time required for stabilization of blockage in group B) values of the animals of groups B and C and those of the animals of group A. On the other hand, there was a statistically significant difference (p < 0.02 being considered significant) in the n.bl/5'% (magnitude of neuromuscular blockage 5 min after the administration of succinylcholine) values only between the animals of group A and B. Our results indicate that under hypoglycemic conditions, the amount of succinylcholine required for final neuromuscular blockage is two times greater than that needed under normal glucose blood levels. This finding suggests that the integrity of the neuromuscular junction is altered during hypoglycemia.

Animals↗
PubMed2000

Clinical observation and experimental study on compound hypoglycemic decoction for hyperglycemia.

PURPOSE: To observe the clinical efficacy of Compound Hypoglycemic Decoction (CHD) and its effect on serum total cholesterol in model mice. METHOD: The paired t test was used to analyze the data recorded before and after administration of drugs for hyperglycemia induced by intraperitoneal injection of 75% egg yolk emulsion in experimental mice. CHD and Fenofibrate were administered as prevention measures. RESULTS: The total effective rate of serum total cholesterol (TC) decrease in 60 cases of hyperglycemia was 86.66% and that of serum total triglyceride (TG) decrease was 81.81%. The total effective rate of high-density lipoprotein-cholesterol (HDL-C) increase was 75%. The decrease in TC and TG, and the increase of HDL-C after treatment by in-group comparison were all significant (P < 0.05). 21.9% and 22.2% decrease in the total cholesterol was respectively found in the CHD and Fenofibrate groups (both P < 0.05), with no significant difference. CONCLUSION: The hypoglycemic action of Compound Hypoglycemic Decoction was remarkable in clinical practice, and it is very effective in preventing hyperglycemia in experimental mice.

Adult↗
PubMed2003

Hypoglycemic neuronal death and cognitive impairment are prevented by poly(ADP-ribose) polymerase inhibitors administered after hypoglycemia.

Severe hypoglycemia causes neuronal death and cognitive impairment. Evidence suggests that hypoglycemic neuronal death involves excitotoxicity and DNA damage. Poly(ADP-ribose) polymerase-1 (PARP-1) normally functions in DNA repair, but promotes cell death when extensively activated by DNA damage. Cortical neuron cultures were subjected to glucose deprivation to assess the role of PARP-1 in hypoglycemic neuronal death. PARP-1-/- neurons and wild-type, PARP-1+/+ neurons treated with the PARP inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone both showed increased resistance to glucose deprivation. A rat model of insulin-induced hypoglycemia was used to assess the therapeutic potential of PARP inhibitors after hypoglycemia. Rats subjected to severe hypoglycemia (30 min EEG isoelectricity) accumulated both nitrotyrosine and the PARP-1 product, poly(ADP-ribose), in vulnerable neurons. Treatment with PARP inhibitors immediately after hypoglycemia blocked production of poly(ADP-ribose) and reduced neuronal death by >80% in most brain regions examined. Increased neuronal survival was also achieved when PARP inhibitors were administered up to 2 hr after blood glucose correction. Behavioral and histological assessments performed 6 weeks after hypoglycemia confirmed a sustained salutary effect of PARP inhibition. These results suggest that PARP-1 activation is a major factor mediating hypoglycemic neuronal death and that PARP-1 inhibitors can rescue neurons that would otherwise die after severe hypoglycemia.

Animals↗
PubMedDate not supplied

Hypoglycemic action and disposition of gliclazide in normal and analbuminemic rats.

The hypoglycemic action and disposition of gliclazide, an oral antidiabetic drug, was investigated in normal and analbuminemic rats. Orally administered gliclazide exhibited a stronger hypoglycemic action in analbuminemic rats than in normal rats. However, the plasma concentration of the drug in the mutant was much lower than that in the normal. This apparent discrepancy may be clarified by measuring the plasma concentration of unbound gliclazide. Analbuminemic rats gave larger values for the total body clearance and steady state volume of distribution of gliclazide than normal rats. The biliary and urinary excretion rates of radioactivity after intravenous bolus administration of [3H]-gliclazide were much greater in the mutant than in the normal. The binding of gliclazide to serum in analbuminemic rats was much lower than that in normal rats. Furthermore, the radioactivities of some tissues after oral administration of [3H]-gliclazide were found to be significantly higher in the mutant than in the normal. These results clearly indicate that albumin plays an important role in the hypoglycemic activity and disposition of gliclazide in rats.

Animals↗