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PubMed1991

Teicoplanin does not modify the hypoglycemic effects of phenformin or glibenclamide, nor the anticoagulant action of warfarin. Experimental study.

Eventual pharmacological interactions induced by teicoplanin administration associated with oral hypoglycemic (phenformin and glibenclamide) and oral anticoagulant (warfarin) drugs have been experimentally evaluated. The administration of teicoplanin (3-15 mg/kg/die by endoperitoneal route) to the rat for 4 days did not significantly (P greater than 0.05) modify glycemia, prothrombin and partial thromboplastin times, the hypoglycemic effect of phenformin (2.5 mg/kg/die/4 days) or glibenclamide (0.5 mg/kg/die/4 days) nor the anticoagulant effect of warfarin (0.5 mg/kg/die/4 days). In conclusion, our results document that teicoplanin does not interfere with the activity of phenformin, glibenclamide or sodium warfarin.

Administration, Oral↗
PubMed1975

Effects of carbohydrate restriction on glucose tolerance of normal men and reactive hypoglycemic patients.

Normal individuals ingesting a low carbohydrate diet frequently develop an impairment of glucose tolerance as measured by the oral glucose tolerance test; most of these diets, however, have been high in fat content. Our present studies demonstrate that a low carbohydrate diet (57 g/day) did not impair the glucose tolerance of normal men if the fat content was similar to values on a standard (301 g/day) carbohydrate diet. However, a low carbohydrate diet did lead to impaired glucose tolerance when the fat content was 16 per cent higher than on the control diet. Thus our present and previous studies demonstrate that normal men maintain normal glucose tolerance on low carbohydrate diets and suggest that the deterioration of the glucose tolerance observed on high fat diets is related to the increased fat content rather than to the reduced carbohydrate content of these diets. Seven patients with reactive hypoglycemia were exquisitely sensitive to carbohydrate deprivation. Whereas the glucose tolerance tests of normal men were not altered by a low carbohydrate, high protein diet, a significant deterioration of glucose tolerance occurred when reactive hypoglycemic patients were changed from control diets to low carbohydrate, high protein diets. These hypoglycemic patients also showed an exaggerated deterioration of the glucose tolerance after a 48-hour fast when compared tothe response of normal men. Our observations suggest that a low carbohydrate, high protein diet is not the best therapeutic diet for certain patients with reactive hypoglycemia because this diet does not provide symptomatic improvement and, in addition, leads to impaired glucose tolerance.

Adolescent↗
PubMed2005

Brief report: parent perceptions of hypoglycemic symptoms of youth with diabetes; disease disclosure minimizes risk of negative evaluations.

OBJECTIVE: Based on a theoretical model, this study explored the effects that the disclosure of diabetes has on parental perceptions of a hypothetical child experiencing hypoglycemia. METHODS: Parents (N = 610) first read vignettes that varied in a 2 x 2 design (Male vs. Female Character x Preventative Disclosure of Illness vs. Nondisclosure) and then answered several questions regarding the hypothetical child, resulting in four subscales that were validated using confirmatory factor analysis. RESULTS: Disclosure of diabetes significantly increased perceptions of a medical problem, decreased suspicions of drug use, and presented a lower risk of parental restrictions on future contact with their child. CONCLUSIONS: Individuals who disclose their diabetes may prevent negative social consequences and restrictions on social contact. Those who choose not to disclose may risk having a hypoglycemic event perceived as a drug or alcohol problem, which may ultimately interfere with appropriate medical intervention in a hypoglycemic event.

Adolescent↗
PubMed2001

Insulinoma-induced hypoglycemic death in mice is prevented with beta cell-specific gene therapy.

OBJECTIVE AND SUMMARY BACKGROUND DATA: Tumor-specific gene therapy can be achieved if a tumor-specific promoter can be identified. In this study the authors investigated the use of the rat insulin promoter (RIP) for insulinoma-specific expression of a reporter gene. Insulinoma-specific cytotoxicity using the suicide gene thymidine kinase (tk) was studied both in vitro and in vivo. RIPtk gene therapy, delivered by a nontoxic, noninflammatory liposomal delivery system, was used in an insulinoma ICR/SCID mouse model to prevent hypoglycemic death. METHODS: Rat insulin promoter (0.502 kb) was ligated to the reporter gene lacZ and ligated to the tk gene. These two genes were transfected into a mouse insulinoma (NIT) cell line to ascertain insulinoma-specific expression and insulinoma-specific cytotoxicity in vitro. Reverse transcriptase-polymerase chain reaction and electrophoretic mobility-shift assays were performed on NIT-1 cell RNA and nuclear extract, respectively, to determine the transcription factors present and responsible for RIP activation in NIT-1 cells. A mouse insulinoma model was created with NIT-1 cells. These mice were treated with the RIPtk gene, and both blood sugars and animal viability were monitored. RESULTS: Only NIT-1 cells stained blue after X-gal staining or had detectable levels of beta-galactosidase protein. A significant decrease in cell survival was observed in NIT-1 cells transfected with RIPtk in vitro. Messenger RNA for both BETA2 and PDX-1 was found in NIT-1 cells, and a supershift was observed for both BETA2 and PDX-1. Experimental mice treated with the RIPtk gene, delivered by a liposomal gene delivery system, maintained their blood glucose levels, and the animals did not die of hypoglycemia. CONCLUSIONS: The data suggest that the RIP is an insulinoma-specific promoter. An ICR/SCID mouse insulinoma model was used to show that insulinoma-specific cytotoxicity can be accomplished by RIP coupled to a suicide gene in vivo, preventing hypoglycemic death.

Animals↗
PubMed1992

Release of excitatory amino acids from cultured hippocampal astrocytes induced by a hypoxic-hypoglycemic stimulation.

An excess release of excitatory amino acids (EAA) is an important factor for postischemic brain damage. In the present communication, we demonstrate that cultured hippocampal cells release EAA after hypoxic-hypoglycemic treatment. The amounts of EAA released from astrocytes were appreciably above those released from neurons. Furthermore, the amount of aspartate released from astrocytes was comparable to that of glutamate, although the endogenous content of aspartate was one-fifth that of glutamate. The endogenous content of aspartate in astrocytes increased even after hypoxic-hypoglycemic treatment. These results suggests that ischemic neuronal death is due, at least in part, to the excitotoxicity of aspartate and glutamate derived from surrounding astrocytes.

Amino Acids↗
PubMed1984

Reactive hypoglycemic tendency among arsonists.

A reactive hypoglycemic tendency during the glucose tolerance test was connected with fire-setting behavior. These hypoglycemic arsonists not only fulfilled the criteria for either intermittent explosive disorder or violent antisocial personality, but also those for borderline personality disorder. They seemed to differ from other arsonists in alcohol abuse and behavior during the fire-setting acts, and, in personality profile in MMPI, also differed from classical violent offenders with intermittent explosive disorder.

Adult↗
PubMed1969

Hypoglycemic activity of endotoxin. II. Mechanism of the phenomenon in BCG-infected mice.

The mechanism of the hypoglycemic activity of endotoxin in hyperreactive BCG mice was investigated. The mechanism was found to be an inhibition of the synthesis of glucose from noncarbohydrate sources. The possibilities of an induced hypermetabolic state and an induced release of insulin in response to endotoxin as causes for the hypoglycemic response were essentially ruled out. In addition, no clear-cut evidence of an insulin-like action by endotoxin was found in the in vivo setting.

Animals↗
PubMed1989

The hypoglycemic effect of the crude drug prescription resources from Taiwan on experimental diabetic-mellitus (II)--the antihyperglycemic effect of tang-niao-tung no. 2 and no. 3.

The water extracts of crude drugs of Taiwan Tang-Niao-Tung (T.N.T.) No. 2 and No. 3 were administered to normal and diabetic rats for investigating the antihyperglycemic effect of these two prescriptions. It was found that the blood glucose level in normal rats was temporarily increased after T.N.T. No. 2 and No. 3 administration; this may be caused by the starch content of the drugs component. In contrast, the diabetic rats have shown a significant decrease (P less than 0.01) of blood glucose in 2, 4, 6 hours after T.N.T. No. 2 and No. 3 have been given. The blood glucose percentage at 6 hours was 78.1% of T.N.T. No. 2 and 79.2% of T.N.T. No. 3 as compared to the original level. The hypoglycemic effect of T.N.T. No. 2 and No. 3 on alloxan-induced diabetic rats have suggested that action mechanism might not mediate through the release of insulin or positive feedback of glucose to insulin, neither acted on insulin receptor. It might be possible by the indirect promoting of enzyme activity. However, the pharmacological effect of some drugs could elucidate the hypoglycemic action of these prescriptions. Temporary promotion of blood glucose in normal rats will decline to normal level by 12 hours after T.N.T. No. 2 and No. 3 administration. The pharmacological effect of these herb prescriptions for diabetic rats is valuable for further study.

Animals↗
PubMed1991

Opiate blockade enhances hypoglycemic counterregulation in normal and insulin-dependent diabetic subjects.

To examine the impact of opiate blockade on glucose counterregulation we performed two hypoglycemic insulin clamp studies with and without naloxone in healthy subjects and well-controlled insulin-dependent (IDDM) patients with defective glucose counterregulation. During both studies plasma glucose fell to 55-60 mg/dl and was then maintained at that level using a variable glucose infusion. In normal subjects, naloxone increased glucose production, thereby reducing the exogenous glucose dose needed to maintain the hypoglycemic plateau. Epinephrine and cortisol responses to hypoglycemia were increased during naloxone plus insulin compared with insulin alone; glucagon responses were unaffected. IDDM patients with suppressed hepatic and hormonal responses to insulin-induced hypoglycemia also demonstrated greater stimulation of glucose production as well as epinephrine, growth hormone, and cortisol release during the naloxone study. In the absence of hypoglycemia, naloxone did not significantly affect glucose production or glucoregulatory hormones. We conclude that opiate blockade augments glucoregulatory responses to insulin-induced hypoglycemia, even in IDDM patients with preexisting defects in glucose counterregulation. This effect is at least in part due to enhanced counterregulatory hormone release during hypoglycemia. Endogenous opiates may modulate hormonal responses during hypoglycemia; their blockade could provide a means of ameliorating defective counterregulation in IDDM patients.

Adult↗
PubMed1993

Response to intravenous injections of amylin and glucagon in fasted, fed, and hypoglycemic rats.

The actions of intravenous glucagon and amylin, a newly discovered hyperglycemic pancreatic islet hormone, have been compared in 20-h fasted and fed, lightly anesthetized rats, and in rats made hypoglycemic with an insulin infusion. In fasted animals, amylin (75 nmol/kg) was more effective than glucagon (90 nmol/kg) in increasing plasma glucose (glucose increment 4.55 vs. 1.71 mM, P < 0.001). Amylin elicited a marked increase in plasma lactate, as previously reported, whereas glucagon did not alter plasma lactate. In fed animals, glucagon elicited twice as much increase in plasma glucose as did amylin; amylin again elicited a marked lactate increase that was greater (increment 1.45 vs. 0.97 mM, P < 0.05) and more prolonged than in the fasted state, whereas glucagon was without effect on lactate levels. These findings are consistent with glucagon's known action to promote hyperglycemia from hepatic glycogenolysis and amylin's demonstrated action to promote muscle glycogenolysis and increase lactate supply to the liver. Infusions of sodium lactate that produced plasma lactate increments similar to those evoked by 75 nmol/kg amylin evoked patterns of glucose response in fasted and fed rats similar to those evoked by amylin. Thus increased lactate supply to the liver may account for amylin's hyperglycemic effects. Amylin and glucagon could each restore plasma glucose to control levels in fasted animals made hypoglycemic by insulin infusion (plasma glucose reduced to 3.3 mM). A bolus of 75 nmol/kg amylin was more effective than 180 nmol/kg glucagon, restoring basal glucose levels for > 3 h, whereas glucagon restored it for < 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed2001

Effects of antecedent hypoglycemia, hyperinsulinemia, and excess corticosterone on hypoglycemic counterregulation.

This study aimed to differentiate the effects of repeated antecedent hypoglycemia, antecedent marked hyperinsulinemia, and antecedent increases in corticosterone on counterregulation to subsequent hypoglycemia in normal rats. Specifically, we examined whether exposure to hyperinsulinemia or elevated corticosterone per se could impair subsequent counterregulation. Four groups of male Sprague-Dawley rats were used: 1) normal controls (N) had 4 days of sham antecedent treatment; 2) an antecedent hypoglycemia group (AH) had 7 episodes of hyperinsulinemic hypoglycemia over 4 days; 3) an antecedent hyperinsulinemia group (AE) had 7 episodes of hyperinsulinemic euglycemia; and 4) an antecedent corticosterone group (AC) had 7 episodes of intravenous corticosterone to simulate the hypoglycemic corticosterone levels in AH rats. On day 5, hyperinsulinemic euglycemic-hypoglycemic clamps were performed. Epinephrine responses to hypoglycemia were impaired (P < 0.05 vs. N) after antecedent hypoglycemia and hyperinsulinemia. This correlated with diminished (P < 0.05 vs. N) absolute glucose production responses in AH rats and diminished incremental glucose production responses in AE rats. Paradoxically, norepinephrine responses were increased (P < 0.05 vs. N) after antecedent hypoglycemia. Glucagon and corticosterone responses were unaffected by antecedent hypoglycemia and hyperinsulinemia. In AC rats, incremental but not absolute glucose production responses were decreased (P < 0.05 vs. N). However, neuroendocrine counterregulation was unaltered. We conclude that both antecedent hypoglycemia and hyperinsulinemia impair epinephrine and glucose production responses to subsequent hypoglycemia, suggesting that severe recurrent hyperinsulinemia may contribute to the development of hypoglycemia-associated autonomic failure.

Animals↗
PubMed1983

Hyperammonemia in hypoglycemic preterm neonates.

Plasma glucose, blood urea nitrogen, and ammonia were measured simultaneously in 44 newborns a few hours after birth. When the concentration of plasma glucose was below 30 mg/dl, plasma ammonia concentration was significantly higher (129 +/- 67 mumol/l) than in normoglycemic infants (74 +/- 33 mumol/l; p less than 0.01). Blood urea nitrogen was slightly lower in hypoglycemic infants (3.65 +/- 0.7 mmol/l) than in the control group (4.5 +/- 1 mmol/l) but the difference was not significant. These data show that hyperammonemia can be associated to hypoglycemia in low birth weight infants. Therefore, further investigations are required to determine the link between urea and glucose production rates in hypoglycemic newborns and whether hyperammonemia participates in the deleterious effects of hypoglycemia on the neonatal brain.

Alanine↗
PubMed1983

Synergistic effect of a tumor-promoting phorbol ester and a hypoglycemic sulfonylurea upon insulin release.

The tumor-promoting phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and the hypoglycemic sulfonylurea gliclazide both stimulate insulin release from rat pancreatic islets incubated at a low concentration of glucose (2.8 mM). The increment in secretion rate evoked by the combination of these two secretagogues was at least 7 times higher than the sum of increments evoked by each agent alone. TPA augmented insulin release evoked by gliclazide more efficiently than that induced by glucose. The enhancing action of TPA could not be attributed solely to changes in the capacity of gliclazide to inhibit 86Rb outflow, to provoke an exchange between influent 40Ca and effluent 45Ca, or to stimulate the net uptake of 45Ca by the islets. Nevertheless, the facilitation by TPA of gliclazide-induced insulin release suggests that a biophysical interference with the handling of cations at the plasma membrane level represents the primary site of action of hypoglycemic sulfonylureas in the pancreatic B cell.

Animals↗
PubMed1975

Stimulation of the secretion of parathyroid hormone during hypoglycemic stress.

The effect and the mechanism of insulin-induced hypoglycemic stress on parathyroid hormone (PTH) secretion in man was evaluated. Porcine crystalline insulin (0.1 U/kg,iv) caused symtomatic hypoglycemia in all subjects. The maximum hypoglycemia occurred between 25 and 35 min following the insulin administration. A significant increase in the serum PTH concentration occurred promptly at 5 min following the time of maximum hypoglycemia, achieving peak levels between 5 and 15 min. Thereafter the serum PTH concentration gradually declined, reaching baseline values of 60 min. Serum cortisol levels were increased, but not until 30 min following the maximum hypoglycemia, and remained significantly elevated at 60 min. Therefore the stimulation of PTH secretion was not caused by elevated levels of serum cortisol. The serum calcium and magnesium levels remained unchanged throughout the procedure. A significant and sustained decline in the serum inorganic phosphate levels occurred following insulin administration. The results indicate that hypoglycemic stress stimulates PTH secretion, presumably via increased epinephrine levels, and further suggest that adrenergic stimuli play an important role in the physiology of PTH secretion.

Adult↗
PubMed1983

Study of hypoglycemic patients by the glucose clamp technique using the artificial pancreas.

Using the artificial pancreas, blood glucose levels were maintained at 80 mg/dl in nine hypoglycemic patients (four with histologically proven insulinomas and five with nontumoral hypoglycemia) and in four normal subjects during a 24-h fast. The amount of glucose used, serum insulin levels, and glucose clearance were higher in patients with nontumoral hypoglycemia than in normal subjects and highest in the patients with an insulinoma. Surgical or pharmacological treatment resulted in normalization of all parameters. In contrast to the 72-h fast, the 24-h glucose clamp technique allowed the study of hypoglycemic patients without inducing hazardous hypoglycemia.

Adenoma, Islet Cell↗
PubMed1998

Imaging of the buffering effect of insulin antibodies in the autoimmune hypoglycemic syndrome.

Insulin autoimmune hypoglycemia is characterized by recurrent hypoglycemia and high levels of immunoreactive insulin in the presence of insulin autoantibodies. The mechanisms inducing hypoglycemia are largely unknown. An [123I]insulin scintigraphic scanning was performed to directly demonstrate the effect of antibodies on insulin biodistribution in one patient with this syndrome both before and after treatment. The patient had insulin autoantibodies IgG3 lambda, which had a single site dissociation constant (Kd = 10(-7) mol/L, by Scatchard analysis), a very fast dissociation rate of immune complexes, and a very rapid association of [125I]insulin. Insulin receptors on red blood cells were down-regulated. The [123I]insulin scintigraphic study imaged the buffering effect of antibodies on insulin bioavailability. [123I]Insulin was not removed from the blood, and no liver or kidney uptake of the hormone occurred. The frequency and severity of hypoglycemic episodes required treatment. Insulin antibody levels decreased and [123I]insulin biodistribution improved after treatment with plasmapheresis and prednisone. Improved hormone bioavailability was further evidenced by the reduction in the hypoglycemic delay after i.v. insulin from 90 min before any treatment to 60 min after plasmapheresis and 30 min after steroid administration. Glucose tolerance was normal after treatment. Plasmapheresis followed by steroid treatment can lower the insulin antibody concentration, abolish severe hypoglycemia, and improve insulin biodistribution and glucose tolerance in insulin autoimmune hypoglycemia.

Autoantibodies↗
PubMed1993

Hypoglycemic activity of polygonati rhizoma in normal and diabetic mice.

The hypoglycemic effect of different dose of Polygonati Rhizoma, i.e., "Ousei", was investigated in both normal and streptozotocin-induced diabetic mice. The methanol extract of Polygonati Rhizoma (OM) (800 mg/kg) reduced the blood glucose of normal mice from 202 +/- 7 to 144 +/- 13 mg/100 ml 4 h after intraperitoneal administration (p < 0.01), and also lowered significantly the blood glucose of streptozotocin-induced diabetic mice from 589 +/- 34 to 396 +/- 15 mg/100 ml under similar conditions (p < 0.001). However, the hypoglycemic effects were not accompanied by any alteration in the serum insulin in these mice. OM also suppressed epinephrine-induced hyperglycemia in mice. These results support, therefore, the use of Polygonati Rhizoma in patients with diabetes and confirm its role as a traditional medicine. In addition, one of the active components of OM was identified as a spirostanol glycoside (PO-2).

Animals↗
PubMed1992

Influence of blood proteins on biomedical analysis. XII. Effects of glycation on gliclazide (oral hypoglycemic drug)-binding with serum albumin in diabetics.

The sera of diabetic patients showed an inverse correlation (r = -0.67, n = 57) between free gliclazide (oral hypoglycemic drug) level and the fructosamine value. The binding capacity of the primary binding site for gliclazide in the albumin molecule was increased from 4.5 x 10(-4) to 8.0 x 10(-4) M-1 by glycation of albumin, but not that of the secondary binding site (1.2 x 10(-4) M-1). This suggests that the glycation of albumin increases its total binding capacity for gliclazide, resulting in a low free gliclazide level. Therefore, a low hypoglycemic activity of the drug is observed when it is administered to diabetic patients with hyperglycemia.

Blood Proteins↗