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At least 793 records · Page 44Linked to original sources
PubMed2002

Simultaneous analyses of hypoglycemic agents and C-peptide are essential in a homicide case with the combined dosing insulin and insulin-releasing drug.

A 5-year-old girl was given a sulfonylurea hypoglycemic agent, 25 mg of glibenclamide (ten tablets of Euglucon) with two benzodiazepine drugs, 2 mg of estazoram and 0.75 mg of triazolam (one tablet of Eurodin and three tablets of Halcion), by her 37-year-old pharmacist father and then injected with 70 units of insulin (NovoLet 40R). She died several hours after the injection of insulin. Autopsy was carried out 12 h after the death. A glibenclamide level of 103 ng/ml was detected in the serum collected from the heart at autopsy. The serum insulin and C-peptide concentrations were 295 microU/ml and 0.5 ng/ml, respectively. The high level of insulin and the low level of C-peptide indicated that most of the serum insulin was exogenous. The determination of the serum C-peptide concentration was useful to the diagnosis of hypoglycemia caused by exogenous insulin even in the case of co-administration with an endogenous-insulin-releasing agent.

Journal Article↗
PubMed1999

Recent developments in oral hypoglycemic agents.

Recent large-scale studies in patients with type 2 diabetes have suggested that improved glycemic control will reduce the incidence and severity of chronic complications. However, it is difficult to maintain the blood glucose levels of diabetic patients within a narrow range. Since insulin resistance and impaired insulin secretion cause hyperglycemia in type 2 diabetes, both improvement of insulin resistance and compensation for defective insulin secretion are necessary. Recently, the first insulin sensitizer was released, and a short-acting insulinotropic agent, which should be more convenient for strict glycemic control than sulfonylureas, has also been launched. This review focuses on these two new classes of hypoglycemic agents.

Journal Article↗
PubMed2000

Differences in the dynamics of frontal sharp transients in normal and hypoglycemic newborns.

OBJECTIVE: This study focuses on the characteristics of frontal sharp transients (FST), a normal variant of neonatal EEG, in newborns with hypoglycemia. METHODS: The EEG from 20 newborns with symptomatic hypoglycemia were compared with a control group of normal newborns matched by conceptional age. The dynamics of these transients were evaluated concerning sleep stages. The density, type and bilateral synchrony of FST were also calculated. The results were compared in the two groups by Student's t test. RESULTS: When compared with controls, hypoglycemic newborns have increased density of frontal sharp transients in all sleep stages but less bilateral synchrony (P<0.05). FST density was even higher in small for gestational age newborns. CONCLUSIONS: The data suggests that normal patterns of neonatal EEG as FST can be influenced by systemic disturbances.

Electroencephalography↗
PubMed1995

Bilateral temporal lobe MRI changes in uncomplicated hypoglycemic coma.

We report bilateral temporal lobe MRI findings in a patient following an episode of prolonged hypoglycemia uncomplicated by coexisting anoxia, hypotension, acidosis, drug intoxication, infection, or status epilepticus. The MRI findings are discussed in relation to the experimental and human data on hypoglycemic neuronal injury.

Adult↗
PubMed1979

Discriminant--analytical investigation on the structural dependence of hyperglycemic and hypoglycemic activity in a series of substituted o-toluenesulfonylthioureas and o-toluenesulfonylureas.

The influence of a series of substituted o-toluenesulfonylthioureas and o-toluenesulfonylureas on the level of blood sugar was investigated in rats. According to the observed response the compounds were divided into three classes corresponding to hypoglycemic, hyperglycemic, and no activity. The distribution of the compounds over these classes can be described by discriminant functions using substituent constants, RM values, and indicator variables. Most important for the separation of classes are hydrophobic and/or steric properties as well as the presence or absence of the thiomide group. The results indicate that two different mechanisms of action with opposite effect overlap in the case of the series studied.

Animals↗
PubMed1976

Hypoglycemic alpha-cycloalkylphenylmehtyl, furanalkyl, and thiophenealkyl lactamimides.

A series of alpha-cycloalkylphenylmethyl lactamimides and a series of furan- and thiophenealkyl lactamimides were prepared for biological evaluation as an extension of earlier finding of hypoglycemic activity in lactamimides. Compounds 7, 20, 23, 25, 29, and 32 produced pronounced hypoglycemia after oral administration to fasted, glucose-primed rats.

Animals↗
PubMed2000

Intracranial malignant meningioma with abdominal metastases associated with hypoglycemic shock: a case report.

A thirty-year-old male with an intracranial malignant meningioma, first diagnosed 9 years ago, with three recurrences was admitted with a hypoglycemic shock. The blood glucose level was 17 mg/dl, requiring treatment with high doses of intravenous and oral dextrose for improvement. A large metastatic tumor in the liver was noted. All hormones and peptides influencing blood glucose levels were in their normal levels. Chemo-embolization and injection of anti-cancer drugs was employed in the management of the metastatic tumor. Positron emission tomography was performed to measure the glucose metabolism of the abdominal tumor and it indicated that glucose consumption within the tumor was much elevated than the surrounding abdominal organs. Hypoglycemia secondary to primary hepatoma or islet-cell cancer has been frequently described, but a complication of metastatic meningioma is an exceedingly rare event. Elevated glucose consumption within the tumor might be addressed as one of the reasons for hypoglycemia, not due to the elevated serum levels of insulin or IGF, but due to the closely related blood glucose level.

Abdominal Neoplasms↗
PubMed1998

Inactivation of protein kinase C in rat liver during late hypoglycemic phase of sepsis.

Changes in protein kinase C (PKC) (calcium- and phospholipid-dependent protein kinase) activity in rat liver during different metabolic phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Experiments were divided into three groups: control, early sepsis, and late sepsis. Early and late sepsis refers to those animals sacrificed at 9 and 18 h, respectively, after CLP. Hepatic PKC was extracted and partially purified by ammonium sulfate fractionation and DEAE-cellulose chromatography. PKC activity was assayed based on the rate of incorporation of 32p from [gamma-32P]ATP into histone. The results show that during early sepsis, both membrane-associated and cytosolic PKC activities remained relatively unaltered. During late sepsis, membrane-associated PKC was unaffected while cytosolic PKC activity was decreased by 19.5-34.4%. Kinetic analysis of the data on cytosolic PKC during late phase of sepsis reveals that the Vmax values for ATP, histone, Ca2+, phosphatidylserine, and diacylglycerol were decreased by 23.4, 22.1, 19.5, 25, and 34.4%, respectively, with no changes in their Km values. These data indicate that cytosolic PKC activity was inactivated in rat liver during late hypoglycemic phase of sepsis. Since PKC-mediated phosphorylation plays an important role in regulating hepatic glucose metabolism, an inactivation of cytosolic PKC may contribute to the development of hypoglycemia during late phase of sepsis.

Animals↗
PubMed1990

Regional neuroprotective effects of the NMDA receptor antagonist MK-801 (dizocilpine) in hypoglycemic brain damage.

Current evidence points to an important role of N-methyl-D-aspartate (NMDA) receptor activation in the pathogenesis of hypoglycemic neuronal death. MK-801 [dizocilpine maleate, (+)-5-methyl-10,11-dihydro-5H-di[a,d]cyclohepten-5,10-imine] is an anticonvulsant compound also known to be a potent noncompetitive antagonist at NMDA receptors, readily crossing the blood-brain barrier after parenteral administration. Treatment of rats with dizocilpine (1.5-5.0 mg/kg) injected intravenously during profound hypoglycemia (blood glucose levels 1.5-2.0 mM) at the stage of delta-wave (1-4 Hz) slowing of the EEG mitigated selective neuronal necrosis in the hippocampus and striatum, assessed histologically after 1-week survival. The degree of neuroprotection in the striatum and in the CA1 pyramidal cells of the hippocampus was dose dependent. Because of concern for a possible hypothermic mechanism of brain protection by MK-801, core temperature was closely monitored and was found not to decrease significantly. Since CBF is normal or increased in hypoglycemia, a fall in brain temperature during hypoglycemia is unlikely to play a role in the mechanism of the neuroprotection seen with the drug. The findings indicate that in profound hypoglycemia, intravenous administration of the NMDA antagonist dizocilpine, even after the appearance of delta-wave EEG slowing, can reduce the number of necrotic neurons in several brain regions and suggest that the neuroprotective effect of MK-801 is not related to hypothermia.

Animals↗
PubMed1993

Recovery of mitochondrial and plasma membrane function following hypoglycemic coma: coupling of ATP synthesis, K+ transport, and changes in extra- and intracellular pH.

The primary objective of the present study was to evaluate the recovery of plasma and mitochondrial membrane functions after 30 min of hypoglycemic coma and to establish whether a lingering accumulation of free fatty acids (FFAs) delays the recovery. A secondary objective was to study whether production of metabolic acids following glucose infusion leads to a fall in intracellular pH (pHi). Phosphocreatine, creatine, ATP, ADP, and AMP, as well as glycogen, glucose, lactate, pyruvate, and FFAs of rat brain cortex and caudoputamen were measured, and "free" ADP was calculated from the creatine kinase equilibrium. Extracellular pH (pHe) and K+ concentration (K+e) were measured with ion-sensitive microelectrodes, and pHi was derived by the CO2 method. Glucose injection was followed by resumption of oxidative phosphorylation within approximately 2 min and by an equally rapid restoration of normal K+e levels. These functions recovered although tissue FFAs remained elevated for at least 7-8 min. Tissue lactate content increased only moderately and production of metabolic acids did not lead to intracellular acidosis. After 15 min of recovery, pHi was moderately increased, although pHe fell toward 7.0. It is speculated that the dissociation between intra- and extra-cellular pH is compatible with an up-regulation of an Na+/H+ antiporter, e.g., by phosphorylation.

Adenosine Triphosphate↗
PubMed1997

Increased expression of calbindin D28k via herpes simplex virus amplicon vector decreases calcium ion mobilization and enhances neuronal survival after hypoglycemic challenge.

Disruption of Ca2+ homeostasis often leads to neuron death. Recently, the function of calcium-binding proteins as neuronal Ca2+ buffers has been debated. We tested whether calbindin D28k functions as an intracellular Ca2+ buffer by constructing bicistronic herpes simplex virus vectors to deliver rat calbindin cDNA to hippocampal neurons in vitro. Neurons were infected with vectors delivering calbindin or a negative control or were mock-infected. After 12 or 24 h of hypoglycemia, infected cells were made aglycemic during fura-2 calcium ratiometric imaging. In response to this challenge, neuronal overexpressing calbindin had less Ca2+ mobilized as compared with negative controls or mock-infected cells. Cells were assayed for survival after 12- or 24-h hypoglycemia or aglycemia. The calbindin vector decreased neuronal death due to hypoglycemia but not aglycemia. Here we demonstrate, in response to hypoglycemic challenge, both decreased Ca2+ mobilization and increased survival of cells infected with the calbindin vector.

Animals↗
PubMed2001

Hypoglycemic brain injury.

Hypoglycemia frequently occurs in newborn infants who previously have suffered asphyxia, who are offspring of diabetic mothers, or who are low birthweight for gestational age (IUGR). Many infants who are hypoglycemic do not exhibit clinical manifestations, while others are symptomatic and at risk for the occurrence of permanent brain damage. This review emphasizes the clinical, neuropathologic, and neuro-imaging features of hypoglycemia in newborn infants, especially those who are symptomatic. Neurologic morbidity occurs particularly in those infants who have suffered severe, protracted, or recurrent symptomatic hypoglycemia. Experimental observations emphasize the resistance of the immature brain to the damaging effect of hypoglycemia; such resistance occurs as a consequence of compensatory increases in cerebral blood flow, lower energy requirements, higher endogenous carbohydrate stores, and an ability to incorporate and consume alternative organic substrates to spare glucose for energy production. Hypoglycemia combined with hypoxia-ischemia (asphyxia) is more deleterious to the immature brain than either condition alone.

Brain Injuries↗
PubMed1976

Isolated corticotrophin-deficiency found through alcohol-induced hypoglycemic coma.

A case of hypoglycemic coma after alcohol ingestion was observed in a chronic alcoholic. Upon close examination isolated corticotrophin-deficiency was found. It is suggested that ethanol-induced hypoglycemia may be consistent with dysfunction of mitochondria in hepatic cells and that there may be disorder of the hypothalamus in the chronic drinker.

Adrenocorticotropic Hormone↗
PubMed1986

Antiketogenic and hypoglycemic effects of aminocarnitine and acylaminocarnitines.

DL-Aminocarnitine (DL-3-amino-4-trimethylaminobutyrate) is a potent, noncovalent inhibitor of carnitine palmitoyltransferase (palmitoyl-CoA:L-carnitine O-palmitoyltransferase, EC 2.3.1.21). Here we show that decanoyl-DL-aminocarnitine and palmitoyl-DL-aminocarnitine inhibit carnitine palmitoyltransferase in vitro about 7-fold and 100-fold more effectively than does aminocarnitine. Aminocarnitine and its decanoyl and palmitoyl derivatives are active in vivo following oral or parenteral administration and, at doses of 0.3 mmol/kg or less, inhibit the oxidation of [14C]palmitate to 14CO2 by 45-70% in mice. Larger doses do not significantly increase the extent of inhibition, a finding suggesting that substantial carnitine palmitoyltransferase-independent long-chain fatty acid oxidation may occur in vivo. Small doses of aminocarnitine and palmitoylaminocarnitine prevent the development of ketoacidemia in fasted, normal mice and reverse the ketoacidemia observed in diabetic mice. Aminocarnitine has a strong hypoglycemic effect in fasted diabetic mice; a single dose (0.3 mmol/kg) normalizes plasma glucose levels within 4-8 hr and remains effective for at least 12 hr.

Acyltransferases↗
PubMed2002

Lethal hypoglycemic ketosis and glyceroluria in mice lacking both the mitochondrial and the cytosolic glycerol phosphate dehydrogenases.

The activities of either the mitochondrial or cytosolic glycerol phosphate dehydrogenase (mGPD, cGPD) plus that of glycerol kinase are required for the use of glycerol in aerobic metabolism and gluconeogenesis. A knockout mouse lacking mGPD has reduced body weight and fertility but shows remarkably normal liver and muscle metabolite levels. The BALB/cHeA mouse strain, which lacks cGPD, breeds well and is phenotypically normal, although it demonstrates metabolite abnormalities in certain tissues. Crosses were made between these two strains, and mice were generated that lacked both dehydrogenases. These mice, although active and nursing well for several days, failed to grow, and usually died within the first week. Liver glycerol phosphate levels were elevated 30-fold, whereas liver ATP, ADP, and AMP levels were reduced by 30-40%. Plasma glycerol was elevated 30- to 50-fold to 30-50 mm, and urine glycerol exceeded 0.45 m (4% w/v). GPD-deficient mice were hypoglycemic, had a 50% increase in plasma free fatty acids, and developed ketonuria within the first day of life. Uncoupling protein-1 mRNA in brown adipose tissue was reduced 60%. These mice share some features of both glycerol kinase deficiency and hereditary fructose intolerance, suggesting the phenotype may be due to the combined effects of the loss of a gluconeogenic substrate, the osmotic effects of glycerol, and the metabolic effects of the accumulation of a phosphorylated metabolite.

Animals↗
PubMed2003

Double liposomes: hypoglycemic effects of liposomal insulin on normal rats.

The biopharmaceutical characteristics of double liposomes (DLs) containing insulin were examined, and the usefulness of DLs in combination with aprotinin is discussed. Encapsulation of insulin was influenced by lipid composition, and the highest efficiency was observed with positively charged liposomes. Insulin encapsulated in liposomes, especially in DLs, was protected from enzymatic proteolysis. A portion of insulin molecules was adsorbed on the surface of the membrane when liposomes were prepared using a lipid with a positive charge and was degraded by enzymes. Remarkable hypoglycemic effects were observed after intragastric administration of DLs containing insulin at a dose of 20 IU/kg to normal male Wistar rats. The highest mean relative efficacy to administration was obtained with insulin-loading DLs containing aprotinin as a protease inhibitor. These results suggest that DLs are applicable as an oral dosage form for peptide drugs such as insulin etc., especially in combination with protease inhibitors.

Animals↗
PubMed2006

Evaluation of the accuracy of a microdialysis-based glucose sensor during insulin-induced hypoglycemia, its recovery, and post-hypoglycemic hyperglycemia in humans.

BACKGROUND: These studies were designed to evaluate the accuracy of a microdialysis-based subcutaneous glucose sensor (GlucoDay, A. Menarini Diagnostics, Firenze, Italy) compared with a standard reference method of plasma glucose measurement during insulin-induced hypoglycemia. RESEARCH DESIGN AND METHODS: Nine subjects without diabetes were studied in eu-, hypo-, and hyperglycemia (clamp technique). The GlucoDay was calibrated against one arterialized plasma glucose measurement (Glucose Analyzer, Beckman, Brea, CA), and plasma glucose estimates every 3 min were compared with paired plasma glucose values. RESULTS: Accuracy of glucose estimates was not homogeneously distributed among subjects and depended on stability of the sensor's current signal during spontaneous euglycemia (R +/- -0.68). Linear regression analysis showed a good correlation between the two methods of measurement (R = 0.9), Deming regression showed the inclusion of the unit in the confidence interval of the slope (slope 0.95, 95% confidence interval 0.87-1.02), and the accuracy of the GlucoDay reached 40 +/- 15% (American Diabetes Association criteria). The mean relative difference was 6 +/- 8% in euglycemia, 13 +/- 14% during plasma glucose fall, 5 +/- 22% in the hypoglycemic plateau, and -14 +/- 16% during recovery from hypoglycemia. The Bland-Altman analysis indicated a bias of -1.9 +/- 16.6 mg/dL, whereas the Error Grid Analysis showed 94% of the Gluco- Day measurements in the acceptable zones of the grid. The time to reach the glycemic nadir was longer when measured with the GlucoDay (90 +/- 5 vs. 72.5 +/- 9 min, P < 0.05). However, absolute values of glycemic nadir, time spent in hypoglycemia, and the rate of fall of glycemia and the rate of recovery from the hypoglycemia were not statistically different. CONCLUSIONS: GlucoDay closely monitors changes in plasma glucose before, during, and after hypoglycemia. However, these results can be achieved only if calibration of the GlucoDay is performed under conditions of sensor signal stability. Similar studies have to be performed in subjects with diabetes to validate the GlucoDay system.

Adult↗
PubMed1990

Cornstarch ingestion after oral glucose loading: effect on glucose concentrations, hormone response, and symptoms in patients with postprandial hypoglycemic syndrome.

In susceptible individuals ingestion of glucose can lead to clinical symptoms of hypoglycemia as well as a reflex rise of counterregulatory hormones. We hypothesized that cornstarch, a slowly absorbed starch, might prevent hypoglycemic-symptom episodes. Eight patients who had characteristic signs, symptoms, and reflex hormonal responses of hypoglycemia at the glucose nadir after ingesting 75 g glucose (OGTT) participated. Patients ingested 75 g glucose followed by 75 g raw cornstarch (OGTT + CS). None of the patients reported symptoms or had signs of hypoglycemia in response to OGTT + CS. The glucose nadir concentration during OGTT + CS (3.8 +/- 0.6 mmol/L) was significantly higher than during OGTT (3.2 +/- 0.6; P less than 0.03). The responses of cortisol (331 +/- 166 nmol) and epinephrine (491 +/- 589 pmol/L) at the glucose nadir during OGTT + CS were significantly lower than the responses of cortisol (524 +/- 193 nmol/L; P less than 0.003) and epinephrine 1834 +/- 1135 pmol/L (P less than 0.0005) during OGTT. A slowly absorbed starch such as cornstarch may be an effective component in dietary management of this disorder.

Administration, Oral↗