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PubMed1984

The distribution of hypoglycemic brain damage.

Rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose, they were allowed to wake up and survive for 1 week. Control rats were recovered at the stage of EEG slowing. After sub-serial sectioning, the number and distribution of dying neurons was assessed in each brain region. Acid fuchsin was found to stain moribund neurons a brilliant red. Brains from control rats showed no dying neurons. From 10 to 60 min of cerebral isoelectricity, the number of dying neurons per brain correlated positively with the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min. Neuronal necrosis was found in the major brain regions vulnerable to several different insults. However, within each region the damage was not distributed as observed in ischemia. A superficial to deep gradient in the density of neuronal necrosis was seen in the cerebral cortex. More severe damage revealed a gradient in relation to the subjacent white matter as well. The caudatoputamen was involved more heavily near the white matter, and in more severely affected animals near the angle of the lateral ventricle. The hippocampus showed dense neuronal necrosis at the crest of the dentate gyrus and a gradient of increasing selective neuronal necrosis medially in CA1. The CA3 zone, while relatively resistant, showed neuronal necrosis in relation to the lateral ventricle in animals with hydrocephalus. Sharp demarcations between normal and damaged neuropil were found in the hippocampus. The periventricular amygdaloid nuclei showed damage closest to the lateral ventricles. The cerebellum was affected first near the foramina of Luschka, with damage occurring over the hemispheres in more severely affected animals. Purkinje cells were affected first, but basket cells were damaged as well. Rare necrotic neurons were seen in brain stem nuclei. The spinal cord showed necrosis of neurons in all areas of the gray matter. Infarction was not seen in this study. The possibility is discussed that a neurotoxic substance borne in the tissue fluid and cerebrospinal fluid (CSF) contributes to the pathogenesis of neuronal necrosis in hypoglycemic brain damage.

Animals↗
PubMedDate not supplied

Chromium in plants. Comparison between the concentration of chromium in Brazilian nonhypo and hypoglycemic plants.

Chromium is an essential trace element and is associated with some biological pathways, especially with glucose tolerance. For these reasons, we decided to determine the concentration of chromium in two sets of Brazilian medicinal plants. The first group consisted of plants that are considered as antidiabetic, whereas the second included plants that do not have this therapeutic property. The concentration of chromium was determined by flameless atomic absorption. All the plants analyzed contain chromium in the normal range for this element, but the hypoglycemic plants contain more chromium than the others (1-4 micrograms/g compared to 0.5-1.5 micrograms/g).

Brazil↗
PubMed1986

Insulin autoimmune syndrome with insulin-resistant diabetes at the incipient stage prior to hypoglycemic attacks.

Insulin autoimmune syndrome is characterized by spontaneous hypoglycemia, glucose intolerance, hyperinsulinemia and insulin-binding antibodies in serum without previous immunization. A 31-year-old man with Graves' disease developed insulin autoantibodies after therapy with methimazole. The patient was unique in that persistent hyperglycemia with polyuria and polydipsia had continued for several days before frequent hypoglycemic attacks appeared. We were able to extract a huge amount of immunoreactive insulin (116,000 microU/ml) with acid-ethanol from his serum obtained in the diabetic stage, and serum C-peptide immunoreactivity was as high as 268 ng/ml. The insulin-binding activity of his serum was quite potent, and when 1:5,000 diluted serum was incubated with 125I-porcine insulin, 71.2% of the label could be precipitated by polyethylene glycol. The insulin-binding protein was identified as mainly IgG with kappa light chains. Insulin-binding activity was not detected in serum obtained before methimazole therapy, suggesting that the drug was responsible for the induction of antibodies in this patient. The antibodies recognized porcine, sheep, bovine and horse insulins as well as human insulin. The mechanisms by which the antibodies produced hyper- and hypoglycemia have also been discussed.

Adult↗
PubMed2000

Adrenal crisis presenting as hypoglycemic coma.

An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. Plasma levels of ACTH and cortisol remained undetectable. Renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. Intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.

Adrenal Cortex↗
PubMed1994

Recovery of epinephrine response but not hypoglycemic symptom threshold after intensive therapy in type 1 diabetes.

PURPOSE: Patients with intensively treated insulin-dependent diabetes mellitus (IDDM) exhibit more severe defects in counterregulatory hormone secretion and symptom recognition during hypoglycemia than do conventionally treated patients. In this prospective study in patients with preexisting defects in counterregulation, we examined the induction and reversibility of impaired symptomatic and adrenomedullary responses to hypoglycemia in 5 patients with IDDM (diabetes duration of 2 to 16 years; aged 19 to 36 years; 3 women, 2 men) who were receiving intensive therapy. METHODS: Counterregulatory responses were assessed by using a single-step (approximately 2.8 mmol/L plasma glucose) and multiple-step (from approximately 5 mmol/L to 2.2 mmol/L plasma glucose) clamped hypoglycemia procedure. Patients were first studied after a stable period of conventional insulin therapy (glycosylated hemoglobin [HbA1c] 9.5 +/- 1.2%), then after 3 to 5 months of intensive therapy (HbA1c 6.6 +/- 0.2%), and a third time after resuming conventional therapy (HbA1c 8.7 +/- 0.9%). RESULTS: Intensive therapy was associated with a 44% decline (P < 0.01) in the average plasma epinephrine increase during hypoglycemia, and the plasma glucose level required to stimulate epinephrine secretion fell from 3.7 +/- 0.2 to 3.0 +/- 0.1 mmol/L (P < 0.01). The threshold, but not the magnitude, of the plasma norepinephrine response was similarly altered. Hypoglycemic symptoms also decreased in intensity (by 67%, P < 0.01), and the glucose level required for symptom activation fell from 3.4 +/- 0.3 to 2.7 +/- 0.2 mmol/L, P < 0.01). When conventional therapy was resumed, the abnormalities in the epinephrine response due to intensive therapy were almost completely reversed. However, the reduction in symptoms and the altered thresholds for plasma norepinephrine were not reversed. CONCLUSIONS: There is dissociation between the treatment-associated defects in hypoglycemia counterregulation in IDDM, and an increase in average glycemia produced by a return to conventional insulin therapy is not sufficient to reverse hypoglycemia unawareness worsened by intensive therapy.

Adult↗
PubMed1985

Mechanism responsible for the hypoglycemic action of 2-alkoxy-2-propenylidene methanaminiums.

2-Alkoxy-2-propenylidene methanaminiums inhibited gluconeogenesis and stimulated glycolysis by hepatocytes isolated from 48-h-fasted rats and fasted-refed rats, respectively. The order of effectiveness of these compounds was the same as the hypoglycemic response of intact rats found in other studies, i.e., butoxy greater than propoxy greater than ethoxy derivative. Lactate/pyruvate and beta-hydroxybutyrate/acetoacetate ratios were elevated whereas cellular ATP concentration was decreased by these compounds. The butoxy derivative inhibited the oxidation of [U-14C]glucose to 14CO2 but increased glucose utilization and lactate accumulation by isolated rat diaphragms. The butoxy derivative also inhibited site I reversed electron transfer and the oxidation of NAD+-linked substrates but not succinate by isolated rat liver mitochondria. Methanaminium-induced hypoglycemia in intact rats was accompanied by an increase in blood lactate concentration as well as blood beta-hydroxybutyrate to acetoacetate ratio. The hypoglycemia caused by these compounds is proposed to be due to inhibition of glucose synthesis in the liver along with increased glucose utilization in peripheral tissues, both for want of ATP as a consequence of inhibition of site I electron transfer.

Adenosine Triphosphate↗
PubMed1983

Recovery after hypoglycemic brain injury. Action of some biological substances on the cerebral metabolism.

In artificially ventilated beagle dogs a severe hypoglycemic condition was induced by insulin injection, while the posthypoglycemic recovery was induced by glucose treatment at the end of a 20-min period of spontaneous electroencephalographic silence. The motor area of the cerebral cortex was analyzed for glycolytic metabolites, related amino acids, energy mediators, fatty acids, phospholipids and free fatty acids. The effects on the posthypoglycemic recovery of a intracarotid infusion with some agents (i.e. uridine, cytidine, DL-carnitine, DL-acetylcarnitine, papaverine) were tested. Severe hypoglycemia induced an extensive derangement of the brain metabolism, with partial restitution during the posthypoglycemic recovery. During this condition, the intracarotid perfusion with some biological pyrimidines (uridine, cytidine) interfered with the glycolytic and amino acid metabolites, inducing a decrease in glucose, pyruvate and lactate contents, and an increase in succinate, alanine and glutamine cerebral concns. The lipid carriers (DL-carnitine, DL-acetylcarnitine) interfered with the fatty acid degradation inducing a magnification of the decrease in the individual (palmitic acid, oleic acid) and total fatty acids, the vasodilating agent (papaverine) being practically inactive.

Acetylcarnitine↗
PubMed1984

Hypoglycemic properties of taurine: not mediated by enhanced insulin release.

Taurine (2-aminoethanesulfonic acid) has been shown to be a potent hypoglycemic agent in the Wistar Kyoto rat (WKY). Glucose and insulin levels were measured in serum at various times after glucose loading (400 mg/kg, i.p.). Pretreatment with taurine (200 mg/kg, i.p.) attenuated the rise in serum glucose levels at 0.5 hr after glucose administration. In addition, taurine also prevented the rise in serum immunoreactive insulin levels. The taurine analogue hypotaurine produced a similar inhibition in the rise of both serum glucose and insulin levels while beta-alanine, the carboxylic acid derivative of taurine, was totally ineffective. The enhanced glucose clearance can be explained by an increase in deoxyglucose accumulation in skeletal muscle and liver. In the liver, a 50% increase in glycogen synthesis was observed. A possible interrelationship between taurine and insulin receptor is discussed.

Animals↗
PubMed1981

Insulin-induced hypoglycemic coma and regional cerebral energy metabolism.

Swiss-Albino female mice weighing 20 g were rendered hypoglycemic by injecting insulin (2 units/kg). Animals were sacrificed at 40 min (pre-coma), 2 h (coma) and 4.5 h (recovery) after insulin injection by rapid submersion in liquid N2. Following sectioning at 20 micrometer, samples from the ascending reticular activating system and the inferior colliculus were freeze-dried and assayed for glucose, lactate, ATP and phosphocreatine (PCr). There was a preferential effect of hypoglycemia on ATP and PCr in cells of the ascending reticular activating system. ATP was depleted 30%, and PCr 55% in the pre-coma stage. ATP and PCr in cells from the inferior colliculus were not decreased. This selective effect on cells of the ascending reticular activating system followed by coma suggests that the coma per se may not represent total failure of the organism, but rather a compensatory mechanism designed to permit the animal to correct its compromised energy status.

Adenosine Triphosphate↗
PubMed1984

Hypoglycemic activation of focal abnormalities in the EEG of patients considered for temporal lobectomy.

EEGs were recorded in 22 patients with medically refractory complex partial epilepsy undergoing presurgical evaluation and 11 age-matched controls while subjected to moderate levels of hypoglycemia to determine if changes activated were predictive of underlying pathology. Five patients had fasting EEGs showing focal abnormalities not seen in the non-fasting state. With hypoglycemia, EEG tracings in normal individuals showed diffuse background slowing, whereas 7 of 22 patients developed focal temporal changes, including focal spike and focal slow wave activation. The development of focal changes correlated well with clinical data concerning underlying focal pathology; focal abnormalities were not evoked in patients with multifocal disease. Hypoglycemic activation of the EEG may be a useful technique for predicting the presence of pathology in patients considered for anterior temporal lobectomy.

Adult↗
PubMed1984

Potentiation of the hypoglycemic effect of insulin by thiorphan, an enkephalinase inhibitor.

Insulin administration to rats produced a dose-related hypoglycemia. When insulin and the enkephalinase (Enk'ase) inhibitor thiorphan (30 or 100 mg/kg s.c.) were co-administered, there was a potentiation of the hypoglycemic response to insulin; these doses of thiorphan alone had no significant effect on plasma glucose. When tested in vitro against isolated Enk'ase, both insulin and its beta-chain inhibited the catabolism of [Met5]enkephalin. Theoretically, thiorphan blocked the catabolism of insulin by inhibiting Enk'ase. Alternatively, thiorphan acted as an inhibitor of another insulin-catabolizing enzyme having similar substrate requirements as Enk'ase.

Amino Acids, Sulfur↗
PubMed1993

The hypoglycemic sulphonylurea tolbutamide increases N-methyl-D-aspartate- but not kainate-activated currents in hippocampal neurons in culture.

The effects of the hypoglycemic sulphonylurea tolbutamide, a marker of K(+)-ATP channels, on the N-methyl-D-aspartate- (NMDA) and kainate-activated currents were studied in rat hippocampal neurons in culture, using the patch-clamp technique in a whole-cell configuration. Tolbutamide (500 microM) reversibly increased the peak amplitude and the steady state level of NMDA- but not kainate-evoked currents. This effect was not glycine dependent as it was observed at low and saturated concentrations of glycine. The affinity of the NMDA receptor-channel complex for glycine did not change in the presence of tolbutamide. The action of tolbutamide on the NMDA-activated current was not mediated by K(+)-ATP channels since CsCl was added intracellularly at concentrations which completely blocked all K+ channels. Possible mechanisms explaining the effect of tolbutamide via the modulation of intracellular messengers are discussed.

Animals↗
PubMed1985

Fetal heart rate in maternal hypoglycemic coma.

In pregnancies complicated by diabetes mellitus fetal heart rate (FHR) monitoring is widely utilized to detect early fetal compromise. Never, however, was the fetal heart rate monitored during a maternal hypoglycemic coma. Such a case is here presented.

Adult↗
PubMed1992

Blunted ACTH response to hypoglycemic stress in depressed patients but not in patients with schizophrenia.

In this study, 7 hospitalized patients with major depression (MD), 5 hospitalized patients with schizophrenia (S), and 13 control subjects (C) were administered 0.15 units/kg of regular insulin at 1600 h by intravenous bolus infusion. ACTH, cortisol, and glucose levels were measured intermittently for 2h following infusion. Baseline ACTH, cortisol and glucose levels were similar in Cs, MDs, and Ss. The mean glucose nadir was equivalent for Cs, patients with MD, and patients with S. Patients with MD had a blunted ACTH response (F = 3.28; df = 12,126; p = .0004) and cortisol response (F = 4.20; df = 12,132; p = .0001) to hypoglycemia when compared to Cs and patients with S. Carroll Depression Rating Scale scores in patients with S (23 +/- 10) were similar to patients with MD (30 +/- 8) and significantly higher than in controls (1 +/- 2) (F = 55.2; df = 2.22; p = .0001). These findings suggest that patients with MD show different ACTH and cortisol responses to hypoglycemic stress which are not explained by negative feedback of baseline ACTH or cortisol, glucose nadir, or the number of depressive symptoms per se.

Adrenocorticotropic Hormone↗
PubMed1995

Pancreatic polypeptide enhances plasma glucocorticoid concentration in rats: possible role in hypoglycemic stress.

The acute bolus intraperitoneal (i.p.) administration of pancreatic polypeptide (PP) dose-dependently enhanced the plasma concentration of corticosterone (PBC) in hypophysectomized/ACTH replaced rats, but not that of aldosterone. Minimal and maximal effective doses were 10(-12) and 10(-10) mol/rat, respectively, and maximal PBC increase occurred between 60 and 120 min after PP injection. Insulin (1 U/kg, i.p.) evoked a net decrease in the blood glucose concentration, and marked rises in the plasma levels of PP and PBC, that attained their maximum at 60 and 120 min, respectively. The effects of insulin were annulled by the simultaneous injection of 0.5 mg/kg atropine. The effects of 1 U/kg insulin and 10(-10) mol/rat PP on PBC were not additive; atropine did not affect PBC response to PP or PP plus insulin, though annulling that to insulin alone. Taken together these findings suggest that PP plays a physiologic role in the rat as modulator of the adrenal response to the insulin-induced hypoglycemic stress.

Aldosterone↗
PubMed1982

Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions.

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion. We recently showed that GTG treatment also produces an early decrease and a later increase in sensitivity to insulin hypoglycemic convulsions. We report here that BPM also produces a similar biphasic change in sensitivity to insulin hypoglucemic convulsions. For both, the differences are in the brain's convulsive response to hypoglycemia, rather than in the degree of hypoglycemia in response to insulin. Thus, GTG and BPM cytotoxic lesions appear similar in this regard as well. BPM is another way of producing a relatively discrete brain lesion which alters the brain's functional adjustment to hypoglycemia. The significance of this control center and its relationship to the control(s) of feeding and systemic metabolism are discussed.

Animals↗
PubMed1989

Blood-brain barrier permeability after electrically induced seizure in normoglycemic, hypoglycemic, and hyperglycemic rats.

The influence of hyperglycemia and moderate hypoglycemia plus electroconvulsive seizure on the permeability of the blood-brain barrier to protein was studied in rats. Evans blue was used as a blood-brain barrier tracer. Following a single electroconvulsive seizure, slight staining of brain tissue was seen. After 10 electroconvulsive stimuli followed by sustained seizure activity, this phenomenon was more pronounced in moderate hypoglycemic animals. In this group, Evans blue albumin extravasation occurred in all regions of the hemispheres, but the most severe protein leakage was seen in the thalamus, hypothalamus, amygdala nuclei, and frontal, parietal, and occipital cortex. Ten repeated electroconvulsive stimuli applied in case of hyperglycemia made no important difference in blood-brain barrier dysfunction according to normoglycemic group. Our results suggest that moderate hypoglycemia provokes the effect of electroconvulsive seizure on the permeability of the blood-brain barrier.

Animals↗