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PubMed1980

Plasma cyclic nucleotide responses to insulin-induced hypoglycaemia and methacholine in patients with hyperthyroidism.

The effect of insulin-induced hypoglycaemia and methacholine on plasma cAMP and cGMP levels was studied in normal volunteers, hyperthyroid and hypothyroid patients. A significant positive correlation existed between the maximal increase in plasma cAMP and the maximal decrease in plasma glucose in normals during insulin-induced hypoglycaemia. Therefore, the plasma cAMP response is considered to be dependent on the degree of hypoglycaemia, rather than the dose of insulin. The cAMP response to hypoglycaemia was significantly higher in hyperthyroid patient, and was lower in patients with hypothyroidism than in normals. The cAMP response of the hyperthyroid patients was normalized when their hyperthyroidism was controlled after 3 months of treatment. The plasma level of cGMP was slightly elevated during hypoglycaemia, but there was no significant difference between controls and hyperthyroid patients. The cGMP response to methacholine, which is probably mediated by cholinergic receptors, was significantly potentiated in hyperthyroid patients. The cAMP response, which is presumably dependent on endogenous catecholamines secreted during methacholine-induced hypotension, was also enhanced in hyperthyroid patients. It is likely that beta-adrenergic receptor responses and cholinergic receptor responses are both enhanced in hyperthyroidism.

Adolescent↗

PubMed1990

The effect of alpha-adrenergic blockade on responses of peripheral blood cells to acute insulin-induced hypoglycaemia in humans.

Acute hypoglycaemia provokes rapid changes in peripheral blood cell counts. To examine possible adrenergic mechanisms modulating these changes, counts of peripheral blood cells including lymphocytes, granulocytes and erythrocytes were measured in response to acute hypoglycaemia in a group of six normal subjects in control conditions (study 1), and during alpha-adrenergic blockade with phentolamine (study 2). In study 1 hypoglycaemia provoked a biphasic leucocyte response, with an early rise in lymphocyte count and a later rise in granulocyte count. The erythrocyte count increased modestly following hypoglycaemia. During alpha-adrenergic blockage, the rise in total leucocyte count was diminished, with the rise in the lymphocyte count being greatly obtunded. These findings suggest that the increments of peripheral lymphocyte and erythrocyte counts in response to acute insulin-induced hypoglycaemia are mediated via alpha-adrenoreceptors.

Adult↗

PubMed1991

Plasma volume changes during hypoglycaemia: the effect of autonomic blockade.

To investigate the role of the autonomic nervous system in changes in blood volume and composition induced by acute hypoglycaemia in man, seven healthy subjects participated in three experiments on separate days: insulin-induced hypoglycaemia with concomitant alpha-adrenoceptor blockade; insulin-induced hypoglycaemia with total autonomic blockade (alpha-adrenoceptor blockade combined with beta-adrenoceptor blockade and atropine); and insulin-induced hypoglycaemia without any autonomic blockade. In the experiments without autonomic blockade the peripheral venous hematocrit increased, plasma volume decreased, intravascular albumin content decreased and the transcapillary escape rate of albumin increased. In both experiments with autonomic blockade the increase in venous haematocrit was abolished, yet plasma volume decreased, intravascular albumin content decreased and the transcapillary escape rate of albumin increased in these experiments. Thus, the changes in plasma volume and composition in response to hypoglycaemia are due to the combined actions of adrenaline and of insulin.

Adult↗

PubMed1992

Cognitive function, insulin-dependent diabetes and hypoglycaemia.

A series of seven psychometric tests, to evaluate mental concentration and the ability to retain selective attention, lexical fluency, wordlist memorizing and psychomotor speed, was performed on 25 non-diabetic control subjects and 55 insulin-dependent diabetes (IDD) patients of similar social background and professional status. When tested, none of the diabetics was hypoglycaemic and these patients were divided into two groups: Group I: 30 IDD patients unaware of hypoglycaemia, and experiencing frequent and severe episodes of hypoglycaemia. Group II: 25 IDD patients aware of hypoglycaemia. Groups I and II had experienced the disease for the same period of time (17 +/- 13 vs. 14 +/- 11 years, respectively) and they had similar HbA1c levels (7.14 +/- 1.25% vs. 8.6 +/- 1.88%, respectively) and degenerative complications. Compared with the scores of the controls, the Group I scores were lower in four tests: trail-making part A (psychomotor speed; P less than 0.001) and part B (retaining selective attention; P less than 0.01), lexical fluency (P less than 0.01) and Rey auditory-verbal learning test (wordlist learning; P less than 0.05). Group II scores were lower in two tests: trail-making part A (P less than 0.01) and part B (P less than 0.05). In word memorizing, the performance of Group I was inferior to that of Group II (P less than 0.05). In general, these psychometric tests showed that IDD scores were lower than those of the controls, with an average of 67% for Group II and 80% for Group I. Chronic hyperglycaemia and severe hypoglycaemia may have a deleterious effect on cognitive performance. In particular, several severe episodes of hypoglycaemia could be responsible for permanent memory impairment.

Adolescent↗

PubMed1986

Frequency of daytime biochemical hypoglycaemia in insulin-treated diabetic patients: relation to daily median blood glucose concentrations.

The frequency and distribution of daytime biochemical hypoglycaemia (capillary blood glucose concentration below 3 mmol/l) was assessed in type 1 diabetic patients on conventional twice daily insulin therapy (n = 79) and on continuous subcutaneous insulin infusion (n = 20). Patients collected and mailed to the hospital blood for seven-point blood glucose profiles. For both treatment regimens the frequency of biochemical hypoglycaemia on individual days was inversely related to the median blood glucose concentration in a curvilinear manner (p less than 0.001). Hypoglycaemia was more frequent pre-prandially than post-prandially (p less than 0.01), and was evenly distributed during the day in patients on continuous subcutaneous insulin infusion. In patients on conventional therapy, however, pre-lunch hypoglycaemia was four times more frequent than pre-breakfast or pre-dinner hypoglycaemia (p less than 0.0001).

Adolescent↗

PubMedDate not supplied

A prospective study of symptomatic hypoglycaemia in childhood diabetes.

A prospective study of symptomatic hypoglycaemia was conducted in 47 children over a 14-week period using a questionnaire completed at home for each episode of hypoglycaemia. Twenty-nine children (62%) experienced 150 episodes during the study. The average incidence was once every 33 days (range 0-5.2 mo-1). Hypoglycaemia occurred more frequently in children with lowest haemoglobin A1 levels. Episodes were not randomly distributed in time; hypoglycaemia occurred significantly more frequently in the evening, in the early morning and around midday. The majority of episodes were judged to be mild but 2 children had nocturnal convulsions and glucagon was used on three occasions. Symptomatic nocturnal hypoglycaemia occurred one or more times in 30% of the children. Daytime episodes were manifested by tremor, feeling weak, dizziness, pallor, and other symptoms and signs. In 46% of cases the cause was not evident to parents or children, but 25% were related to physical activity.

Child↗

PubMed1990

Postprandial hyperglycaemia following a morning hypoglycaemia in type 1 diabetes mellitus.

The occurrence of hyperglycaemia following a morning hypoglycaemic episode was studied in nine patients with Type 1 diabetes. Each patient was studied twice, once following induced hypoglycaemia and once in a control study when hypoglycaemia was prevented by glucose infusion. After the initial hypoglycaemic/control period the patients were maintained on their regular insulin regimens and were given standard meals. Hypoglycaemia induced postprandial hyperglycaemia (3.1 +/- 0.8 mmol l-1 above control) which lasted for about 8 h. Maximal growth hormone levels were seen 40 min after glucose nadir (control 7.8 +/- 3.2, hypoglycaemia 74.0 +/- 12.3 mU l-1) and the magnitude of the hyperglycaemia was related to the growth hormone levels following the hypoglycaemia (r = 0.80, p less than 0.01).

Adult↗

PubMed2004

Hypoglycaemia with insulin aspart: a double-blind, randomised, crossover trial in subjects with Type 1 diabetes.

AIMS: To compare the effects of the rapid-acting insulin analogue insulin aspart and soluble human insulin on hypoglycaemia and glycaemic control in patients with Type 1 diabetes when injected immediately before meals as part of intensive insulin therapy. METHODS: In this multinational, double-blind, randomised, crossover trial, 155 patients with Type 1 diabetes (HbA(1c) < 8.0%) were symmetrically randomised to two 16-week treatment periods on either type of insulin, both injected 0-5 min before meals. NPH insulin was given as basal insulin once or twice daily as needed, and insulin dosages were regularly adjusted using pre-defined algorithms to maintain tight glycaemic control. Treatment periods were separated by a 4-week washout. RESULTS: The rate of major nocturnal (24.00-06.00 h) hypoglycaemic episodes was 72% lower with insulin aspart than with human insulin (0.067 vs. 0.225 events/month; P = 0.001). Total rate of major hypoglycaemia did not differ significantly between treatments (insulin aspart/human insulin relative risk 0.72; 95% CI 0.47-1.09, P = 0.12). The rate of minor events was significantly reduced by 7% with insulin aspart (P = 0.048). Reductions in rate of hypoglycaemia were achieved with maintained overall glycaemic control: Mean HbA(1c) remained constant, slightly below 7.7% on both treatments. CONCLUSIONS: The use of insulin aspart in an intensive insulin regimen in patients with tightly controlled Type 1 diabetes led to clinically significant reductions in major nocturnal hypoglycaemia with no deterioration in glycaemic control. Major nocturnal hypoglycaemia appears to be a strong clinical indication for the use of rapid-acting insulin analogues during intensive insulin therapy.

Adolescent↗

PubMed1979

The significance of abnormal glucose tolerance (hyperglycaemia and hypoglycaemia) in pregnancy.

Maternal hypoglycaemia (plasma glucose below 5th centile) had a highly significant association with fetal growth retardation, and perinatal mortality was significantly increased in the presence of both hypoglycaemia and hyperglycaemia (plasma glucose above 95th centile) when pregnancy outcome was analyzed in 5000 consecutive patients who had a glucose tolerance test performed during the third trimester of pregnancy. This study confirms the significance of abnormal glucose tolerance as a causative factor of feto-placental dysfunction. The flat glucose tolerance test pattern had no significance beyond the presence of associated hypoglycaemia, but reactive hypoglycaemia, and persistent abnormalities of plasma glucose levels during the test, were associated with higher incidences of complicated outcome. Hypertonic dextrose therapy administered to the patient with persistently subnormal urinary oestriol excretion was less likely to cause a favourable response in oestriol excretion if glucose tolerance was abnormal, perhaps because the adverse influences of abnormal glucose tolerance were not reversible by the third trimester of pregnancy. Hypoglycaemia and hyperglycaemia, additional to diabetes mellitus, are significant factors in the aetiology and diagnosis of abnormal pregnancy, and point to the need to investigate therapeutic measures.

Blood Glucose↗

PubMed2006

Effect of chronic hypoglycaemia on glucose concentration and glycogen content in rat brain: A localized 13C NMR study.

While chronic hypoglycaemia has been reported to increase unidirectional glucose transport across the blood-brain barrier (BBB) and to increase GLUT1 expression at the endothelium, the effect on steady-state brain d-glucose and brain glycogen content is currently unknown. Brain glucose and glycogen concentrations were directly measured in vivo using localized 13C magnetic resonance spectroscopy (MRS) following 12-14 days of hypoglycaemia. Brain glucose content was significantly increased by 48%, which is consistent with an increase in the maximal glucose transport rate, Tmax, by 58% compared with the sham-treated animals. The localized 13C NMR measurements of brain glucose were directly validated by comparison with biochemically determined brain glucose content after rapid focused microwave fixation (1.4 s at 4 kW). Both in vivo MRS and biochemical measurements implied that brain glycogen content was not affected by chronic hypoglycaemia, consistent with brain glucose being a major factor controlling brain glycogen content. We conclude that the increased glucose transporter expression in chronic hypoglycaemia leads to increased brain glucose content at a given level of glycaemia. Such increased brain glucose concentrations can result in a lowered glycaemic threshold of counter-regulation observed in chronic hypoglycaemia.

Animals↗

PubMed1995

Altered cAMP response after isoprenaline stimulation of mononuclear leucocytes from insulin-dependent diabetic patients with hypoglycaemia unawareness.

Loss of adrenergic hypoglycaemic symptoms is the most distinctive feature in insulin-dependent diabetes mellitus (IDDM) patients with hypoglycaemia unawareness. Previous reports from in vivo studies show reduced heart rate responsiveness both to adrenergic agonists and antagonists in these patients. This study was carried out to investigate whether the reduced adrenergic sensitivity in IDDM patients with hypoglycaemia unawareness (IDDM-unaware) also could be demonstrated as reduced increase in cAMP production in mononuclear leucocytes induced by isoprenaline stimulation, or reduced inhibition by ICI-118551 (a selective beta 2-adrenergic receptor blocker) of isoprenaline induced cAMP production. We found that the slope of the concentration-response curves of isoprenaline/cAMP and the maximal cAMP concentrations obtained after isoprenaline stimulation were reduced in IDDM-unaware compared to control and IDDM patients with normal hypoglycaemia awareness (IDDM-aware). We did not find any significant differences in the response to ICI-118551 between control, IDDM-aware and IDDM-unaware. This study supports the reports of reduced sensitivity of adrenergic agonists as a part of the pathophysiological changes in hypoglycaemia unawareness, but we have not been able to confirm the reports of an association between hypoglycaemia unawareness and reduced effect of adrenergic antagonists.

Adrenergic beta-Agonists↗

PubMed1975

Endocrinological aspects at follow-up studies in neonatal hypoglycaemia.

Thirty-seven cases of neonatal hypoglycaemia were studied at follow-up at the age of 2 6/12-r 9/12 years. Two of them had had hypoglycaemia were stuafter the newborn period, and another patient died in a hypoglycaemic state following surgery at 10 weeks of age. Twenty-three children had oral glucose tolerance tests and intravenous insulin tolerance tests performed. Diabetic glucose tolerance was noted in 3 children. None of them showed symptoms of diabetes mellitus, neither was there any family history of diabetes. One of these patients had experienced hypoglycaemia after the newborn period and responded with hyperinsulinism during the glucose tolerance test. The other hypoglycaemic patient showed an exaggerated insulin release in response to tolbutamide. Deficient serum cortisol response to insulin-induced hypoglycaemia was demonstrated in 7 patients and 6 of these had concomitant minimal growth hormone response. One of these patients also had a diabetic glucose tolerance. None were of short stature. It is probable that a disturbance in the hypothalamic-pituitary-adrenal axis may contribute to an impaired carbohydrate metabolism in some patients with neonatal hypoglycaemia.

Blood Glucose↗

PubMed1997

Cognitive function in type 1 diabetic children with and without episodes of severe hypoglycaemia.

We assessed the effect of diabetes and of episodes of severe hypoglycaemia on cognitive function in 28 diabetic children. Fifteen diabetic children (age 12.9 (SD 2.0) years) had experienced 1-4 episodes of severe hypoglycaemia. Five of these children diseased before the age of 5 years (SH-eod subgroup), and ten diseased after this age (SH-lod subgroup). Thirteen diabetic children (age 13.1 (SD 2.0) years) had not experienced episodes of severe hypoglycaemia (non-SH group). Each diabetic child was compared with a healthy control child of the same age and gender and with a similar social background. Neuropsychological assessment was blinded. The neuropsychological tests were grouped into one of seven cognitive domains. We found no effect on cognitive performance from diabetes per se or from severe hypoglycaemia in children with late-onset diabetes. However, early-onset diabetes was associated with low scores in two cognitive domains: psychomotor efficiency and attention. The SH-eod subgroup had lower scores than the SH-lod subgroup in psychomotor efficiency (p < 0.05) and also had lower scores than the SH-lod subgroup and the non-SH group in measures of attention (p < 0.05). Our results may indicate a slight cognitive dysfunction in children with early-onset diabetes who have experienced episodes of severe hypoglycaemia early in childhood.

Adolescent↗

PubMed1997

High-molecular weight IGF-2 expression in a haemangiopericytoma associated with hypoglycaemia.

Spontaneous hypoglycaemia is usually caused by an insulin-producing islet-cell tumour of the pancreas. Rarely, it can be caused by non-islet cell tumours. Most of the tumours are of mesenchymal type, large, and slowly growing. One representative is haemangiopericytoma (HAP). The present report describes a case of a large recurrent retroperitoneal HAP associated with severe hypoglycaemia. Blood serum insulin and proinsulin concentrations were low. By means of acid-gel chromatography and dot-blot techniques, an increased amount of a high-molecular-weight IGF-2 peptide was found. By using antigen retrieval procedures, IGF-2-immunoreactive tumour cells were found in specimens of the recent tumour recurrence-but not in the original. When the in situ hybridization technique was used it could be shown that IGF-2 mRNA labelling had already occurred in the original tumour specimen, 11 years before the onset of hypoglycaemic symptoms. These observations confirm the hypothesized hypoglycaemic effects of high-molecular-weight (HMW) IGF-2, but also point to the presence of a prolonged compensation of this effect. A literature review, based on 17 similar cases of haemangiopericytoma with hypoglycaemia, is presented. Our observation and findings in the literature review support the idea that non-islet-cell tumour hypoglycaemia is caused by an overproduction of a HMW IGF-2 peptide. The insulin-like effect is mediated via non-specific binding to the insulin receptors. To anticipate patients at risk of developing this kind of hypoglycaemia, the histopathological investigation should include not only immunohistochemical analyses of the presence of IGF-2 peptide, but also in situ hybridization of the IGF-2 mRNA expression.

Aged↗

PubMed1986

Intravenous uridine treatment antagonizes hypoglycaemia-induced reduction in brain somatostatin-like immunoreactivity.

By means of radioimmunoassay procedures, cholecystokinin-(CCK) and somatostatin-(SRIF) like immunoreactivity have been studied in the dorsal hippocampal formation and in the frontoparietal cortex of the male rat in insulin-induced hypoglycaemia, leading to an isoelectric EEG pattern. It has been demonstrated that severe hypoglycaemia of 40-min-duration produces a disappearance of SRIF but not of CCK-like immunoreactivity in both cortical regions. It was found that an i.v. injection of uridine but not of saline could significantly counteract the disappearance of SRIF-like immunoreactivity induced by severe hypoglycaemia in both cortical areas. Uridine did not by itself change plasma glucose levels. It is suggested that uridine may prevent release and/or increase synthesis of cortical SRIF peptides in severe hypoglycaemia, possibly due to an action on the metabolism (e.g. by enhancing the resynthesis of phosphatidyl inositol) within the tissue of the cerebral cortex and/or on putative pyrimidine binding sites in the brain controlling SRIF synthesis and/or release. It is possible that uridine in this way may improve recovery of neuronal function within SRIF-immunoreactive neurons of the cerebral cortex after severe hypoglycaemia (which also may be true in other states of reduced metabolic support). These findings suggest a possibility to use uridine in the treatment of Alzheimer's disease and Status epilepticus.

Animals↗

PubMed1980

The effects of hypoglycaemia on cerebral blood flow and metabolism in the new-born calf.

1. The effects of insulin hypoglycaemia on cerebral blood flow and metabolism have been examined in unanaesthetized, unrestrained calves between 1 and 26 days after birth. 2. Cerebral blood flow was measured with an inert gas technique using molecular hydrogen, and cerebral metabolism was quantified by determination of arterio-cerebral venous (A--V) concentration differences for oxygen, glucose, lactate, pyruvate, acetoacetate, beta-D-hydroxybutyrate and ammonia. 3. During normoglycaemia the mean (A--V) difference for glucose was close to one sixth that of oxygen, on a molar basis. A small net loss of pyruvate from the brain was found, but there was no significant (A--V) difference for lactate. Arterial concentrations of acetoacetate and beta-D-hydroxybutyrate were low, and no utilization of ketone bodies by the brain was demonstrated. 4. Moderate hypoglycaemia (arterial plasma glucose concentration 1--2 m-mole/l.) had no measurable effect on either cerebral blood flow or metabolism. 5. During profound hypoglycaemia (arterial plasma glucose concentration less than 1.0 m-mole/l.) cerebral glucose uptake was sufficient to account for only 56% of the cerebral oxygen consumption. Cerebral oxygen consumption fell in comatose animals, but increased during hypoglycaemic convulsions, as did cerebral blood flow. 6. In day-old calves hypoglycaemia was associated with a rise in blood lactate concentration and uptake of lactate by the brain. 7. A net loss of ammonia by the brain was observed during hypoglycaemia in calves at all ages examined. The loss was greater in convulsing than in comatose animals.

Ammonia↗

PubMed1991

Rapid resetting of human baroreflex working range: insights from sympathetic recordings during acute hypoglycaemia.

1. Human muscle nerve sympathetic activity (MSA), which is governed by baroreflexes and involved in blood pressure homeostasis, is increased during acute insulin-induced hypoglycaemia. 2. To elucidate the detailed relationship between MSA and blood pressure during hypoglycaemia, 0.15 i.u. (kg body weight)-1 regular human insulin was given intravenously to eight fasting, healthy volunteers. Microneurographic recording of MSA in the peroneal nerve was made with simultaneous monitoring of arterial blood pressure by a finger cuff (Finapres). The course of MSA and blood pressure was monitored for 30 min before and 60 min after insulin injection. In three subjects control recording without insulin injection was made for the same duration. 3. Stimulus-response regression lines were constructed by plotting diastolic blood pressure against the occurrence frequency of MSA for the period of initial rest, the period of maximal MSA outflow during hypoglycaemia and the period of glucose counter-regulation. The control experiments were analysed for the corresponding periods. 4. The stimulus-response line was stable throughout the control experiments, whereas it was shifted either to the left or to the right during hypoglycaemia, and regularly shifted to the left (i.e. towards a lower blood pressure) during glucose counter-regulation, without change of slope. 5. It is concluded that the changes in MSA during acute hypoglycaemia are not secondary to baroreflex regulation but instead are characterized by acute resetting of the baroreflex working range without change of sensitivity.

Adult↗

PubMed2007

Ionic currents underlying the response of rat dorsal vagal neurones to hypoglycaemia and chemical anoxia.

A proportion of dorsal vagal neurones (DVN) are glucosensors. These cells respond to brief hypoglycaemia either with a K(ATP) channel-mediated hyperpolarization or with depolarization owing to an as yet unknown mechanism. K(ATP) currents are observed not only during hypoglycaemia, but also in response to mitochondrial inhibition. Here we show that similarly to the observations for K(ATP) currents, both hypoglycaemia and inhibition of mitochondrial function elicited a small inward current that persisted in TTX in DVN of rat brainstem slices. Removal of glucose from the bath solution induced this inward current within 50 +/- 4 s in one subpopulation of DVN and in 279 +/- 36 s in another subpopulation. No such subpopulations were observed for the response to mitochondrial inhibition. Biophysical analysis revealed that mitochondrial inhibition or hypoglycaemia inhibited an openly rectifying K+ conductance in 25% of DVN. In the remaining cells, either an increase in conductance, with a reversal potential between -58 and +10 mV, or a parallel inward shift of the holding current was observed. This current most probably resulted from inhibition of the Na+-K+-ATPase and/or the opening of an ion channel. Recordings with electrodes containing 145 mm instead of 5 mm Cl- failed to shift the reversal potential of the inward current, indicating that a Cl- channel was not involved. In summary, glucosensing and non-glucosensing DVN appear to use common electrical pathways to respond to mitochondrial inhibition and to hypoglycaemia. We suggest that differences in glucose metabolism rather than differences in the complement of ion channels distinguish these two cell types.

Action Potentials↗