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PubMed1989

The role of cortisol in the peripheral granulocyte response to insulin-induced hypoglycaemia in man.

Peripheral blood leukocyte counts and plasma hormonal changes in response to acute insulin-induced hypoglycaemia were examined in 16 patients undergoing assessment of pituitary function. Eight subjects had a normal cortisol secretory response (Group 1), and 8 patients had definite hypopituitarism in whom the cortisol responses were deficient or absent (Group 2). An equivalent degree of hypoglycaemia was achieved in both groups. In Group 1a biphasic rise in leukocyte count occurred following hypoglycaemia, with an early rise in lymphocytes at 15 minutes after the acute hypoglycaemic reaction, and a later rise in granulocytes. A similar rise in lymphocytes was observed in Group 2, but the rise in the granulocyte count was attenuated, increasing from a basal value of 3.6 +/- 0.6 x 10(9) cells/L to a peak of 7.4 +/- 1.1 x 10(9) cells/L, compared with a peak of 11.7 +/- 1.2 x 10(9) cells/L in Group 1 (P less than 0.05). The usual increment in plasma cortisol in response to hypoglycaemia occurred in Group 1, but plasma cortisol did not rise in Group 2. A correlation was observed between the magnitude of the granulocyte rise and the increment in plasma cortisol in individual subjects (r = 0.64, P less than 0.02). This suggests that the rise in peripheral granulocytes following insulin-induced hypoglycaemia in man is mediated by cortisol released from the adrenal gland, following activation of the hypothalamic-pituitary-adrenal axis.

Blood Glucose↗

PubMed1986

The erythrocyte insulin receptor response to insulin induced hypoglycaemia.

The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (+/- S.D.) specific insulin binding following the 5 hour insulin infusion was unchanged (6.9 +/- 2.1 to 6.65 +/- 2.2% bound per 2.25 X 10(9) erythrocytes). In the presence of mild hypoglycaemia, mean (+/- SD) specific insulin binding rose from 6.6 +/- 2.3 to 7.6 +/- 2.5% bound per 2.25 X 10(9) erythrocytes (P less than 0.01), after 5 hours. This increase was due to increased receptor affinity. It was not correlated with the increase in the concentration of any individual counter-regulatory hormone. Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P less than 0.01). Thus, acute hyperinsulinaemia, when associated with hypoglycaemia, does not result in downregulation of insulin receptors on erythrocytes but rather results in increased receptor binding. Consequently, the insulin receptor may not play an active role in protecting the individual against acute hypoglycaemia.

Adult↗

PubMed1997

Detection of hypoglycaemia by microdialysis measurements of glucose in subcutaneous adipose tissue.

The aim of the present investigation was to study how various fractional sampling times affect the detection of hypoglycaemia, using microdialysis of the adipose tissue. We therefore studied eight healthy subjects during a standardized hyperinsulinaemic hypoglycaemic clamp. The glucose concentration in the adipose tissue dialysate was determined in timed fractions of 15 min, 30 min and 60 min and compared to those in arterialized venous plasma. Before and after hypoglycaemia, the plasma and adipose tissue glucose concentrations were similar. However, during hypoglycaemia, the adipose tissue glucose nadir, as measured in 15-min fractions of the tissue dialysate, was significantly lower than that in plasma (2.1 +/- 0.1 vs. 2.4 +/- 0.1 mmol/l, p = 0.05) and during the increase in plasma glucose, the corresponding increase in adipose tissue glucose was delayed by approximately 20 min (p = 0.004). When the microdialysate was sampled over 30 or 60 min periods, there was a close agreement between the plasma and adipose tissue glucose nadirs. We conclude that there is a protracted fall in subcutaneous adipose tissue glucose levels in response to insulin-induced hypoglycaemia. While shorter microdialysis sampling periods improve the resolution of the hypoglycaemic event, 30-min fractions seem sufficient to detect hypoglycaemia in a clinically relevant way.

Adipose Tissue↗

PubMed2006

Ambulatory blood glucose measurement, dietary composition and physical activity levels in otherwise healthy women reporting symptoms that they attribute to hypoglycaemia.

Reactive hypoglycaemia (RH) is a condition that has been popularised in the media and lay literature, particularly that targeting women, over the past 30 years. The objective of the present study was to investigate whether a non-patient group reporting symptoms that they attributed to a low blood glucose level would demonstrate biochemical hypoglycaemia when symptomatic and whether their habitual diet and activity level differed from those of controls. Thirty non-obese, healthy women (aged 19-45 years) reporting symptoms more than once a week that they attributed to hypoglycaemia (RH group), and eighteen controls, measured their finger-prick blood glucose level 3 h after breakfast and lunch, and recorded their diet and activity daily for 7 d. The RH group also measured their blood glucose when symptoms were being experienced. Symptoms less than 4 h after eating were classed as postprandial. The mean postprandial blood glucose level in the RH group when asymptomatic (4.66 (SEM 0.08) mmol/l) was significantly lower than that of controls (5.05 (SEM 0.11) mmol/l; P<0.01). Symptoms occurred 2.6 (SEM 0.13) h after eating, at a lower blood glucose level (4.18 (SEM 0.10) mmol/l; P<0.001) than when the women were asymptomatic. On symptomatic days, the RH group were more physically active than the controls (1.64 (SEM 0.04) v. 1.50 (SEM 0.03) multiples of resting energy expenditure; P<0.05), with a lower energy intake (7901 (SEM 311) v. 9332 (SEM 227) kJ; P<0.001). In conclusion, subjects reporting symptoms they associated with hypoglycaemia generally did not demonstrate biochemical hypoglycaemia but did have significantly lower blood glucose levels than controls. Higher physical activity and a failure to match energy intake to estimated energy requirement may be important in the aetiology of symptoms.

Adolescent↗

PubMed2001

Skeletal muscle glucose uptake, glycogen synthase activity and GLUT 4 content during hypoglycaemia in type 1 diabetic subjects.

In healthy subjects, hypoglycaemia induces a profound 80% reduction in skeletal muscle glucose uptake and a similar suppression of glycogen synthase activity. The aim of this study was to examine the efficacy of this counterregulatory mechanism in type 1 diabetic subjects, who are especially prone to hypoglycaemic incidents. Nine type 1 diabetic male subjects were examined twice; during 120 min of hyperinsulinaemic (1.5 mU x kg(-1) x min(-1)) euglycaemia followed by (i) 240 min of graded hypoglycaemia (glucose nadir 2.8 mM) or (ii) 240 min of euglycaemia. At 345-360 min a muscle biopsy was taken and indirect calorimetry was performed at 210-240 and 320-340 min. The sensitivity of glycogen synthase to glucose-6-P was reduced by hypoglycaemia, as shown by an increase in A0.5 for glucose-6-P (at 0.07 mmol/L) from 0.21+/-0.02 to 0.28+/-0.03 mM (p=0.06). Likewise, the fractional velocity for glycogen synthase was reduced by 25%; i.e. from 20.8+/-2.0 to 15.5+/-1.4% (p<0.05). Total glucose disposal was decreased during hypoglycaemia (5.3+/-0.6 vs. 8.3+/-0.7 mg x kg(-1) x min(-1) (euglycaemia), n = 9; p<0.05), primarily due to a reduction of non-oxidative glucose disposal (2.7+/-0.3 vs. 5.1+/-0.6 mg x kg(-1) x min(-1) (euglycaemia), n=7; p<0.05). Forearm arteriovenous glucose differences were decreased by 50% in the hypoglycaemic situation (0.7+/-0.1 vs. 1.4+/-0.3 mmol/L (320-340 min)), and counterregulatory hormonal responses seemed less conspicuous than described in healthy subjects. We conclude that hypoglycaemia induces decrements of forearm glucose uptake and glycogen synthase activity in type 1 diabetic subjects. The study indicates a decreased magnitude of these responses, but this remains to be confirmed.

Adult↗

PubMed2002

Performance of a continuous glucose monitoring system during controlled hypoglycaemia in healthy volunteers.

It has been suggested that the continuous glucose monitoring system may be a useful tool for detecting unrecognised hypoglycaemia, especially at times when finger prick testing is difficult or impossible (e.g., at night). Studies suggest that subcutaneous glucose levels closely mimic blood glucose levels with a lag time of only a few minutes. However, no studies have been published to show how well the sensor performs during sustained or in recovery from hypoglycaemia. This study involved using a hyperinsulinaemic glucose clamp (60 mU/m2) in nine healthy volunteers. Each subject had two sensors inserted the day before the study. Blood glucose levels were maintained at euglycaemia for the first 60 min, then decreased to 45 mg/dL (2.5 mmol/L) for 60 min, and finally restored to euglycaemia. Blood glucose measurements were compared with interstitial values recorded by the sensor. Sensor profiles showed acceptable agreement with blood glucose levels at each of the three plateaus with a correlation coefficient of 0.79, slope of 0.85, and mean absolute error of 7%. The sensor drop closely matched the drop in blood glucose, but the recovery from hypoglycaemia was delayed by an average of 26 min. Continuous glucose sensing provides a useful means of detecting unrecognised hypoglycaemia in type 1 diabetes, although the duration of hypoglycaemia may be overestimated.

Adult↗

PubMed1991

Lack of knowledge of symptoms of hypoglycaemia by elderly diabetic patients.

The knowledge of symptoms of hypoglycaemia of 45 consecutive elderly diabetic patients was assessed during a structured interview and compared with that of an age-matched non-diabetic control group. Twenty-three (88%) patients taking oral hypoglycaemic agents (OHAs) and six (32%) insulin-treated patients denied any knowledge of hypoglycaemia. There was no significant difference in knowledge of 14 symptoms of hypoglycaemia between the non-diabetic controls and the combined diabetic (OHA and insulin) groups, but insulin-treated patients were slightly more knowledgeable than patients taking OHAs. Fourteen (54%) of the OHA group were taking either glibenclamide or chlorpropamide which have been associated with severe and prolonged hypoglycaemia. Elderly diabetic patients are unlikely to respond to the warning symptoms of hypoglycaemia and caution should therefore be exercised when prescribing for these patients.

Administration, Oral↗

PubMed1997

Differentiation of hypoglycaemia induced cognitive impairments. An electrophysiological approach.

Effects of hypoglycaemia on distinct cognitive processes were assessed with event-related brain-potential (ERP) measures and reaction times in a hybrid selective-attention/response-choice task. One group of subjects received a euglycaemia-hypoglycaemia-euglycaemia treatment order and a second group a euglycaemia-placebo(euglycaemia)-euglycaemia sequence of treatments. During hypoglycaemia, ERP measures of selective attention (selection negativity), response choice (lateralized readiness potential) and reaction time were delayed compared with baseline performance. After restoration of euglycaemia, the onset of the selection negativity returned to baseline, whereas the lateralized readiness potential was still delayed, and error frequencies remained elevated. These results suggest that hypoglycaemia delays both the stimulus selection and the motor-response selection. They further suggest that the stimulus-selection process recovers quickly after restoration of euglycaemia, but that the response-selection process does not. Slow shifts in cortical potentials with a broad frontal distribution that occurred during hypoglycaemia, are discussed in relation to frontal lobe mechanisms involved in the control of subordinate, modality-specific selection mechanisms.

Adult↗

PubMed1993

Hypoglycaemia: a common problem among uncomplicated newborn infants in Nepal.

Among a cross-sectional sample (stratified by weight and age after birth) of 226 uncomplicated term newborns from the delivery and postnatal wards of a busy government maternity hospital in Kathmandu, the period prevalence of hypoglycaemia (corrected blood glucose of < 2.6 mmol/l) during the first 50 hours after birth was 38 per cent. (This compares with a reported prevalence rate of 12 per cent from studies of uncomplicated term newborns in the UK.) Hypothermia, young maternal age, low birth weight and early sampling after birth were independent risk factors for hypoglycaemia. Of 31 infants studied longitudinally during the same period, 27 (87 per cent) had at least one blood glucose measurement of < 2.6 mmol/l and 25 (81 per cent) a rectal temperature of < 35.5 degrees C. Fourteen infants (44 per cent) had three or more episodes of hypoglycaemia and seven infants (22 per cent) had three or more episodes of hypothermia. Hypoglycaemia is a common, preventable and neglected problem in many maternity hospitals in developing countries. Simple low-cost measures to reduce the incidence of hypoglycaemia may have a major impact on early infant mortality and neurodevelopmental sequelae of perinatal origin.

Adolescent↗

PubMed1982

Effect of metoprolol and alprenolol on the metabolic, hormonal, and haemodynamic response to insulin-induced hypoglycaemia in hypertensive, insulin-dependent diabetics.

Insulin hypoglycaemia was induced three times in 6 insulin-dependent, hypertensive diabetics: before instituting antihypertensive long-term treatment and after obtaining a satisfactory blood pressure with either alprenolol or metoprolol given in a randomized order. The blood glucose concentration (1.6-1.9 mmol/l) at which the hypoglycaemia necessitated intravenous administration of glucose was almost identical on all three occasions. During hypoglycaemia the systolic and diastolic blood pressures increased significantly by a mean maximal rise of 27/14 mmHg on alprenolol treatment, but remained unchanged on metoprolol. The responses of adrenaline, noradrenaline, cortisol, and growth hormone did not differ significantly on the three occasions. None of the beta-adrenergic drugs counteracted the early hormone defence mechanisms in hypoglycaemia and the signs of hypoglycaemia were not masked. The haemodynamic response was altered only by the non-selective (alprenolol) and not by the selective beta-adrenergic blocking agent (metoprolol).

Adult↗

PubMed1994

Reduced sensitivity to beta-adrenoceptor stimulation and blockade in insulin dependent diabetic patients with hypoglycaemia unawareness.

Nine IDDM-patients with hypoglycaemia unawareness, seven IDDM-patients with hypoglycemia awareness and a control group of nine healthy persons were included in this study. The patients were recruited from the medical out-patients' department of the University Hospital of Tromsø. The pathophysiological changes which cause hypoglycaemia unawareness are today not clear. Reduced peripheral tissue sensitivity to catecholamines is suggested as one of several mechanisms which may contribute. For further investigation of beta-adrenergic sensitivity an isoprenaline/metoprolol sensitivity test was performed. Isoprenaline and metoprolol were administered intravenously, and the effects on heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and plasma levels of adrenaline (ADR) and noradrenaline (NA) were measured. All subjects were given the same doses of isoprenaline (0.25-8 micrograms) and metoprolol (0.5-8 mg). Metoprolol was given together with the dose of isoprenaline which increased heart rate by 25 beats min-1. The dose/response curves of both isoprenaline/HR and metoprolol/HR were significantly shifted to the right in IDDM-patients with hypoglycaemia unawareness compared with controls and IDDM-patients with hypoglycaemia awareness (P < 0.05). Reduced sensitivity of isoprenaline stimulation has also been shown before, whereas reduced sensitivity of a blocking agent has not earlier been shown. These findings support the hypothesis of reduced beta-adrenergic sensitivity as one pathophysiological component in hypoglycaemia unawareness.

Adult↗

PubMed1992

Phospholipid-containing toxic malaria antigens induce hypoglycaemia.

Hypoglycaemia is associated with severe malaria and is an important prognostic indicator. Molecules liberated during overnight incubation of erythrocytes infected with Plasmodium yoelii induce marked hypoglycaemia in normal mice, with a delayed time course compared with insulin; some, though weaker, activity could also be obtained by overnight incubation of uninfected erythrocytes. The active component shares many properties with the phospholipid-containing molecules which we have previously shown to be toxic and to induce the release of tumour necrosis factor (TNF) from macrophages. However a MoAb which neutralizes the cytotoxicity of tumour necrosis factor in vitro did not prevent this induction of hypoglycaemia, whereas antiserum against the toxic antigens did, as did immunization of normal (but not the immunoglobulin-deficient SCID) mice with the same material. Furthermore, normal mice injected with the antigens after immunization with phosphatidyl inositol or inositol monophosphate did not develop hypoglycaemia; the latter compound was also inhibitory when mixed with the antigens before injection. These compounds were previously shown to block the induction of TNF by the antigens and to induce the production of inhibitory antibodies. The role of these molecules in the etiology of the hypoglycaemia of malaria is discussed.

Animals↗

PubMed1982

The effect of adrenergic and cholinergic mechanisms on the secretion of pancreatic polypeptide and gastrin following hypoglycaemia in man.

The changes of plasma pancreatic polypeptide (PP) and plasma gastrin following acute insulin-induced hypoglycaemia (0 . 15 U/kg) were examined in six normal subjects, six tetraplegic subjects (preganglionic sympathectomy) and six tetraplegic subjects given atropine (combined adrenergic denervation and cholinergic blockade). Adequate hypoglycaemia was achieved in all three groups. The normal rise of plasma PP following hypoglycaemia was present in the tetraplegic group without atropine but was abolished in the tetraplegic subjects given atropine. There was no significant rise in plasma gastrin following hypoglycaemia except in the tetraplegic group given atropine. These results confirm that the secretion of PP in response to acute hypoglycaemia is mediated via cholinergic activity, while gastrin secretion appears to be inhibited in normal subjects by a vagal cholinergic mechanism.

Adult↗

PubMed1984

Studies on the mechanisms of somatostatin release after insulin induced hypoglycaemia in man.

Insulin-induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. In order to assess the mechanisms involved in this rise, six normal volunteers connected to a Biostator for continuous glucose monitoring were studied, on three separate occasions. On each occasion after basal blood sampling, 0.15 i.u./kg body weight of insulin was administered i.v. and further samples were obtained intermittently over 150 min. On one occasion, dextrose was infused by the Biostator to prevent hypoglycaemia, while on the other two, a constant infusion of either normal saline or the specific H2 antagonist cimetidine was administered. Insulin plus dextrose caused no significant changes in circulating somatostatin levels, whereas insulin plus saline was associated with a marked, sustained and significant rise in all subjects; insulin plus cimetidine also produced a rise but it was delayed; the area under the curve was significantly (P less than 0.05) greater with insulin plus saline than with insulin plus cimetidine. These results show that in man insulin itself does not stimulate somatostatin secretion directly, but indirectly via hypoglycaemia. Further, the inhibition of gastric acid secretion with cimetidine reduces somatostatin release during insulin-induced hypoglycaemia. This suggests that gastric acid may mediate somatostatin secretion associated with insulin-induced hypoglycaemia.

Adult↗

PubMed1985

Evidence for the participation of endogenous opioids in the sympathoadrenal response to hypoglycaemia in man.

The effects of the long acting met-enkephalin analogue D-Ala2-MePhe4-met-enkephalin-O-ol (DAMME) and the opiate antagonist naloxone on the plasma catecholamine responses to insulin-induced hypoglycaemia have been investigated in two separate studies. DAMME depressed basal noradrenaline and adrenaline at 15 min, and blunted both the noradrenaline and adrenaline responses to hypoglycaemia. Naloxone did not alter basal plasma catecholamines, but caused a significant enhancement of the adrenaline response to hypoglycaemia. Neither DAMME nor naloxone altered the blood glucose response to insulin-induced hypoglycaemia. These data are consistent with an inhibitory modulation of endogenous opioids in the sympathoadrenal response to insulin-induced hypoglycaemia in man.

Adrenal Medulla↗

PubMed1990

Metabolic effects of an insulin-like factor causing hypoglycaemia in a patient with a haemangiopericytoma.

We have studied a patient with fasting hypoglycaemia and skin lesions (sign of Leser-Trélat) related to a retroperitoneal haemangiopericytoma in whom removal of the tumour resulted in immediate cure of hypoglycaemia. Before removal of the tumour, severe fasting hypoglycaemia was associated with undetectable insulin and C-peptide levels. She required 16.9 mumol/kg/min (10.4 g/h) of glucose intravenously to prevent hypoglycaemia and endogenous glucose production (measured using tritiated glucose) was suppressed to 1.3 mumol/kg/min while the whole-body glucose utilization rate was elevated at 18.2 mumol/kg/min. After removal of the tumour both endogenous glucose production rate and utilization rate returned to normal (11.5 mumol/kg/min). Resting energy expenditure, measured by indirect calorimetry, was markedly elevated at 2109 kcal/day (161% of predicted) and fell to 1205 (97% of predicted) after the tumour was removed. Glucose oxidation was also enhanced at 8.5 mumol/kg/min and fell to 3.3 mumol/kg/min after removal of the tumour. Other metabolites and hormones measured, and their response to oral glucose, were all consistent with the presence of a circulating substance with similar properties to insulin. We conclude that her hypoglycaemia resulted primarily from suppression of endogenous glucose production but also from enhanced glucose utilization. These effects were the result of a circulating growth factor sharing many metabolic effects with insulin, but with a much greater effect on resting energy expenditure and glucose oxidation.

Adult↗

PubMed1994

Insulin-like growth factor binding protein 1 response to acute insulin induced hypoglycaemia in type 1 diabetes.

OBJECTIVES: Insulin is believed to be the prime regulator of insulin-like growth factor binding protein 1 (IGFBP-1) secretion, and in normal subjects acute insulin induced hypoglycaemia exerts a rapid effect on concentrations of IGFBP-1, and may also influence insulin-like growth factor I (IGF-I) concentrations. The rise in IGFBP-1 concentrations in normal subjects following hypoglycaemia has been suggested to be due to suppression of endogenous insulin secretion. We have examined this further by studying diabetics with no endogenous insulin secretion. DESIGN: We have compared the IGFBP-1 response to acute insulin induced hypoglycaemia in normal subjects and patients with Type 1 (insulin dependent) diabetes mellitus. METHODS: Insulin tolerance tests were performed using a bolus of insulin (0.15 U/kg), in six control subjects and six patients with Type 1 diabetes. MEASUREMENTS: Serum levels of IGFBP-1, insulin, glucose, and IGF-I were measured at regular intervals during the insulin tolerance test. RESULTS: Blood glucose fell to a nadir which coincided with the onset of the acute autonomic reaction 'R' in both groups. The basal concentration of IGF-I was significantly lower in the diabetic group at 0.4 +/- 0.1 kU/l, compared to 0.9 +/- 0.1 kU/l in the control group, but there was no significant change in IGF-I concentrations in response to hypoglycaemia in either group. Hypoglycaemia provoked a fall in IGFBP-1 in patients with Type 1 diabetes, from 38 +/- 9 micrograms/l basally to 17 +/- 3 micrograms/l at R + 120 minutes, with a return to basal values of 45 +/- 11 micrograms/l at R + 180 minutes. In the control subjects there was no fall in IGFBP-1, but a significant increase to 71 +/- 14 micrograms/l at R + 180 minutes. CONCLUSION: This difference in the IGFBP-1 response in the presence of a similar glucose response suggests that in Type 1 diabetes there may be different sensitivities to the actions of exogenous insulin on IGFBP-1 regulation.

Adult↗

PubMed1995

Octreotide exacerbated fasting hypoglycaemia in a patient with a proinsulinoma; the glucostatic importance of pancreatic glucagon.

Octreotide, a long-acting somatostatin analogue, has been used to alleviate hypoglycaemia in patients with insulinomas. Transient worsening of fasting hypoglycaemia following octreotide has also been described (Stehouwer et al., 1989). We describe a patient with a 'proinsulinoma' in whom octreotide caused rapid and prolonged symptomatic worsening of fasting hypoglycaemia. Catecholamine and cortisol counterregulatory hormonal responses were normal but those of glucagon and GH were impaired. Acute neuroglycopaenic symptoms were present during octreotide induced hypoglycaemia, which was accompanied by and attributed to an acute reduction in pancreatic glucagon secretion in the presence of persistent and unsuppressed hyperproinsulinaemia. This suggests that glucagon may be important in maintaining glucose homeostasis in chronic hypoglycaemia due to endogenous hyperinsulinism even though its concentration in the peripheral blood is not raised.

Blood Glucose↗