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PubMed2002

Heterogeneity of persistent hyperinsulinaemic hypoglycaemia. A series of 175 cases.

UNLABELLED: Hyperinsulinism is a heterogeneous disorder characterised by severe hypoglycaemia due to an inappropriate oversecretion of insulin. In a personal series of 175 patients investigated for hyperinsulinaemic hypoglycaemia over the last 20 years, we review clinical presentations, molecular studies and therapeutic management of hyperinsulinism. There were 98 neonatal-onset patients, including 86 permanent hyperinsulinism and 12 transient forms, 68 with infancy-onset and nine with childhood-onset. Hyperammonaemia was found in 12 out of 69 patients tested, 4 neonates and 8 infants. Neonates were clinically more severely affected than infants. Diagnosis of infancy-onset hyperinsulinism was often delayed because of less profound hypoglycaemia and better tolerance to hypoglycaemia. Neonates required higher rates of i.v. glucose than infants to maintain normal plasma glucose levels (16 mg/kg per min versus 12 mg/kg per min). Only 16% of neonates were diazoxide-sensitive compared to 66% of the infants. Neonates with hyperammonaemia or transient hyperinsulinism were diazoxide-sensitive. Most neonates were pancreatectomised whereas 65% of the infants were treated medically. Among surgically-treated patients, 47% had a focal adenomatous hyperplasia (31 neonates and 13 infants) and 53% a diffuse form of hyperinsulinism (39 neonates and 11 infants). Diazoxide-responsiveness in the focal and diffuse forms did not differ in both neonates and infants; it depended only upon the age of onset of hypoglycaemia. One or two mutations, SUR1 or KIR6.2, were found in 41 of 73 neonates who were investigated and in 13/38 infants using polymerase chain reaction-single strand conformational polymorphism analysis of both genes. Almost all patients with SUR1 (38/41) or KIR6.2 (5/7) mutations were resistant to diazoxide. Ten patients with hyperinsulinism-hyperammonaemia syndrome had a mutation in the glutamate dehydrogenase gene (three neonates and seven infants) after reverse transcriptase-polymerase chain reaction and sequence analysis of cDNA. No mutation was found by polymerase chain reaction-single strand conformational polymorphism in the glucokinase gene. Eight of nine patients with childhood onset hyperinsulinism were treated surgically and histological examination confirmed an adenoma in each case. CONCLUSION: the clinical severity of hyperinsulinism varies mainly with age at onset of hypoglycaemia. The heterogeneity of hyperinsulinism has major consequences in terms of therapeutic outcome and genetic counselling.

Age of Onset↗

PubMed1998

Post-transplantation hypoglycaemia in type 1 diabetic pancreas allograft recipients.

Physiologic replacement of insulin in patients with type 1 (insulin-dependent) diabetes following pancreas allograft transplantation results in normoglycaemia during fasting and postprandial states. However, this is achieved at the expense of peripheral hyperinsulinaemia in the heterotopic pancreas allograft recipients with systemic insulin drainage. In addition, the pancreas allograft is denervated and thus devoid of autonomic nervous regulation of pancreatic beta-cell secretion. Recent reports of hypoglycaemia (symptomatic and asymptomatic), which can be fatal, have raised serious concerns regarding the aetiology of the hypoglycaemic epiphenomenon in type 1 diabetic pancreas allograft recipients. Although the prevalence of significant hypoglycaemia following pancreas transplantation remains unknown, it is important to conduct studies to determine the mechanisms, the natural history, predictors and treatment as well as the long-term prognosis (graft and patient survival rates) of type 1 diabetic patients who develop pancreas-allograft-associated hypoglycaemia. Indeed, predictors of hypoglycaemia following pancreas allograft could significantly impact on the selection of appropriate therapeutic options for pancreas allograft transplantation. Finally, whether postpancreas allograft transplantation-associated hypoglycaemia in type 1 diabetic patients carries greater morbidity and mortality when compared to those without hypoglycaemia deserves to be investigated.

Diabetes Mellitus, Type 1↗

PubMed1996

Use of the DIAS model to predict unrecognised hypoglycaemia in patients with insulin-dependent diabetes.

The Diabetes Advisory System (DIAS) is a model of human glucose metabolism implemented in a causal probabilistic network. It handles data on insulin dose, carbohydrate intake and blood glucose concentration to predict hourly blood glucose concentrations and thus provide an indication of blood glucose values between home blood tests. DIAS was used to predict blood glucose profiles in eight patients with well-controlled insulin-dependent diabetes, who are at increased risk of hypoglycaemia (abnormally low blood glucose levels). DIAS predicted nocturnal hypoglycaemia in six patients and daytime hypoglycaemia in one patient. The occurrence of nocturnal hypoglycaemia was not recognised by the patient or suspected by their doctor but was subsequently confirmed by blood testing in five patients. It is known that unrecognised nocturnal hypoglycaemia is common in patients with well-controlled diabetes. The ability of DIAS to identify such periods of hypoglycaemia with reasonable accuracy illustrates how the advanced technology it employs may provide reliable decision support to clinicians.

Adolescent↗

PubMed1997

Auditory information processing during acute insulin-induced hypoglycaemia in non-diabetic human subjects.

Acute insulin-induced hypoglycaemia impairs performance on tests of general mental ability in humans. It is recognized that different brain functions vary in their sensitivity to neuroglycopenia, but little is known about the effects of neuroglycopenia on specific brain processes. The effect of controlled hypoglycaemia on two aspects of auditory information processing (auditory temporal processing and simple auditory processing) was examined in a homogeneous group of 20 healthy non-diabetic human subjects. Auditory temporal processing (temporal order discrimination) and simple auditory processing (pitch discrimination, single-tone duration and single-tone loudness discrimination) tests were part of the Test of Basic Auditory Capabilities (TBAC). Two tests of general cognitive performance (Digit Symbol Substitution and Trail Making B) were included to provide a measure of general brain functioning during hypoglycaemia. Hypoglycaemia lead to a significant deterioration in auditory temporal processing (P < 0.01), and a deterioration in one of three tasks of simple auditory processing (discrimination of single-tone loudness, P < 0.05). Significant disruptions also occurred in both tests of general brain functioning. These results are congruent with other studies in human subjects, showing a disruptive effect of hypoglycaemia on visual information processing when examined under conditions of limited perceptual time, and they provide further evidence of the importance of sensory processing speed in basic perceptual and cognitive functions. The disruptive effect of moderate insulin-induced hypoglycaemia on auditory perception may have implications for insulin-treated diabetic humans exposed to this metabolic stress, because of the importance of hearing in everyday life.

Acoustic Stimulation↗

PubMed1996

Effect of caffeine on recognition of and physiological responses to hypoglycaemia in insulin-dependent diabetes.

BACKGROUND: For the patient with diabetes, hypoglycaemia unawareness--ie, the warning signs of falling blood glucose are missing--is potentially dangerous. One study has suggested that, in healthy volunteers, caffeine might be a helpful treatment. Our study looked at two effects of caffeine ingestion (250 mg) on the brain--namely, a decrease in cerebral blood flow and an increase in brain glucose use--to see if the recognition of and physiological responses to hypoglycaemia were altered in patients with insulin-dependent diabetes mellitus (IDDM). METHODS: 12 patients were studied twice. A hyperinsulinaemic glucose clamp was used to maintain plasma glucose at 5 mmol/L for 90 min, followed by 60 min at 3.8 mmol/L, and then 2.8 mmol/L for a further hour. After 30 min at 5 mmol/L, patients consumed, in a double-blind, crossover design, 250 mg caffeine or matched placebo. We recorded middle cerebral artery velocity (VMCA), counterregulatory hormone levels, and cognitive function, and patients recorded hypoglycaemia symptoms on a visual analogue scale. RESULTS: Caffeine caused an immediate and sustained fall in VMCA of 10 cm/s, from 60 to 50 cm/s (95% CI -5 to -15 cm/s; p < 0.001). At a blood glucose of 3.8 mmol/L, plasma adrenaline levels were twice as high after caffeine than after placebo (difference 524 pmol/L). When glucose was lowered to 2.8 mmol/L, caffeine ingestion was associated with: greater awareness of hypoglycaemia in 9 patients, significantly more intense autonomic and neuroglycopenic symptoms, and higher levels of adrenaline, cortisol, and growth hormone. Cognitive function (latency of P300 evoked potentials) deteriorated to the same extent in both studies at this glucose level. INTERPRETATION: The sustained fall in VMCA and augmented sympathoadrenal and symptomatic responses during moderate hypoglycaemia suggest caffeine as a potentially useful treatment for diabetic patients who have difficulty recognising the onset of hypoglycaemia.

Adult↗

PubMed2003

Emotional changes during experimentally induced hypoglycaemia in type 1 diabetes.

Emotional changes during experimentally induced hypoglycaemia in type 1 diabetic patients were investigated using a hyperinsulinaemic glucose clamp. In the experimental group (n=11), blood glucose was stabilised at euglycaemia (5.6 mmol/l, phase 1), then lowered to 2.5 mmol/l (phase 2) and raised to 5.6 mmol/l (phase 3). In the control group (n=11), euglycaemia was maintained during all phases. Hypoglycaemia elicited the expected endocrine, symptomatic and neuroglycopenic effects. During hypoglycaemia negative mood states increased significantly, whereas positive mood states decreased. Hypoglycaemia prolonged rating time of emotional stimuli (drawn from IAPS) significantly. The arousal ratings of the slides were higher during hypoglycaemia. Valence and dominance ratings were not affected. Epinephrine and norepinephrine release correlated with a higher arousal rating and a decrease in positive mood states. Deterioration in neuropsychological tasks correlated with an increase in negative mood states. Experimental induction of hypoglycaemia can offer a new research model to study emotional processes.

Adult↗

PubMed1993

Hypoglycaemia in pregnancy.

Normally there is a very close relationship between maternal and fetal glucose concentrations during both early and late gestation. Maternal hypoglycaemia during pregnancy will therefore not only affect the mother herself but also the conceptus. As can be judged from the literature, acute hypoglycaemic episodes are only rarely seen in non-diabetic pregnancies. In recent years it has become increasingly evident that insulin-dependent diabetic patients, whether pregnant or not, run a much increased risk of having severe hypoglycaemia (SH) attacks (i.e. the patient needs the assistance of another person to relieve the attack) whenever attempts are made to introduce tight blood glucose control. Very high incidence rates of SH between 19% and 44% have been reported in diabetic pregnancy. Episodes of SH could have serious consequences; neuroglycopenia seems especially hazardous for the mother particularly during the performance of a critical task like driving a car. While hypoglycaemia has embryopathic effects in rodents, there are no data in the human to support a teratogenic effect. Insulin-induced hypoglycaemia in the last trimester of diabetic pregnancy may increase fetal body movement and decrease the fetal heart rate variability. A number of very rare conditions such as insulinoma, severe malaria, HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count), severe fulminating liver disease, and ACTH and/or growth hormone deficiency have been reported to be associated with SH. Relative hypoglycaemia--i.e. low fasting blood glucose and 'flat' glucose tolerance test--is frequently seen in normotensive pregnant women with intrauterine fetal growth retardation. This pattern of maternal carbohydrate metabolism could lead to fetal hypoglycaemia and hypoinsulinaemia and contribute to poor fetal growth.

Diabetes Mellitus, Type 1↗

PubMed1999

Diabetic emergencies: Part 1. Hypoglycaemia.

Diabetes mellitus is a chronic, lifelong condition which can affect people of all ages, and is increasing in prevalence. Hypoglycaemia is probably the most common acute problem suffered by patients with diabetes. It is also a serious medical emergency with potentially fatal outcomes, and is the most common reason for patients with diabetes attending an accident and emergency (A&E) department. It is also a major source of anxiety for diabetics, particularly those controlled on insulin, and unfortunately, in the move towards ever tighter glycaemic control, it is inevitable that diabetics will continue to suffer from hypoglycaemia. This article examines the pathophysiology of hypoglycaemia and some of its main causes, and will look at the clinical management of the patient with hypoglycaemia, both in the community and in the A&E department. The importance of the recognition and prompt treatment of hypoglycaemia, and of the investigation of hypoglycaemia with no obvious cause are also discussed. Part 2 of the series will explore the pathophysiology and clinical management of diabetic emergencies involving hyperglycaemia, including both diabetic ketoacidosis and the rarer hypernatremic, non-ketotic coma.

Diabetes Mellitus, Type 1↗

PubMed2003

Neurocognitive functioning in children with type-1 diabetes with and without episodes of severe hypoglycaemia.

Previous studies have shown that recurrent severe hypoglycaemia can cause long-term cognitive impairment in children with type-1 diabetes, but the results are controversial, possibly due to the heterogeneity of samples and lack of comprehensive neuropsychological assessments of children. The aim of this study was to assess the effects of diabetes and severe hypoglycaemia on the neurocognitive functioning of children with a standardized, wide age-range neuropsychological test battery designed for the assessment of children. Eleven children with diabetes and a history of severe hypoglycaemia, 10 children with diabetes without a history of severe hypoglycaemia, and 10 healthy control children (a total of 31 children: 14 males and 17 females, age range 5 years 6 months to 11 years 11 months, mean 9 years 4 months, SD 1 year 11 months) were studied using the Wechsler Intelligence Scale for Children-Revised (WISC-R) and the NEPSY, a Developmental Neuropsychological Assessment. The NEPSY assessed development in attention and executive functions, language, sensorimotor functions, visuospatial processing, and learning and memory. Children with a history of severe hypoglycaemia had more neuropsychological impairments, more learning difficulties (as reported by parents), and needed more part-time special education than those in the other groups. Significant differences were found in verbal short-term memory and phonological processing. Results suggest that severe hypoglycaemia is a risk factor for learning due to deficits in auditory-verbal functioning.

Child↗

PubMed1996

Reversal of hypoglycaemia in murine malaria by drugs that inhibit insulin secretion.

We have investigated the metabolic disturbances in 2 murine models of blood-stage malaria, Plasmodium chabaudi and Plasmodium yoelii. Blood glucose, plasma insulin and parasitaemia were measured in normal and infected mice before and after treatment with diazoxide, adrenaline, Sandostatin and quinine. Severe hypoglycaemia and marked hyperinsulinaemia developed during both infections. A single injection of diazoxide (25 mg/kg i.p.) or adrenaline (0.03 mg s.c.) lowered insulin concentrations in normal mice, reversed the hypoglycaemia in both infections and significantly reduced the hyperinsulinaemia in P. chabaudi-infected mice (P < 0.0001). Higher doses of Sandostatin (500 micrograms/kg s.c.) were required to reverse hypoglycaemia. Quinine (25 mg/kg i.p.) significantly increased blood glucose in normal and infected mice (P < 0.0010 and no hypoglycaemia was observed in mice with normal blood glucose for more than 3 h. This study shows that the major cause of hypoglycaemia in murine malaria is hyperinsulinaemia rather than high consumption of glucose by host and parasites or chemotherapy with quinine, and that hypoglycaemia can be reversed by correcting the hyperinsulinaemia.

Animals↗

PubMed2000

Review of prandial glucose regulation with repaglinide: a solution to the problem of hypoglycaemia in the treatment of Type 2 diabetes?

Type 2 diabetes mellitus is characterised by abnormal beta-cell function (present at the time of diagnosis) that is often associated with insulin resistance. An important and consistent pathophysiological finding is the failure to produce adequate increments in insulin secretion in response to carbohydrate intake. Therefore, insulin secretagogue therapy, particularly when focused on prandial glucose regulation, is a logical approach to treatment because it addresses one of the most fundamental pathophysiological aspects of the disease. However, the traditional secretagogues-the sulphonylureas--have long been associated with the unwanted effect of hypoglycaemia. This is particularly likely to occur when drugs with lengthy plasma half-lives, prolonged drug-receptor interactions, active metabolites or a reliance on renal clearance are used. The problem is most prevalent in elderly patients, where sulphonylurea-induced hypoglycaemia may be related to failure to comply with strict mealtimes or the need for supplementary food intake, often in the context of compromised renal function. Data from large-scale outcome studies demonstrate that when tight glycaemic control is achieved through aggressive antidiabetic therapy, late diabetic complications can be significantly reduced. However, the pursuit of stricter HbA1c targets with more aggressive interventions may increase the risk of hypoglycaemia. This is an irony because the clinical need to avoid hypoglycaemia and patients' apprehension of it present barriers to the achievement of beneficial glycaemic targets. However, an increased risk of hypoglycaemia may not be inevitable with insulin secretagogue therapy. The recently introduced carbamoylmethyl benzoic acid derivative, repaglinide, has pharmacological properties that are well suited to its intended role as a prandial glucose regulator. When taken prior to main meals, the rapid onset and relatively short duration of action of repaglinide aid disposal of the mealtime glucose load, without continued stimulation of pancreatic beta-cells in the postprandial fasting period. Repaglinide is also characterised by hepatic metabolism and elimination, which is an advantage in the context of impaired renal function. Prandial glucose regulation with repaglinide selectively increases insulin secretion, and hence limits glucose excursions, in the prandial phase. If a meal is omitted, so too is the corresponding dose. This more flexible approach to the management of Type 2 diabetes has a number of advantages when compared with the fixed daily dosing regimens of sulphonylureas, among them a reduced risk of hypoglycaemia--a benefit that is particularly marked in the context of missed or irregular meals.

Blood Glucose↗

PubMed2002

Reducing hypoglycaemia with insulin analogues.

Numerous studies have demonstrated that tight glycaemic control reduces long-term complications in both Type 1 and Type 2 diabetes. However, current intensive insulin regimens increase the risk of hypoglycaemia, dissuading many attempting this approach. Normal physiological insulin profiles consist of a stable, basal component and meal-related surges in secretion. Conventional insulin regimens cannot mimic this profile accurately due to pharmacokinetic limitations. Human insulin has a slow onset of action, thus patients are advised to inject about 30 min before a meal, ensuring peak insulin concentrations coincide with postprandial glucose excursions. This is clearly impractical for many and can lead to pre-meal hypoglycaemia if the meal is delayed. Furthermore, it only partially overcomes the unphysiological insulin profile and patients experience postprandial hyperglycaemia and are vulnerable to postabsorptive hypoglycaemia. Insulin aspart and insulin lispro are rapid-acting analogues that allow a more physiological replacement of mealtime insulin secretion. They reduce postprandial glucose and usefully reduce the incidence of hypoglycaemia when used in a basal-bolus regimen in tightly controlled patients. Pre-mixed insulins, containing a combination of rapid-acting and intermediate-acting insulin, are widely used, particularly in Type 2 diabetes. They have limitations achieving tight glucose targets but early data suggest that the combination of 30% insulin aspart and 70% protaminated insulin aspart may also reduce severe hypoglycaemia. On-going clinical trials will establish whether they can be used to achieve better glycaemic control with less hypoglycaemia.

Blood Glucose↗

PubMed1991

Autonomic mechanisms underlying intraocular pressure changes during insulin-induced hypoglycaemia in normal human subjects: effects of pharmacological blockade.

1. A fall in intraocular pressure is induced by acute hypoglycaemia in humans. The role of the autonomic nervous system in mediating this response was investigated in 24 normal volunteers in whom hypoglycaemia was induced with intravenous soluble insulin, under four experimental conditions: (1) control (n = 6), (2) non-selective alpha-adrenoceptor blockade (phentolamine) (n = 6), (3) non-selective beta-adrenoceptor blockade (propranolol) (n = 6) and (4) cholinergic blockade (atropine) (n = 6). Intraocular pressure was measured by using an applanation tonometer. In 12 subjects intraocular pressure was measured during each type of pharmacological blockade of similar duration without induction of hypoglycaemia, to assess the effects of individual antagonists. 2. In the control study intraocular pressure fell during hypoglycaemia from 15 +/- 1.0 to 10 +/- 1.3 mmHg (P less than 0.01) 10 min after the autonomic reaction. beta-Adrenoceptor blockade caused a reduction in intraocular pressure from 15 +/- 1.1 to 9 +/- 1.0 mmHg (P less than 0.001) before the administration of insulin, and when hypoglycaemia was induced intraocular pressure decreased further to 7 +/- 1.0 mmHg (P less than 0.05, compared with immediately before insulin). A decrease in intraocular pressure of similar magnitude was observed with propranolol alone (16 +/- 1.0 to 10 +/- 1.0 mmHg, P less than 0.05). 3. Cholinergic blockade had no immediate effect on intraocular pressure, and the reduction in intraocular pressure during hypoglycaemia was of similar magnitude to that observed during the control study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Effects of acute insulin-induced hypoglycaemia on haemostasis, fibrinolysis and haemorheology in insulin-dependent diabetic patients and control subjects.

1. The effects of acute hypoglycaemia on haemostasis, fibrinolysis, blood viscosity and erythrocyte aggregation were examined after acute insulin-induced hypoglycaemia in six normal male subjects and in six male patients with poorly controlled insulin-dependent diabetes. In the control subjects hypoglycaemia caused a significant increase in the concentration of von Willebrand factor, with no change in the concentrations of fibrinogen and cross-linked fibrin degradation products. Fibrinolysis was enhanced, as indicated by significant increases in tissue plasminogen activator concentration and the fibrin plate lysis area, with a fall in plasminogen-activator inhibitor activity, suggesting complex formation. Whole-blood and plasma viscosity increased significantly after hypoglycaemia, but there was no significant change in erythrocyte aggregation tendency. 2. In diabetic patients the increase in the concentration of von Willebrand factor was significantly greater than in the control group (analysis of variance, P less than 0.02). The basal concentration of tissue plasminogen activator was reduced at 3.7 +/- 0.7 mg/l (mean +/- SEM) in the diabetic group compared with 8.5 +/- 1.3 mg/l in the control group (Student's t-test, P less than 0.01), but thereafter the increase in response to hypoglycaemia was similar. The changes in the other variables were not significantly different from the changes in the control group. 3. During acute hypoglycaemia in poorly controlled diabetic patients there is promotion of haemostasis with a greater increase in the concentration of von Willebrand factor, which, in association with the increase in viscosity, might reduce perfusion in diabetic microangiopathy, leading to aggravation of the microvascular complications of diabetes.

Acute Disease↗

PubMed1999

Increased QT dispersion during hypoglycaemia in patients with type 2 diabetes mellitus.

OBJECTIVES: To study effects of insulin-induced hypoglycaemia on the cardiac repolarization, using QT interval measurements, in patients with type 2 diabetes. DESIGN: Hypoglycaemia was induced by an i.v. insulin-infusion and blood glucose was clamped at 2.7 mmol L-1 for 60 min (T = 90-150 min) in two experiments, with (+GLIB) and without (-GLIB) glibenclamide. In a third experiment, with similar hyperinsulinaemia, glucose was clamped at a euglycaemic level (;5 mmol L-1). ECG was continuously recorded for arrhythmia-monitoring, and 12-lead ECGs were recorded at T = 0 and 150 min. QT intervals were measured, and we determined QT dispersion (difference between the maximum and the minimum QT interval) reflecting interlead variability of repolarization. SUBJECTS: Thirteen patients with type 2 diabetes, on combined insulin and glibenclamide treatment, were studied during hypoglycaemia, and eight of them participated in the euglycaemic experiment. RESULTS: No significant arrhythmias were seen during hypoglycaemia but the mean QT intervals and QT dispersion increased significantly (P < 0.001), with no differences between -GLIB and +GLIB. During the euglycaemic clamp all QT measurements remained unchanged. Serum potassium decreased significantly (P < 0.001) during all three clamps, but the decrease was more pronounced during hypoglycaemia. The change in potassium was not correlated to the degree of QT prolongation or QT dispersion. CONCLUSIONS: Significant changes in the repolarization of the heart can be seen during hypoglycaemia in patients with type 2 diabetes, indicating an increased risk of arrhythmia at low blood glucose levels.

Aged↗

PubMed2002

Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycaemia in long-term type 1 diabetes.

OBJECTIVES: To evaluate the influence of residual beta-cell function on glucagon secretion and glucose counter-regulation following hypoglycaemia in type 1 diabetes. DESIGN AND SUBJECTS: The hormonal counter-regulatory responses to standardized insulin-induced hypoglycaemia were investigated, 18 patients with type 1 diabetes of long duration and 12 healthy subjects were investigated. Nine of the diabetic patients (diabetes duration 17 +/- 1 years) had residual insulin secretion, as reflected by persistent urinary C-peptide excretion. The other nine diabetic patients (diabetes duration 21 +/- 1 years) were C-peptide negative. RESULTS: Similar hypoglycaemic nadirs were found in all groups (2.1-2.3 mmol L-1), whereas the recovery of plasma glucose levels was delayed similarly in the diabetic groups. In the control subjects, plasma glucagon increased ( approximately 50%). No significant glucagon response was registered in either of the two diabetic groups. The maximum plasma adrenaline and pancreatic polypeptides (PP) responses to hypoglycaemia were comparable in the two diabetic patient groups; the peak values being lower (P < 0.05) than in the controls. Plasma noradrenaline, growth hormone and cortisol responses to hypoglycaemia were similar in all three groups. CONCLUSION: Residual beta-cell function in patients with long-term type 1 diabetes is not accompanied by preservation of the glucagon response to hypoglycaemia. As the two markers of autonomic function (adrenaline and PP) were similarly reduced in the two diabetic groups, the findings instead favour the concept that the defective glucagon secretory response to hypoglycaemia is because of autonomic nervous dysfunction.

Adult↗

PubMed1984

Insulin-induced hypoglycaemia stimulates secretion of parathyroid hormone.

In-vitro and in-vivo studies have suggested a role for the adrenergic system in the regulation of secretion of parathyroid hormone (PTH). In the present study the effects of insulin induced hypoglycaemia on serum concentrations of PTH, cortisol, calcium and phosphate were evaluated in ten healthy subjects. Maximum hypoglycaemia occurred 25 to 35 min after administration of insulin at a standard dose of 0.15 U/kg body weight. All this time there was a slight and transient increase of the serum calcium concentrations whereas there was a marked drop in the serum phosphate levels with a nadir 15 min after maximum hypoglycaemia. Cortisol levels were below baseline when blood glucose was as lowest but increased to a maximum level of 200% 60 minutes after maximum hypoglycaemia. Serum PTH levels increased significantly and reached a maximum of 130% of baseline values concomitant with maximum hypoglycaemia, whereafter they returned to pre-insulin-injection levels within 15 minutes. These findings indicate that during stress endogenous catecholamines affect the secretion of PTH which could be of physiologic importance. In five patients with primary hyperparathyroidism there was, however, no increase in the PTH levels, although they displayed the same response to hypoglycaemia for cortisol and phosphate. This supports previous suggestions that these patients have an impaired capacity to respond to circulating catecholamines.

Adult↗

PubMed2000

Measurement of high resolution ECG QT interval during controlled euglycaemia and hypoglycaemia.

During hypoglycaemia, typically there is a change in the surface ECG characterized by a flattened and prolonged T wave, often accompanied by a fused U wave. The QT interval is a useful parameter for quantifying the ECG morphology. However, reliable measurement of QT is not straightforward, particularly for hypoglycaemic ECG morphology. The objective of this study was to compare the ability of two methods of QT measurement to distinguish between ECGs recorded during euglycaemia and hypoglycaemia. The first method involves manually setting the intersection of the isoelectric line and the T wave or, where this is not possible, the nadir between the T and U wave. The second method is semi-automatic and fits a tangent to the point of maximum gradient on the downward slope of the T wave. Two independent observers used both methods to measure the QT for high resolution ECG data recorded during a study of 17 non-diabetic subjects undergoing controlled euglycaemia and hypoglycaemia. Using the mean results of the two observers, the mean +/- SD increase in heart rate corrected QT, QTc, for ECGs recorded during euglycaemia and hypoglycaemia was 32 +/- 25 ms for the non-tangent method and 60 +/- 24 ms for the tangent method. Therefore, the tangent method provides greater distinction between ECGs recorded during euglycaemia and hypoglycaemia than the non-tangent method. A potential clinical application could be the non-invasive detection of impending hypoglycaemia at night, which would be of significant benefit to adults and young children with diabetes.

Adult↗