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PubMed1998

Impact of improved glycaemic control on rates of hypoglycaemia in insulin dependent diabetes mellitus.

Increased emphasis on strict glycaemic control of insulin dependent diabetes mellitus (IDDM) in young patients may be expected to cause increases in rates of significant hypoglycaemia. To evaluate whether this is the case for a large population based sample of IDDM children and adolescents rates of severe (coma, convulsion) and moderate (requiring assistance for treatment) hypoglycaemia were studied prospectively over a four year period. A total of 709 patients were studied yielding 2027 patient years of data (mean (SD) age: 12.3 (4.4); range 0-18 years, duration IDDM: 4.9 (3.8) years). Details of hypoglycaemia were recorded at clinic visits every three months when glycated haemoglobin (HbA1c) was also measured. Overall the incidence of severe hypoglycaemia was 7.8 and moderate was 15.4 episodes/100 patient years. Over the four years mean (SD) clinic HbA1c steadily fell from 10.2 (1.6)% in 1992 to 8.8 (1.5)% in 1995. In parallel with this there was a dramatic increase in the rate of hypoglycaemia, especially in the fourth year of the study, when severe hypoglycaemia increased from 4.8 to 15.6 episodes/100 patient years. This increase was particularly marked in younger children (< 6 years) in whom severe hypoglycaemia increased from 14.9 to 42.1 episodes/100 patient years in 1995. It is concluded that attempts to achieve improved metabolic control must be accompanied by efforts to minimise the effects of significant hypoglycaemia, particularly in the younger age group.

Adolescent↗

PubMed1991

Risk of severe hypoglycaemia in insulin treated diabetic patients transferred to human insulin: a case control study.

OBJECTIVE: To examine whether transfer from animal insulin to human insulin is associated with an increased risk of severe hypoglycaemia. DESIGN: Matched case-control study of insulin treated diabetic patients admitted to hospital because of hypoglycaemia during 1984-7, the period when human insulin was introduced into treatment. SETTING: Case admissions and control admissions were obtained from eight public hospitals within the Swiss canton of Berne and a second control group comprised members of the Bernese section of the Swiss Diabetes Association. SUBJECTS: 94 patients with insulin treated diabetes with a total of 112 admissions for hypoglycaemia during 1984-7 (case admissions), 182 patients with insulin treated diabetes seen in the same hospitals for reasons other than hypoglycaemia with a total of 225 admissions (control admissions), and 86 insulin treated diabetic patients who were members of the Bernese section of the Swiss Diabetes Association. MAIN OUTCOME MEASURES: Type of insulin used at time of admission, glycaemic control as measured by amount of glycated haemoglobin or glucose concentration; severity of hypoglycaemia. RESULTS: Treatment with human insulin at admission was more common in cases than controls (52/112 (46%) admissions v 77/225 (34%); p = 0.003). 116 out of 129 (90%) of admissions taking human insulin had been transferred from animal insulin, mainly because of non-availability of porcine insulins. The ratio of rate of hypoglycaemia in those taking human insulin to the rate in those taking animal insulin was 2.4 (95% confidence interval 1.3 to 4.4). Other risk factors for hypoglycaemia were a history of hypoglycaemic coma (rate ratio of history to no history 3.8, 2.3 to 6.4) and good glycaemic control (rate ratio of good to poor control 3.9, 1.4 to 7.5). With multivariate analysis the increase in rate ratio associated with use of human insulin rose to 3.0 (1.4 to 6.4). Comparison with the diabetes association controls also showed an increased risk associated with use of human insulin (2.2; 1.1 to 4.8). CONCLUSIONS: Transfer of treatment from animal insulin to human insulin was associated with an increased risk of severe hypoglycaemia. Caution should be exercised when transferring diabetic patients to human insulin. Further studies are required to elucidate why this effect occurs.

Adolescent↗

PubMed2000

Neonatal hypoglycaemia in Nepal 1. Prevalence and risk factors.

AIMS: To measure the prevalence of hypoglycaemia among newborn infants in Nepal, where classic risk factors prevail, and to evaluate their importance. METHODS: A cross sectional study was done of 578 term newborn infants aged 0 to 48 hours on the postnatal wards of a government maternity hospital in Kathmandu, with unmatched case-control analysis of risk factors for moderate hypoglycaemia (less than 2.0 mmol /l). RESULTS: Two hundred and thirty eight (41%) newborn infants had mild (less than 2.6 mmol/l) and 66 (11%) moderate hypoglycaemia. Significant independent risk factors for moderate hypoglycaemia included postmaturity (OR 2.62), birthweight under 2.5 kg (OR 2.11), small head size (OR 0.59), infant haemoglobin >210 g/l (OR 2.77), and raised maternal thyroid stimulating hormone (TSH) (OR 3.08). Feeding delay increased the risk of hypoglycaemia at age 12-24 hours (OR 4.09). Disproportionality affected the risk of moderate hypoglycaemia: lower with increasing ponderal index (OR 0.29), higher as the head circumference to birthweight ratio increased (OR 1.41). Regression expressing blood glucose concentration as a continuous variable revealed associations with infant haemoglobin (negative) and maternal haemoglobin (positive), but no other textbook risk factors. CONCLUSIONS: Neonatal hypoglycaemia is more common in a developing country, but may not be a clinical problem unless all fuel availability is reduced. Some textbook risk factors, such as hypothermia, disappear after controlling for confounding variables. Early feeding could reduce moderate hypoglycaemia in the second 12 hours of life. The clinical significance of raised maternal TSH and maternal anaemia as prenatal risk factors requires further research.

Adolescent↗

PubMed1999

Ambulance visits for severe hypoglycaemia in insulin-treated diabetes.

AIM: To determine, in insulin-treated diabetes the incidence and risk factors for severe hypoglycaemia requiring ambulance visits. METHODS: A cross-sectional, questionnaire survey was made of patients with type 1 diabetes, who received help for severe hypoglycaemia from Ambulance Association personnel, during the period 1/6/95 to 31/5/96. RESULTS: The ambulance service made 386 emergency visits to 247 persons with type 1 diabetes. Of these, 128 respondents (52%) completed a questionnaire detailing personal and diabetes history, usual diabetes care practices and hypoglycaemia management. Two or more visits for severe hypoglycaemia were made to 26.3% of patients, who reported a longer duration of diabetes than those who required only one visit (28 vs 20 years, p<0.03). Self-blood-glucose monitoring was performed by 98.4% of respondents and 66.4% self-adjusted insulin doses. Intensively treated patients (> or = 3 insulin injections daily) reported less awareness of hypoglycaemia than standard therapy patients (< or = 2 insulin injections daily) (p<0.05). Fifty-four per cent of respondents had glucagon available for emergency use, but those who lived alone and in general practitioner care only (27%) were less likely to have glucagon (p<0.05) compared to those with companions and in shared-care arrangements (62%). Hypoglycaemia management was influenced by the availability of glucagon. Oral glucose was used by 82% before injecting glucagon, whereas 40% of patients without glucagon called for the ambulance when severe symptoms were present even before initiating treatment with oral glucose. CONCLUSION: This survey determined the minimum frequency of severe hypoglycaemia requiring the ambulance at 1.6 episodes patient(-1) year(-1). Precipitating factors and a lack of coping skills and behaviours that might prevent severe hypoglycaemia and ambulance calls were identified.

Aged↗

PubMedDate not supplied

Mental alertness in response to hypoglycaemia in normal man: the effect of 12 hours and 72 hours of fasting.

To study the influence of hypoglycaemia and starvation on mental functions eight healthy male students age 25-34 years with an ideal body mass of 99.9% +/- 2.5% (mean +/- SEM) were recruited. Hypoglycaemia was induced in random order by an insulin-glucose clamp technique (insulin: 2.4 mU/kg/min + glucose at variable rate) keeping the venous blood glucose at 2.2 mmol/l both after an overnight fast and after 72 h fasting. Mental alertness was assessed by measuring the recognition time, moving time and total reaction time to a visual signal and by a verbal mental clearness test and a synonym learning test during normo- as well as hypoglycaemia. Hypoglycaemia prolonged the total reaction time (p less than 0.05) and the time required for the mental clearness test (p less than 0.05). Compared with a control study performed at normoglycaemia the learning effect of the synonym test was reduced by hypoglycaemia. Fasting, which resulted in a body weight reduction of 2.6 +/- 0.3 kg and ketonuria prolonged the total reaction time (p less than 0.005) by increasing the moving time but did not affect the mental clearness test. When hypoglycaemia was preceded by 72 h fasting it did not increase the total reaction time, nor did it modify the mental clearness test. Moreover, the learning effect of the synonym test was less impaired. In conclusion, mental alertness was reduced by moderate hypoglycaemia after an overnight fast while similar hypoglycaemia did not reduce mental alertness after prolonged fasting. This may illustrate a decrease of the glucose dependency of the central nervous system during prolonged fasting.

Adult↗

PubMed1996

Hypoglycaemia and gastric emptying.

The following studies show that insulin-induced hypoglycaemia increases the gastric emptying rate for both liquids and solid food in healthy volunteers and in patients with IDDM of short duration. This response to low blood glucose concentrations may help protect against sustained hypoglycaemia by increasing the uptake of ingested carbohydrates. The results suggest that gastric emptying in patients with diabetes should be examined under conditions that are standardized with respect to blood glucose concentration. The finding that cholinergic muscarinic blockade with atropine inhibited the hypoglycaemia-induced acceleration of gastric emptying indicates that vagal stimulation plays an important role in this mechanism. The fact that plasma pancreatic polypeptide concentrations were unchanged during hypoglycaemic episodes in the presence of atropine indicates that complete inhibition of the cholinergic transmission was achieved. It is not yet established whether hypoglycaemia directly stimulates vagal activity or whether this is achieved through the activation of hormones or other second messengers. It is likely, however, that vagal activity is an important determinant of the varying rate of gastric emptying at different glycaemic levels. The pancreatic polypeptide response in the atropine-treated subjects resembles that seen in diabetic patients with autonomic neuropathy when exposed to insulin-induced hypoglycaemia. Disturbances of vagal function are frequent in diabetic patients with autonomic neuropathy, and can lead to a reduction in the stimulated gastric output. A failure to increase gastric emptying in response to hypoglycaemia would be disadvantageous when ingestion of oral carbohydrates is used to restore normoglycaemia, and diabetic patients with autonomic neuropathy could therefore be at increased risk for severe hypoglycaemia. The influence of glycaemia on vagal activity and gastric emptying rate probably alters the optimal time interval between insulin injections and postprandial increases in the blood glucose concentration in patients treated with short-acting insulin administered at mealtimes. This may cause variations in blood glucose concentrations. Furthermore, it is possible that drugs that have anticholinergic effects (such as tricyclic antidepressants) may deleteriously decrease the gastric emptying rate during hypoglycaemia in diabetic patients.

Adult↗

PubMed2026

Association of Post-Oral Glucose Tolerance Test Hypoglycaemia With Clinical Features, Incident Diabetes and Mortality in the Di@bet.es Cohort.

AIMS: To investigate the association of post-oral glucose tolerance test (OGTT) hypoglycaemia with clinical features, incident diabetes and mortality. MATERIALS AND METHODS: This population-based cohort study included 2924 adults (median age 49 years, 1680 women) without known diabetes who underwent a 75-g OGTT as part of the Di@bet.es Study. Metabolic, demographic and lifestyle variables were collected. Serum glucose and insulin concentrations at 0, 30 and 120 min during the OGTT were obtained, allowing insulin resistance estimation using the HOMA-IR and the Matsuda Index. Participants were grouped according to serum glucose at 120 min: < 70 mg/dL (post-OGTT hypoglycaemia), 70 to < 140 mg/dL (normal result), 140 to < 200 mg/dL, and ≥ 200 mg/dL. The incidence of diabetes (median follow-up, 7.5 years) and mortality (median follow-up, 14.5 years) were assessed. RESULTS: Participants with post-OGTT hypoglycaemia (n = 327, 11.1%) were younger, leaner, less insulin resistant and more frequently active smokers. Despite having the lowest serum glucose at 0, 30 and 120 min, and the lowest serum insulin at 0 and 120 min, these participants tended to have the highest serum insulin concentrations at 30 min. Participants with post-OGTT hypoglycaemia had the lowest incidence of diabetes and mortality, although these associations were attenuated after adjusting for confounders (such as age, sex, body mass index and physical activity) and when compared specifically with the normal result group. CONCLUSIONS: Post-OGTT hypoglycaemia is more frequent in smokers, younger individuals, and those with a favourable metabolic profile. Post-OGTT hypoglycaemia acts as a marker of protection for incident diabetes and mortality. Preserved early insulin secretion together with good insulin sensitivity could explain post-OGTT hypoglycaemia.

Humans↗

PubMed1996

A comparative study of responses to acute hypoglycaemia induced by human and porcine insulins in patients with Type 1 diabetes.

The effects of human and porcine insulins on the symptomatic, physiological, and counterregulatory hormonal responses to acute hypoglycaemia were compared in 40 patients with Type 1 diabetes, 20 of whom were newly diagnosed while 20 had been treated for between 5 and 20 years. In a double-blind, cross-over trial all patients were treated with human or porcine insulin, in random order, for two consecutive 3-month periods. At the end of each treatment period they were subjected to an acute episode of experimental hypoglycaemia induced by a continuous intravenous infusion (2.0 mU kg(-1)min(-1)) of the same insulin species. Haemodynamic, sweating, and tremor responses were measured during both studies, symptom scores were recorded and the arterialized plasma glucose thresholds for autonomic activation and the onset of subjective symptoms were identified. In all patients the glycaemic thresholds for the initiation of the autonomic physiological responses to hypoglycaemia and the onset of the symptomatic response were concurrent and did not differ with insulin species (plasma glucose 1.94 vs 1.96 mmol I(-1), human vs porcine studies). The onset, temporal pattern, nature, and magnitude of the physiological responses (sweating, heart rate, blood pressure, and tremor) during acute experimental hypoglycaemia were also identical with each insulin species. The magnitude and temporal pattern of the response of counterregulatory hormones (adrenaline, noradrenaline, glucagon, ACTH, and GH) to hypoglycaemia as induced by human and porcine insulins were indistinguishable, as were the total and individual scores of autonomic and neuroglycopenic symptoms. In conclusion, in patients who had newly diagnosed and intermediate duration (5-20 years) of diabetes, the symptomatic, physiological, and counterregulatory hormonal responses to acute insulin-induced hypoglycaemia did not differ between human and porcine insulins, and the plasma glucose thresholds at which the symptomatic and autonomic responses were initiated were identical with both insulin species. This study does not support the hypothesis that treatment with human insulin modifies the symptomatic, physiological, and counterregulatory hormonal responses to acute hypoglycaemia.

Acute Disease↗

PubMed1996

Similar physiological and symptomatic responses to sulphonylurea and insulin induced hypoglycaemia in normal subjects.

There is little information concerning the physiological response to hypoglycaemia induced by sulphonylureas. We compared the physiological and symptomatic responses to insulin and tolbutamide induced hypoglycaemia in 8 normal subjects. While infusing either insulin or tolbutamide, we used a glucose clamp to maintain blood glucose at 4.5 mmol l-1 for 30 min and lowered it to 2.9 mmol l-1 for a further 30 min. Mean peripheral insulin levels during the insulin infusion arm in comparison with the tolbutamide infusion were not significantly different during the euglycaemic plateau: 106 +/- 4 vs 77 +/- 15 mU l-1 (mean +/- SEM) (mean difference 29 mU l-1, 95% CI -22 to 80; p = NS) but were greater during the hypoglycaemic plateau: 106 +/- 3.5 vs 21.0 +/- 4.0 mU l-1 (mean difference 85 mU l-1, 95% CI 72 to 98; p < 0.0001). Portal insulin concentrations, calculated from C-peptide data were not significantly different during the euglycaemic plateau with insulin as compared to tolbutamide. However, during hypoglycaemia portal insulin concentrations were significantly higher 15 min from the start of the plateau, during insulin infusion. During hypoglycaemia induced by either insulin or tolbutamide there were similar peak responses of glucagon: 124 +/- 14 vs 128 +/- 7 ng l-1 (mean difference -4, 95% CI -39 to 31; p = NS) and adrenaline: 2.9 +/- 0.4 vs 2.8 +/- 0.3 nmol l-1, (mean difference 0.1, 95% CI -0.9 to 1.0; p = NS). Increases in tremor and sweating and deterioration in reaction time were similar during both periods of hypoglycaemia as were increases in total: 18.5 +/- 1.4 vs 19.6 +/- 2.2 (mean difference -1.0, 95% CI -3.8 to 1.8; p = NS) and autonomic: 8.9 +/- 0.9 vs. 9.9 +/- 1.3 (mean difference -1.1, 95% CI -5.9 to 3.6; p = NS) symptom scores. We conclude that there is no difference in the glucagon, sympathoadrenal, cognitive or symptomatic response during hypoglycaemia induced by either insulin or tolbutamide. This suggests that the different insulin concentrations produced by these contrasting models of hypoglycaemia had no effect on the physiological response and patients taking sulphonylureas can be expected to develop similar warning symptoms to those on insulin.

Adult↗

PubMed1997

Nocturnal hypoglycaemia in IDDM patients younger than 18 years.

The present multicentre study was undertaken to assess the prevalence of nocturnal hypoglycaemia and its determining factors in 117 diabetic children and adolescents, aged 2-18 years and diabetes duration > 1 year in Spain. Each child made 3 measurements of blood glucose (BG) at home at night (between 0000 h and 0600 h) on nine separate nights. A hypoglycaemic event occurred in 12-14% of children in any one night. This is lower than rates for nocturnal hypoglycaemia reported in literature, perhaps because of relatively late mealtimes and different meal content, in Spanish children. Children aged < 7 years were at higher risk of nocturnal hypoglycaemia than older children (p < 0.05). Mean HbA1c from the year before the study and mean HbA1c measured during the closest time to the study were significantly lower in those with nocturnal hypoglycaemia (p < 0.0001). Blood glucose concentrations 2 h before hypoglycaemia did not predict nocturnal hypoglycaemia. The occurrence of low or very low blood glucose concentrations before breakfast was related to a higher risk for nocturnal hypoglycaemia (chi 2 22.97; p < 0.001). No previous symptoms were detectable in 89% of cases.

Adolescent↗

PubMedDate not supplied

Symptomatic and counterregulatory hormonal responses to acute hypoglycaemia induced by insulin aspart and soluble human insulin in Type 1 diabetes.

BACKGROUND: The aim of this study was to assess hypoglycaemia awareness with the insulin analogue, insulin aspart. The counterregulatory hormonal and symptomatic responses to hypoglycaemia induced by insulin aspart were compared with soluble human insulin in a double-blind, randomised, two-period crossover trial in patients with Type 1 diabetes. The primary objective was to compare the blood glucose threshold for autonomic activation during hypoglycaemia induced by insulin aspart and soluble human insulin. Secondary objectives were to compare the counterregulatory, symptomatic and physiological responses to hypoglycaemia. METHODS: 20 patients were screened, 17 were randomised and 16 completed the study. Acute hypoglycaemia was induced by intravenous infusion of insulin aspart or soluble human insulin (100 U ml(-1) at a rate of 2 mU kg(-1) min(-1)). RESULTS: No statistical difference between insulin aspart and soluble human insulin was shown for the primary blood glucose endpoint; mean arterialised blood glucose concentrations (+/-SD) at the onset of autonomic activation were 1. 88+/-0.39 mmol L(-1) for insulin aspart and 1.89+/-0.43 mmol L(-1) for soluble human insulin (not significant). No statistical differences were observed between the two insulins for the secondary endpoints: counterregulatory hormonal responses, autonomic responses, hypoglycaemia symptom scores, cognitive function and blood glucose responses. No serious adverse events were reported during the study. CONCLUSIONS: Insulin aspart and soluble human insulin elicit the same counterregulatory and symptomatic responses to acute hypoglycaemia in patients with Type 1 diabetes.

Adolescent↗

PubMedDate not supplied

Nocturnal hypoglycaemia in type 1 diabetes--consequences and assessment.

Hypoglycaemia is inevitable when striving for low HbA1c values. Nocturnal hypoglycaemia often occurs without symptoms, but results in diminished next day well-being and hypoglycaemia unawareness. Frequency of nocturnal hypoglycaemia was first assessed in research ward settings, but suffered from insufficient glucose sampling frequency. This may have resulted in overestimation of the duration of hypoglycaemic episodes. The advent of the first continuous glucose sensor, the needle-type MedtronicMiniMed Continuous Glucose Measurement System, revolutionized the assessment of glucose values. However, on scrutiny, the first version of this sensor showed a drift into the hypoglycaemic area and delayed recovery from hypoglycaemia. Using the microdialysis-based GlucoDay system, our group reported a lower frequency of nocturnal hypoglycaemia in type 1 diabetes patients using an insulin pump, than that expected from the existing literature. Today, more than 80 years after the introduction of insulin for the treatment of type 1 diabetes, the associated frequency of nocturnal hypoglycaemia still awaits its definitive assessment.

Circadian Rhythm↗

PubMed1989

The prevalence of impaired glucose counter-regulation during an insulin-infusion test in insulin-treated diabetic patients prone to severe hypoglycaemia.

Among 603 patients over the age of 18, with insulin-treated diabetes mellitus, a questionnaire identified 98 patients who during a 12-month period had experienced severe hypoglycaemia, defined as an event which required the help of another person. Twenty of these patients had repeatedly suffered from such episodes, without any obvious reason, for a period of at least three years. The capacity to counter-regulate a standardized, insulin-infusion test (0.034 U.kg-1.h-1 given for 3 h unless severe neuroglucopenia developed) was evaluated in 14 of these patients. In 12, an impaired glucose counter-regulation was registered, defined as blood-glucose values below -2 SD of healthy subjects. In all but one of these patients, a combined deficiency of glucagon and adrenaline was documented, and was believed to be the likely cause of their inclination towards hypoglycaemia. In patients with severe hypoglycaemia, but not in diabetic patients without severe hypoglycaemia or in healthy subjects, a significant relationship between insulin disappearance and glucose rise was found. It is concluded that in insulin-treated diabetic patients, the prevalence of recurrent attacks of severe hypoglycaemia amounts to about 4%. In such patients, a combined deficiency of adrenaline and glucagon responses to hypoglycaemia is the predominant finding and the disappearance rate of insulin becomes critical for recovery of blood glucose after hypoglycaemia.

Blood Glucose↗

PubMed1988

Regional variation in skin blood flow response to hypoglycaemia in type 1 (insulin-dependent) diabetic patients without complications.

Body temperature falls during hypoglycaemia, perhaps as a protective mechanism. To test the hypothesis that the skin blood flow response to hypoglycaemia is specifically designed to facilitate heat loss we studied both nutritional blood flow and arteriovenous shunting of blood in skin during prolonged, controlled hypoglycaemia in man. We studied eight otherwise healthy, male, Type 1 (insulin-dependent) diabetic patients. Under Biostator control blood glucose was clamped at 8.0 (7.9-8.9), mmol/l (median and range) for 30 min, reduced to symptomatic hypoglycaemia, 1.7 (1.0-2.6) mmol/l for 20 min then raised to 4.9 (3.3-6.7) mmol/l. Interdigital skin web blood flow (laser doppler flowmeter, nutritional flow) fell during hypoglycaemia from 3.1 (2.2-3.8) to 2.4 (1.2-2.8) volts and remained depressed. In contrast, finger blood flow (venous occlusion plethysmography, arteriovenous shunt flow) started high at 54.7 (17.4-85.6), remained high at 52.7 (38.1-81.4) during hypoglycaemia but fell sharply to 25.3 (4.2-66.2) ml.min-1.100 ml-1 when symptoms were relieved. Plasma adrenaline and vasopressin both rose during hypoglycaemia from 0.4 (0.05-0.8) to 4.5 (2.3-20.2) nmol/l and from 0.5 (0.5-3.5) to 4.4 (2.0-13.9) pg/ml, respectively, and both fell sharply thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Post-hypoglycaemic hyperketonaemia does not contribute to brain metabolism during insulin-induced hypoglycaemia in humans.

It is controversial as to whether ketone bodies are utilized by the human brain as a fuel alternative to glucose during hypoglycaemia. To clarify the issue, we studied 10 normal volunteers during an experimental hypoglycaemia closely mimicking the clinical hypoglycaemia of patients with Type 1 (insulin-dependent) diabetes mellitus or insulinoma. Hypoglycaemia was induced by a continuous infusion of insulin (0.40 mU.kg-1.min-1 for 8 h, plasma insulin approximately 180 pmol/l) which decreased the plasma glucose concentration to approximately 3.1 mmol/l during the last 3 h of the studies. Subjects were studied on two occasions, i.e. spontaneous, counterregulatory-induced post-hypoglycaemic increase in 3-beta-hydroxybutyrate (from approximately 0.2 to approximately 1.1 mmol/l at 8 h), or prevention of post-hypoglycaemic hyperketonaemia (plasma beta-hydroxybutyrate approximately 0.1 mmol/l throughout the study) after administration of acipimox, a potent inhibitor of lipolysis. In the latter study, glucose was infused to match the hypoglycaemia observed in the former study. The glycaemic thresholds and overall responses of counterregulatory hormones, symptoms (both autonomic and neuroglycopenic), and deterioration of cognitive function (psychomotor tests) were superimposable in the control study in which ketones increased spontaneously after onset of hypoglycaemic counterregulation, as compared to the study in which ketones were suppressed (p = NS). The fact that responses of counterregulatory hormones, symptoms and deterioration in cognitive function were not exaggerated when posthypoglycaemic hyperketonaemia was prevented, indicate that during hypoglycaemia, the counterregulatory-induced endogenous hyperketonaemia does not provide the human brain with an alternative substrate to glucose. Thus, it is concluded that during hypoglycaemia, endogenous hyperketonaemia does not contribute to brain metabolism and function.

3-Hydroxybutyric Acid↗

PubMed1995

Evaluation of a standardized hyperglucidic breakfast test in postprandial reactive hypoglycaemia.

The oral glucose tolerance test is not specific for diagnosing postprandial reactive hypoglycaemia, since it too frequently induces low blood glucose values in subjects who have never complained of symptoms of this. By contrast, the mixed meal tests are deceptive for this purpose because they do not induce hypoglycaemia in subjects who have complained of of hypoglycaemic symptoms. We investigated the frequency of hypoglycaemia after a standardized hyperglucidic breakfast test in three groups of subjects:group A, 43 control subjects; group B, 38 postprandial reactive hypoglycaemic patients; group C, 1193 asymptomatic subjects undergoing assessment of glycoregulation. In the 38 subjects with suspected reactive hypoglycaemia the mean blood glucose nadir was 3.48 +/- 0.08 mmol/l, i.e. lower than in control subjects (4.83 +/- 0.13 p < 0.0001). Blood glucose levels less than 3.3 mmol/l were found in 47.3% of subjects with suspected postprandial reactive hypoglycaemia (group B), i.e more frequently than in control subjects (group A: 2.2% p = 1.6 x 10(-6)) and asymptomatic subjects (group C: 1% p = 8 x 10(-22)). This markedly higher frequency of low blood glucose values in subjects with postprandial symptoms compared with control and asymptomatic subjects suggests that this test detects a tendency to hypoglycaemia after a standardized hyperglucidic breakfast. Since this test mimics average French eating habits, the results suggest that the patients undergo such symptoms in their everyday life, and that the hyperglucidic breakfast test is a simple alternative to ambulatory glucose sampling for diagnosis of postprandial reactive hypoglycaemia.

Adult↗

PubMed1996

Monitoring set-up for selection of parameters for detection of hypoglycaemia in diabetic patients.

Recurrent severe hypoglycaemia is often an unsolved problem in diabetic patients under intensified insulin treatment. As no reliable long-term stable blood glucose sensor has yet been developed, registration of other body function changes could help to detect severe hypoglycaemia. A measuring system is described, capable on the one hand of recording EEG, heart rate, peripheral pulse, skin temperature, respiratory movements, skin impedance and arterial blood pressure, and capable of registering plasma glucose, counter-regulatory hormones, symptoms and cognitive performance under experimental conditions during hypoglycaemia, on the other. In a clinical study involving both insulin-induced hypoglycaemia in healthy subjects and insulin-dependent diabetic patients, the practical value and the character of changes of the recorded parameters are investigated. Currently insensitivity to hypoglycaemia, impracticability, complexity or susceptibility to artefacts make use of most parameters unsuitable for hypoglycaemia prevention. It is believed, however, that future efforts could result in indirect registration of hypoglycaemia, including a qualified combination of different parameters, individual adaptation in accordance with particular responses of individual patients, together with new measuring and sensor techniques.

Adult↗

PubMed2002

Effects of acute hypoglycaemia on auditory information processing in adults with Type I diabetes.

AIMS/HYPOTHESIS: Acute hypoglycaemia in humans causes general impairment of cognitive function, but information about its effects on more specific cognitive processes is limited. METHODS: Basic aspects of auditory function were studied in 15 adults with uncomplicated Type I (insulin-dependent) diabetes mellitus. Two separate hyperinsulinaemic glucose clamp procedures were done on different study days, in a counterbalanced fashion, either maintaining euglycaemia (blood glucose 5.0 mmol x l(-1)) or inducing hypoglycaemia (blood glucose 2.6 mmol x l(-1)). During each study, the subjects performed a battery of auditory and cognitive function tasks. RESULTS: Hypoglycaemia caused deterioration in mental efficiency as assessed by Digit Symbol (p<0.001) and Trail Making B (p=0.004) tasks. Acute hypoglycaemia also caused deterioration in one of three measures of simple auditory processing (single-tone loudness, p=0.001) and in auditory temporal processing (p=0.007). The amplitude and latency of auditory N100, P200 and P300 event-related potentials were not affected, but the amplitude of the N240 potential was reduced during acute hypoglycaemia. CONCLUSION/INTERPRETATION: Our findings are consistent with other recognised disruptive effects of acute hypoglycaemia on sensory information processing in non-diabetic and diabetic adults, including adverse effects on auditory information processing in non-diabetic subjects. These derangements have implications for the everyday activities of people with Type I diabetes who are frequently exposed to acute hypoglycaemia.

Acute Disease↗