Influence of counterregulatory hormones, independently of hypoglycaemia, on cognitive function, warning symptoms and glucose kinetics

D. Kerr, Michael Peter Diamond, W. V. Tamborlane, S. Kerr, R. S. Sherwin

Research output: Contribution to journalArticle

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Abstract

1. To assess the influence of counterregulatory hormones, independently of neuroglycopaenia, on higher cerebral (cognitive) function, 'hypoglycaemic' warning symptoms and glucose kinetics, 10 healthy subjects participated in two hyperinsulinaemic (2 m-units min-1 kg-1) glucose clamp studies. After 100 min of euglycaemia (plasma glucose level 5 mmol/l), the plasma glucose level was either (a) maintained at 5 mmol/l for 120 min by glucose infusion with concomitant replacement of counterregulatory hormones (continuous infusions of glucagon, adrenaline, noradrenaline, cortisol and growth hormone) to mimic the hormonal milieu normally associated with hypoglycaemia (hormone infusion study) or (b) lowered to 2.8 mmol/l for 120 min (hypoglycaemia study). Assessements were made of cognitive function (P300 auditory evoked responses), symptoms (visual analogue scales) and glucose kinetics (3-[3H]glucose). 2. Hypoglycaemia was associated with an increase in all symptoms (facial flushing, palpitations, tingling, trembling, seating, hunger, light-headedness and sleepiness, P<0.01) and all subjects were aware that blood glucose levels had fallen. P300 evoked potential latency increased from 280±6 to 312±5 ms (mean±SEM, P<0.01). In contrast, P300 latency and several individual symptoms (hunger, facial flushing, sweating and light-headedness) did not change from baseline during the hormone infusion study (P<0.05 versus hypoglycaemia). Hepatic glucose production was lower (1.5±0.4 versus 2.3±0.3 mg min-1 kg-1, P<0.05) and peripheral glucose uptake was higher (7.4±1.0 versus 5.6±0.6 mg min-1 kg-1, P<0.01) during infusion of the hormones compared with during hypoglycaemia. 3. In conclusion, the deterioration in cognitive function during hypoglycaemmia is a consequence of a low plasma glucose level and is unaffected by the release of counterregulatory hormones. Counterregulatory hormones mediate some but not all of the symptomatic and kinetic responses to hypoglycaemia.

Original languageEnglish (US)
Pages (from-to)197-101
Number of pages97
JournalClinical Science
Volume85
Issue number2
StatePublished - Jan 1 1993
Externally publishedYes

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Hypoglycemia
Cognition
Hormones
Glucose
Hunger
Dizziness
Auditory Evoked Potentials
Glucose Clamp Technique
Sweating
Glucagon
Visual Analog Scale
Evoked Potentials
Hypoglycemic Agents
Epinephrine
Growth Hormone
Hydrocortisone
Blood Glucose
Norepinephrine
Healthy Volunteers
Liver

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Influence of counterregulatory hormones, independently of hypoglycaemia, on cognitive function, warning symptoms and glucose kinetics. / Kerr, D.; Diamond, Michael Peter; Tamborlane, W. V.; Kerr, S.; Sherwin, R. S.

In: Clinical Science, Vol. 85, No. 2, 01.01.1993, p. 197-101.

Research output: Contribution to journalArticle

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N2 - 1. To assess the influence of counterregulatory hormones, independently of neuroglycopaenia, on higher cerebral (cognitive) function, 'hypoglycaemic' warning symptoms and glucose kinetics, 10 healthy subjects participated in two hyperinsulinaemic (2 m-units min-1 kg-1) glucose clamp studies. After 100 min of euglycaemia (plasma glucose level 5 mmol/l), the plasma glucose level was either (a) maintained at 5 mmol/l for 120 min by glucose infusion with concomitant replacement of counterregulatory hormones (continuous infusions of glucagon, adrenaline, noradrenaline, cortisol and growth hormone) to mimic the hormonal milieu normally associated with hypoglycaemia (hormone infusion study) or (b) lowered to 2.8 mmol/l for 120 min (hypoglycaemia study). Assessements were made of cognitive function (P300 auditory evoked responses), symptoms (visual analogue scales) and glucose kinetics (3-[3H]glucose). 2. Hypoglycaemia was associated with an increase in all symptoms (facial flushing, palpitations, tingling, trembling, seating, hunger, light-headedness and sleepiness, P<0.01) and all subjects were aware that blood glucose levels had fallen. P300 evoked potential latency increased from 280±6 to 312±5 ms (mean±SEM, P<0.01). In contrast, P300 latency and several individual symptoms (hunger, facial flushing, sweating and light-headedness) did not change from baseline during the hormone infusion study (P<0.05 versus hypoglycaemia). Hepatic glucose production was lower (1.5±0.4 versus 2.3±0.3 mg min-1 kg-1, P<0.05) and peripheral glucose uptake was higher (7.4±1.0 versus 5.6±0.6 mg min-1 kg-1, P<0.01) during infusion of the hormones compared with during hypoglycaemia. 3. In conclusion, the deterioration in cognitive function during hypoglycaemmia is a consequence of a low plasma glucose level and is unaffected by the release of counterregulatory hormones. Counterregulatory hormones mediate some but not all of the symptomatic and kinetic responses to hypoglycaemia.

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