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Cited by 138Diabetes Management and ResearchPancreatic function and diabetesNeurological and metabolic disorders

Modest decrements in plasma glucose concentration cause early impairment in cognitive function and later activation of glucose counterregulation in the absence of hypoglycemic symptoms in normal man.

Open access
De Feo, P, Gallai, V, Mazzotta, G, Crispino, G, Torlone, E, Perriello, G, Ventura, M M, Santeusanio, F +2 more·1988·Journal of Clinical Investigation
DOI 10.1172/jci113616PMC PMC303532
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Abstract

To establish the glycemic threshold for onset of neuroglycopenia (impaired cognitive function, measured by the latency of the P300 wave), activation of hormonal counterregulation and hypoglycemic symptoms, 12 normal subjects were studied either under conditions of insulin-induced, glucose-controlled plasma glucose decrements, or during maintenance of euglycemia. A decrement in plasma glucose concentration from 88 +/- 3 to 80 +/- 1 mg/dl for 150 min did not result in changes in the latency of the P300 wave nor in an activation of counterregulatory hormonal response. In contrast, a greater decrement in plasma glucose concentration from 87 +/- 3 to 72 +/- 1 mg/dl for 120 min caused an increase in the latency of the P300 wave (from 301 +/- 12 to 348 +/- 20 ms, P less than 0.01), a subsequent increase in all counterregulatory hormones but no hypoglycemic symptoms. Finally, when plasma glucose concentration was decreased in a stepwise manner from 88 +/- 2 to 50 +/- 1 mg/dl within 75 min, the increase in the latency of the P300 wave was correlated with the corresponding plasma glucose concentration (r = -0.76, P less than 0.001). The glycemic threshold for hypoglycemic symptoms was 49 +/- 2 mg/dl. Thus, in normal man the glycemic threshold for neuroglycopenia (72 +/- 1 mg/dl) is greater than currently thought; the hormonal counterregulation follows the onset of neuroglycopenia; the hypoglycemic symptoms are a late indicator of advanced neuroglycopenia.

Integrity signals

Registry

Crossref · 10.1172/jci113616

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 71 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    In normal subjects, during stepwise plasma glucose decrements, both adrenergic and neuroglycopenic symptoms were reported at 45 minutes when plasma glucose was 49±2 mg/dl.

    “the patients referred both adrenergic and neuroglyco- penic symptoms at 45 min when plasma glucose concentration was 49±2 mg/dl.”
    Quote in the paperNot a substantial claim
  • Findingown data

    In normal subjects, after stepwise plasma glucose decrement, when glucose was normalized at 105 minutes, P300 latency remained higher than control (339±15 vs. 298±10 ms, P<0.05).

    “When plasma glucose concentra- tion was normalized at 105 min, the latency of P300 wave was still greater than in the control study (339±15 vs. 298± 10 ms, P < 0.05).”
    Quote in the paperSubstantial claim
  • Findingown data

    In normal subjects, the peak symptom scores for both adrenergic and neuroglycopenic symptoms occurred at 75 minutes, at the end of the 50 mg/dl plateau.

    “The score peak of both adrenergic and neu- roglycopenic symptoms occurred at 75 min at the end of the plateau plasma glucose concentration of 50 mg/dl.”
    Quote in the paperNot a substantial claim
  • Findingown data

    In normal subjects, P300 latency returned to baseline only after 30 additional minutes of euglycemia (317±13 ms vs. baseline 296±9 ms and control 309±12 ms, P=NS).

    “Only after 30 additional min of euglycemia the latency of P300 wave was normalized (317±13 ms) as com- pared both to baseline values (296±9 ms) and to the control study (309±12 ms) (P = NS).”
    Quote in the paperSubstantial claim
  • Findingown data

    In normal subjects, after plasma glucose was normalized, hypoglycemic symptoms no longer differed from control (neuroglycopenic at 90 minutes; adrenergic at 105 minutes).

    “Following normalization of plasma glucose, the hypoglycemia symptoms were no longer different from those of the control study (neur- oglycopenic symptoms at 90 min; adrenergic symptoms at 105 min).”
    Quote in the paperSubstantial claim
  • May combine two claims. 22
  • Classified as probably not a substantial claim. 9
  • The quote only partly states this claim. 1

  • May combine two claims.

    Findingown data

    In normal subjects, lowering plasma glucose from 87±3 to 72±1 mg/dl for 120 minutes increased P300 latency (301±12 to 348±20 ms, P<0.01) and later increased all counterregulatory hormones, without causing hypoglycemic symptoms.

    “In contrast, a greater decrement in plasma glucose concentration from 87±3 to 72±1 mg/dl for 120 min caused an increase in the latency of the P300 wave (from 301±12 to 348±20 ms, P < 0.01), a subsequent increase in all counterregulatory hormones but no hypoglycemic symptoms.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In normal subjects, during stepwise plasma glucose decrements, plasma growth hormone rose at 45 minutes (13±3.5 vs. 0.7±0.2 ng/ml, P<0.05), peaked at 75 minutes (26±5.3 pg/ml), and remained elevated until 90 minutes (20±3.9 vs. 2.2±0.5 pg/ml, P<0.05).

    “Plasma growth hormone increased significantly at 45 min (13±3.5 vs. 0.7±0.2ng/ml, P < 0.05), peaked at 75 min (26±5.3pg/ml) and remained increased until 90 min (20±3.9ng/ml vs. 2.2±0.5 pg/ml of the control study, P < 0.05).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In normal subjects, during stepwise plasma glucose decrements, plasma FFA and B-OH-B rose at 135 minutes by about 100% and 65% above baseline, respectively, whereas in the control study they only approached baseline.

    “in the study in which plasma glucose concentration was allowed to decrease, plasma FFA and B-OH-B concentration increased at 135 min approximately by 100 and 65%, respectively, as compared to baseline.In contrast, in the control study FFA and B-OH-B concentration just approached the baseline values.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In normal subjects, during the 72±1 mg/dl glucose decrement, plasma FFA and B-OH-B first fell to nadirs (FFA 0.3±0.05 mM at 75 min; B-OH-B 0.126±0.011 mM at 90 min) and then rose despite hyperinsulinemia to values no longer different from baseline.

    “in the study in which plasma glucose concentration was allowed to decrease at 72±1 mg/dl, plasma FFA and B-OH-B initially decreased to nadir values of 0.3±0.05mM at 75 min and 0.126±0.011mM at 90 min, respectively, but subsequently increased despite hyperinsulin- emia to values no longer different from baseline (FFA at 120 min, B-OH-B at 150 min)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In normal subjects, lowering plasma glucose from 88±3 to 80±1 mg/dl and holding it there for 150 minutes produced no change in P300 latency and no activation of counterregulatory hormones.

    “A decrement in plasma glucose concentration from 88±3 to 80±1 mg/dl for 150 min did not result in changes in the latency of the P300 wave nor in an activation of counterregulatory hormonal response.”
    • Also stated in: § Results · plain
      “The latency of the P300 wave and the plasma counterregu- latory hormone concentration did not change either in the control study (euglycemia) or when plasma glucose concen- tration was allowed to decrease from 88±3 to 80±1 mg/dl (Fig. 1).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In normal subjects, during stepwise plasma glucose decrements, plasma glucagon and epinephrine rose at 35 minutes (glucagon 89±9 to 147±15 pg/ml; epinephrine 42±12 to 157±29 pg/ml; both P<0.05), peaked at 75 minutes (215±18 and 389±46 pg/ml), and remained elevated until 90 minutes (P<0.05).

    “Both plasma glucagon and epinephrine increased at 35 min (glucagon from 89±9 to 147±15 pg/ml, epinephrine from 42±12 to 157±29 pg/ml, both P < 0.05), both peaked at 75 min (215±18 and 389±46 pg/ml, respectively) and both remained increased until 90 min (P < 0.05).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In the present study, activation of hormonal counterregulation followed rather than preceded the onset of neuroglycopenia, although the absolute glycemic thresholds for the two were virtually identical.

    “In the present study in which a more sensitive approach to evaluate brain function was used the activation of hormonal counterre- gulation followed rather than preceded the onset of neurogly- copenia, although the absolute glycemic threshold for onset of neuroglycopenia and activation of counterregulation is vir- tually identical.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In the step-wise plasma glucose decrement protocol (study B), plasma glucagon and epinephrine increased at about -60 mg/dl, and growth hormone and cortisol at about -50 mg/dl.

    “When in the present studies the glycemic threshold for hormonal counterregulation was evaluated in the step-wise plasma glucose dec- rement protocol (study B) in which a given plateau plasma glucose concentration was maintained for several minutes, plasma glucagon and epinephrine increased at plasma glucose concentration of -60 mg/dl, and growth hormone and corti- sol at -50 mg/dl.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In the single-step plasma glucose decrease protocol held for at least 120 min (study A), the glycemic threshold for hormonal counterregulation was greater (-72 mg/dl) and identical for all counterregulatory hormones.

    “However, when the glycemic threshold for activation ofhormonal counterregulation was evaluated in the protocol of single-step decrease in plasma glucose, which was held for at least 120 min (study A), the glycemic threshold was found to be greater (-72 mg/dl) and, most important, it was identical for all counterregulatory hormones.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    The generation of the P300 wave requires both perception and cognition of task-relevant stimuli, and its latency reflects the time needed for complete evaluation of the stimulus.

    “The generation of the P300 wave implies both perception and cognition of task relevant stimuli (acoustic, somatosensorial and visual) and its latency expresses the time required for the complete evaluation of the stimulus (28).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [28]

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  • Classified as probably not a substantial claim.

    Study design and conductown data

    In the authors' laboratory, the coefficient of variation for P300 latency measurement in 30 normal volunteers tested on three occasions was 7.2±0.6%.

    “In our laboratory, the coefficient of variation (c.v.) of the determination of latency of P300 wave determined in 30 normal volunteers (17 male, 13 female; 28±0.3 yr) studied in the fasting state between 9 and 10 a.m. on three different occasions at 2-5-d intervals was 7.2±0.6%.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Prior studies in man have shown that brain function becomes impaired when plasma glucose falls about 30-50 mg/dl below normal fasting values, as shown by neuropsychological tests, visual reaction time, and electroencephalogram.

    “several studies in man have shown that brain function be- comes impaired when plasma glucose concentration decreases -30-50 mg/dl below normal fasting values, as demonstrated by the abnormalities of neuropsychological tests (3-5), visual reaction time (6), and electroencephalogram (7,8).”
    Quote in the paperSubstantial claim0 of 6 sources checked
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  • Classified as probably not a substantial claim. May combine two claims. The quote only partly states this claim.

    Study design and conductown data

    The experiments were single-blind, and subjects did not know their plasma glucose concentrations.

    “Three sets of experiments were performed in a single blind in six subjects (three male, three female) on three different occasions in random order, a week apart.”
    • Also stated in: § Methods · plain
      “In all the studies the subjects were unaware of the plasma glucose concentration and were asked to score at 15-min intervals from 0 (none) to 5 (severe) the following symptoms:”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    In normal man, the glycemic threshold for neuroglycopenia is 72±1 mg/dl, which is higher than previously believed.

    “Thus, in normal man the glycemic threshold for neurogly- copenia (72±1 mg/dl) is greater than currently thought;”
    • Also stated in: § Study B · hedged
      “Thus, it appears that the glycemic threshold for the onset of neuroglycopenia is greater than cur- rently appreciated (3-8, 25, 26)”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: Impairment in cognitive function as measured by P300 latency closely reflects impaired brain glucose metabolism (neuroglycopenia).

  • May combine two claims.

    Premisecitation

    Plasma lactate concentration does not change in the early phase of hypoglycemia but increases only during recovery.

    “plasma lactate concentration does not change in an early phase of hypoglycemia, but increases only in the re- covery phase (37).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [37]

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  • May combine two claims.

    Interpretationown data

    In normal man, more profound plasma glucose decrements (about 35 mg/dl below postabsorptive values) further impair brain function, exaggerate hormonal counterregulation, and eventually produce hypoglycemic symptoms.

    “More profound decrements in plasma glucose (-35 mg/dl below the postabsorptive values) further impair brain function, exag- gerate hormonal counterregulation and finally result in symp- toms of hypoglycemia.”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: Impairment in cognitive function as measured by P300 latency closely reflects impaired brain glucose metabolism (neuroglycopenia).

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Aging, dementia, and Huntington's disease are associated with increased P300 latency.

    “since aging (33), dementia (20), Huntington's disease (34) and organic cognitive disorders in children (21) are associated with an increased latency in P300 wave”
    Quote in the paperNot a substantial claim0 of 3 sources checked
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  • May combine two claims.

    Interpretationown data

    In normal man, the absolute glycemic thresholds for neuroglycopenia and for hormonal counterregulation are nearly the same, but counterregulation begins after neuroglycopenia.

    “although the abso- lute glycemic threshold for onset of neuroglycopenia and acti- vation ofhormonal counterregulation is virtually identical, the onset of the latter follows that of the former.”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: Impairment in cognitive function as measured by P300 latency closely reflects impaired brain glucose metabolism (neuroglycopenia).

  • May combine two claims.

    Premisecitation

    Glucose is the obligate fuel for the brain, and more than 90% of the energy for brain function comes from glucose oxidation.

    “Thus, glucose is the obligate fuel for the brain, and more than 90 percent ofthe energy needed for brain function derives from oxidation of glucose (2).”
    Quote in the paperSubstantial claim0 of 2 sources checked
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    Premisecitation

    The brain cannot store or synthesize glucose, so a steady flow of glucose from blood to the central nervous system is required for normal brain function and survival.

    “Since the brain virtually cannot store or synthetize glucose, a constant supply of glucose from the circulation to the central nervous system is essential for normal brain function and whole body survival (1).”
    Quote in the paperSubstantial claim0 of 1 sources checked
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  • May combine two claims.

    Premisecitation

    P300 latency is related to important brain cortical functions in man and may serve as a measure of the physiological integrity of cognitive function.

    “it is concluded that the latency of the P300 wave not only is related to some of the most important brain cortical functions in man, but also that such a parameter might be used as a measure of physiological integrity of cognitive function.”
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  • May combine two claims.

    Interpretationown data

    P300 wave latency is a specific and sensitive measure of cortical cognitive function, which is influenced by brain metabolism.

    “Thus, the assumption that the latency of P300 wave is a specific and sensitive measure of cortical cognitive function, which is in turn influenced by brain metabolism, is validated.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    Statistical significance was assessed by analysis of variance corrected for repeated measures, comparing dependent variables during hypoglycemic and euglycemic clamps to account for variability over time under euglycemia.

    “The statistical significance was evaluated using the analysis of variance corrected for repeated measures (22).The dependent variables were compared dur- ing the hypoglycemic and euglycemic clamps to allow variability in the measurements with time under euglycemic conditions to be factored into the results.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [22]

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    The P300 wave is the main component of event-related potentials and reflects active cognitive processing of stimulus information.

    “The P300 wave is the most prominent component of event-related potentials (19,20) and reflects the active cogni- tive processing of the stimulus information by the subject (27).”
    Quote in the paperSubstantial claim0 of 3 sources checked
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  • Classified as probably not a substantial claim.

    Premisecitation

    In rats, only a 50% decrease in plasma glucose concentration makes glucose substrate availability the rate-limiting step for brain glycolysis.

    “Previous studies in rats have shown that only for a 50% decrease in plasma glucose concentration, the glucose substrate availability becomes the rate limiting step for glycolysis in the brain (2).”
    Quote in the paperSubstantial claim0 of 1 sources checked
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  • May combine two claims.

    Interpretationcitation

    Significant neuroglycopenia and hormonal counterregulation occurred in the absence of hypoglycemic symptoms, reinforcing that hypoglycemic symptoms are a late indicator of plasma glucose decrements below normal.

    “Thus, the ob- servation that significant neuroglycopenia developed and hor- monal counterregulation was activated in the absence of symptoms of hypoglycemia, reinforce the concept that the “hypoglycemic symptoms” are a late indicator of plasma glu- cose decrements below normal values, as recently reported by Schwartz et al. (26).”
    Quote in the paperSubstantial claim0 of 1 sources checked
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  • Classified as probably not a substantial claim.

    Premisecitation

    At present, hypoglycemia is defined as a plasma glucose concentration at which symptoms and signs of brain dysfunction appear, i.e., 55-50 mg/dl.

    “At present, hypoglycemia is defined as a plasma glucose concentration at which symptoms and signs of brain dysfunc- tion appear, i.e., 55-50 mg/dl (3-7).”
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  • May combine two claims.

    Premisecitation

    The glycemic threshold for activation of counterregulation and symptoms of hypoglycemia is increased in chronically hyperglycemic diabetic subjects and decreased in diabetics on intensive insulin therapy with chronically subnormal plasma glucose.

    “Actually, it has been shown that the glycemic threshold for activation of counterregulation and symptoms of hypoglycemia is increased in diabetic subjects chronically hyperglycemic (42), whereas it is decreased in diabetics treated with regimens of intensive insulin therapy (42-47) which result in chronically subnormal plasma glucose concentrations (48).”
    Quote in the paperSubstantial claim0 of 7 sources checked
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28 of 28

  • The authors state this as an assumption.

    Impairment in cognitive function as measured by P300 latency closely reflects impaired brain glucose metabolism (neuroglycopenia).

    “The major finding of the present study, i.e., the exquisite sensitivity of the brain to minor decreases in ambient plasma glucose, relies entirely on the assumption that impairment in cognitive function as measured by means of the latency of the P300 wave, closely reflects impaired brain glucose metabo- lism, i.e., neuroglycopenia.”

  • The paper relies on this without support.

    The potentially deleterious effects of modest plasma glucose decrements on brain function had not been carefully examined before this study.

    “However, because the potentially deleterious effects of modest decrements in plasma glucose concentration on brain function have never been carefully examined, it cannot be excluded that the glycemnic threshold for the onset of neuroglycopenia and brain dysfunction is actually greater than what is currently appreciated.”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Growth-hormone peak is smaller than a later value

    Minor

    The stated peak of 26 pg/ml at 75 minutes is far below the reported 20 ng/ml at 90 minutes. The units make the claimed peak inconsistent with the later measurement.

1 of 1

Cites

Flagged first, then by citations

2 of the 45 references couldn’t be matched to a known paper.

Research works printed but not linked: 5

  1. Tamburrano, G., A. Lala, F. Leonetti, N. Locuratolo, and S. Busco. 1987. Electroencefalography during prolonged hypoglycemia. In Hypoglycemia. D. Andreani, V. Marks, and P. J. Lefebvre, editors. Raven Press, New York. 181-194.
  2. Faloona, G., and R. H. Unger. 1974. Glucagon. In Methods of Hormone Radioimmunoassay. B. Jaffe and H. Behrman, editors. Aca- demic Press, Inc., New York. 317-330.
  3. Peake, G. 1972. Growth Hormone. In Methods of Hormone Radioimmunoassay. B. Jaffe and H. Berhman, editors. Academic Press, Inc., New York. 103-121.
  4. Marks, V. and F. C. Rose. 1981. Hypoglycaemia. Blackwell Scientific Publications, Oxford. 1-521.
  5. Bachelard, H. 1981. Cerebral metabolism and hypoglycaemia. In Hypoglycaemia. V. Marks and F. C. Rose, editors. Blackwell Scien- tific Publications, Oxford. 51-68.

Cited by

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Related

Authors
De Feo, P., Gallai, V, Mazzotta, G., Crispino, G., Torlone, E., Perriello, G., Ventura, M. M., Santeusanio, F., Brunetti, P., & Bolli, G. B.
Affiliations
University of Perugia (IT)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1988-08-01
Volume
82
Issue
2
Pages
436-444
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci113616
PMC
PMC303532
OpenAlex
W2074411447
Semantic Scholar
c941f18c807aae8c70851c0868512fdb413432d8
Cited by
138
References
45
Citations by year
2026: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 4 · 2013: 4 · 2012: 3
FWCI
3.42
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Consiglio Nazionale delle Ricerche
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Neurological and metabolic disorders
Keywords
neuroglycopenia, hypoglycemia, plasma glucose, P300 latency, cognitive impairment, glucose counterregulation, counterregulatory hormones, hypoglycemic symptoms, glycemic thresholds, insulin-induced hypoglycemia, normoglycemia
MeSH terms
Adult, Blood Glucose, Brain, Cognition Disorders, Fatty Acids, Nonesterified, Female, Glucose, Humans, Hydroxybutyrates, Hypoglycemia, Male, Reaction Time, 3-Hydroxybutyric Acid

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