Brain glucose concentrations in healthy humans subjected to recurrent hypoglycemia
Open accessAbstract
Mechanisms responsible for hypoglycemia unawareness remain unknown. Previously, we found that patients with type 1 diabetes and hypoglycemia unawareness had increased brain glucose concentrations as measured by (1)H-magnetic resonance spectroscopy (MRS) compared with controls measured under the same metabolic condition, suggesting that an alteration in brain glucose transport and/or metabolism may play a role in the pathogenesis of hypoglycemia unawareness. To determine whether the brain glucose concentration is altered in normal subjects subjected to recurrent hypoglycemia, we compared the brain glucose concentrations measured in healthy subjects after three episodes of hypoglycemia to blunt the counterregulatory response over 24 hr and compared this value with that measured at a time remote from the antecedent hypoglycemia protocol. Sixteen subjects (9 M/7 F, age 36 +/- 10 years, mean +/- SD) underwent three hypoglycemic clamps for 30 min at 8 AM (0 hr), 5 PM (9 hr), and 7 AM (24 hr). After the third hypoglycemic clamp, subjects underwent a hyperglycemic clamp during which brain glucose concentration was measured by MRS at 4 T. Brain glucose concentration after repeated hypoglycemia was not different from the brain glucose concentration measured in the same subjects during a control study (5.1 +/- 0.8 vs. 4.5 +/- 0.5 mumol/g wet weight, respectively, P = 0.05). These observations suggest that brain glucose transport or metabolism is not altered following short episodes of recurrent hypoglycemia in healthy human volunteers.
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Brain glucose transport is not altered following short episodes of recurrent hypoglycemia in healthy human volunteers.
“since brain glucose transport is not altered following short episodes of recurrent hypoglycemia in healthy human volunteers [25].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [25]
The Discussion (page unavailable) reports no difference in blood-to-brain glucose transport in healthy subjects studied after euglycemia versus after a period of hypoglycemia. It attributes that finding to Segel et al. (2001), but does not say the healthy subjects underwent short episodes of recurrent hypoglycemia; the paper’s own study concerns patients with type 1 diabetes and hypoglycemia unawareness. (LLM, conf=0.83)
Experimental — accuracy not yet measuredBBB adaptation to chronic hyperglycemia represents a dynamic process with a long time constant.
“This mechanism, termed BBB adaptation to chronic hyperglycemia in Fig. 3, represents a dynamic process with a long time constant, since brain glucose transport is not altered following short episodes of recurrent hypoglycemia in healthy human volunteers [25].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [25]
The Discussion (page unavailable) reports no difference in brain glucose transport in healthy subjects studied after euglycemia versus after a period of hypoglycemia. It does not establish that the exposure was short episodes of recurrent hypoglycemia, or a long time constant for BBB adaptation to chronic hyperglycemia. (LLM, conf=0.79)
Experimental — accuracy not yet measuredOverexpression of GLUT-1 has a positive effect on the maximal transport rate TG0 without altering the Michaelis constant KG0.
“Overexpression of GLUT-1 is viewed to have a positive effect on the maximal transport rate, TG0, without altering the Michaelis constant, KG0 [25].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [25]
The Discussion (page unavailable) reports GLUT1 upregulation and increased transporter concentration in animals with chronic hypoglycemia; the introductory passage also links more transporters to increased glucose movement. Our copy does not say that GLUT1 overexpression increases the maximal transport rate TG0 or leaves the Michaelis constant KG0 unchanged. (LLM, conf=0.84)
Experimental — accuracy not yet measuredOnly 54% of the studied subjects developed HAAF, based upon 20% or greater reduction in epinephrine response between the first and the third episode of hypoglycemia.
“Indeed, we found that only 54% of the studied subjects developed HAAF, based upon 20% or greater reduction in epinephrine response between the first and the third episode of hypoglycemia (4, 16).”
From Plasma Epinephrine Contributes to the Development of Experimental Hypoglycemia-Associated Autonomic Failure (2020) · cites this paper as [16]
The Results (page unavailable) report a lower epinephrine response in participants with type 1 diabetes and hypoglycemia unawareness than in controls. The paper does not report that 54% developed HAAF, use a 20% reduction as a criterion, or compare responses between first and third hypoglycemic episodes. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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Background
- Authors
- Criego, A. B., Tkac, I., Kumar, A., Thomas, W., Gruetter, R., & Seaquist, E. R.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Seaquist, Elizabeth R.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2005
- Volume
- 82
- Issue
- 4
- Pages
- 525-530
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W2161962325
- Cited by
- 40
- References
- 32
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 4 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 6 · 2012: 1
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- University of Minnesota
- National Institutes of Health (RR00400, RR08079)
- National Center for Research Resources (P41RR008079)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Neurological and metabolic disorders
- Keywords
- recurrent hypoglycemia, hypoglycemia unawareness, brain glucose transport, brain glucose metabolism, hypoglycemic clamp, counterregulatory response, hyperglycemic clamp, type 1 diabetes
- MeSH terms
- Adult, Brain, Female, Glucose, Humans, Hypoglycemia, Insulin, Male, Middle Aged, Magnetic Resonance Spectroscopy, Time Factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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