Endogenous substrates utilized by rat brain in severe insulin-induced hypoglycemia
(1981) In Journal of Neurochemistry 36(2). p.490-500- Abstract
- Several previous studies have demonstrated that severe hypoglycemia is accompanied by consumption of endogenous brain substrates (glycolytic and citric acid cycle metabolites and free amino acids) and some have shown a loss of structural components as well, notably phospholipids. In the present study, on paralysed and artificially ventilated rats, we measured cerebral oxygen and glucose consumption during 30 min of hypoglycemic coma (defined as hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity) and calculated the non-glucose oxygen consumption. In an attempt to estimate the missing substrate we measured tissue concentrations of phospholipids and RNA.
After 5 min of hypoglycemic coma,... (More) - Several previous studies have demonstrated that severe hypoglycemia is accompanied by consumption of endogenous brain substrates (glycolytic and citric acid cycle metabolites and free amino acids) and some have shown a loss of structural components as well, notably phospholipids. In the present study, on paralysed and artificially ventilated rats, we measured cerebral oxygen and glucose consumption during 30 min of hypoglycemic coma (defined as hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity) and calculated the non-glucose oxygen consumption. In an attempt to estimate the missing substrate we measured tissue concentrations of phospholipids and RNA.
After 5 min of hypoglycemic coma, tissue phospholipid content decreased by about 8% with no further change during the subsequent 55 min. A similar reduction remained after 90 min of recovery, induced by glucose administration following 30 min of coma. Since no preferential loss of polyenoic fatty acids or of ethanolamine phosphoglycerides occurred, it is concluded that loss of phospholipids was due to phospholipase activity rather than to peroxidative degradation. The free fatty acid concentration increased sixfold after 5 min of coma and remained elevated during the course of hypoglycemia. A 9% reduction in tissue RNA content was observed after 30 min of hypoglycemia.
Calculations indicated that available endogenous carbohydrate and amino acid substrates were essentially consumed after 5 min of coma, and that other non-glucose substrates must have accounted for approximately 50μmol·g−1 of oxygen (8.3 μmol·g−1 in terms of glucose equivalents) within the 5–30 min period. The 10% reduction in phospholipid-bound fatty acids was more than sufficient (in four- to fivefold excess) to account for this oxygen consumption. However, since no further degradation occurred in the 5–30 min period, there is no simple, direct, quantitative relationship between oxygen consumption and cortical fatty acid oxidation during this interval. The possibility thus remains that unmeasured exogenous or endogenous substrates were utilized. (Less)
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- author
- Agardh, Carl-David LU ; Chapman, Astrid G ; Nilsson, Bengt LU and Siesjö, Bo LU
- organization
- publishing date
- 1981
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Hypoglycemia, Rat brain, Phospholipids, Fatty acids, Amino acids, Glucose
- in
- Journal of Neurochemistry
- volume
- 36
- issue
- 2
- pages
- 490 - 500
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:6162005
- scopus:0019364142
- ISSN
- 1471-4159
- DOI
- 10.1111/j.1471-4159.1981.tb01619.x
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neurology, Lund (013027000), Unit on Vascular Diabetic Complications (013241510)
- id
- 3d8c0f95-1044-4761-bfb1-c64566034f5c (old id 1102835)
- date added to LUP
- 2016-04-01 16:21:30
- date last changed
- 2021-01-03 05:53:20
@article{3d8c0f95-1044-4761-bfb1-c64566034f5c,
abstract = {{Several previous studies have demonstrated that severe hypoglycemia is accompanied by consumption of endogenous brain substrates (glycolytic and citric acid cycle metabolites and free amino acids) and some have shown a loss of structural components as well, notably phospholipids. In the present study, on paralysed and artificially ventilated rats, we measured cerebral oxygen and glucose consumption during 30 min of hypoglycemic coma (defined as hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity) and calculated the non-glucose oxygen consumption. In an attempt to estimate the missing substrate we measured tissue concentrations of phospholipids and RNA.<br/><br>
<br/><br>
After 5 min of hypoglycemic coma, tissue phospholipid content decreased by about 8% with no further change during the subsequent 55 min. A similar reduction remained after 90 min of recovery, induced by glucose administration following 30 min of coma. Since no preferential loss of polyenoic fatty acids or of ethanolamine phosphoglycerides occurred, it is concluded that loss of phospholipids was due to phospholipase activity rather than to peroxidative degradation. The free fatty acid concentration increased sixfold after 5 min of coma and remained elevated during the course of hypoglycemia. A 9% reduction in tissue RNA content was observed after 30 min of hypoglycemia.<br/><br>
<br/><br>
Calculations indicated that available endogenous carbohydrate and amino acid substrates were essentially consumed after 5 min of coma, and that other non-glucose substrates must have accounted for approximately 50μmol·g−1 of oxygen (8.3 μmol·g−1 in terms of glucose equivalents) within the 5–30 min period. The 10% reduction in phospholipid-bound fatty acids was more than sufficient (in four- to fivefold excess) to account for this oxygen consumption. However, since no further degradation occurred in the 5–30 min period, there is no simple, direct, quantitative relationship between oxygen consumption and cortical fatty acid oxidation during this interval. The possibility thus remains that unmeasured exogenous or endogenous substrates were utilized.}},
author = {{Agardh, Carl-David and Chapman, Astrid G and Nilsson, Bengt and Siesjö, Bo}},
issn = {{1471-4159}},
keywords = {{Hypoglycemia; Rat brain; Phospholipids; Fatty acids; Amino acids; Glucose}},
language = {{eng}},
number = {{2}},
pages = {{490--500}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Neurochemistry}},
title = {{Endogenous substrates utilized by rat brain in severe insulin-induced hypoglycemia}},
url = {{http://dx.doi.org/10.1111/j.1471-4159.1981.tb01619.x}},
doi = {{10.1111/j.1471-4159.1981.tb01619.x}},
volume = {{36}},
year = {{1981}},
}