Dietary nonprotein calories and cerebral infarction size in rats.
- 1 April 1992
- journal article
- abstracts
- Published by Wolters Kluwer Health in Stroke
- Vol. 23 (4) , 564-568
- https://doi.org/10.1161/01.str.23.4.564
Abstract
Conventional diets may cause hyperglycemia in patients with neurological injuries. The purpose of this study was to examine the effect on the severity of cerebral infarction of replacing carbohydrates as the primary dietary source of nonprotein calories. Sixty-nine Long-Evans rats were either fasted for 24 hours, fed isocaloric amounts of a control diet containing 51.5% of the calories as carbohydrates, or fed one of five experimental diets before middle cerebral artery occlusion for 45 minutes. In the experimental diets, 60% of the carbohydrate calories were replaced with one or more of the following substrates: 1,3-butanediol, triacetin, tributyrin, and long- and medium-chain triglycerides. The plasma glucose concentration in the fasted animals was 6.4 +/- 1.1 mumol/ml. In the animals receiving the control diet, which contained the greatest number of carbohydrate calories, plasma glucose was 9.1 +/- 1.4 mumol/ml. The 1,3-butanediol diet resulted in an intermediate plasma glucose concentration averaging 7.8 +/- 1.3 mumol/ml. Plasma beta-hydroxybutyrate levels were elevated in the fasted group and with the 1,3-butanediol diet. Plasma acetate levels were increased with the diets supplemented with triacetin. The smallest infarct volume (53 +/- 43 mm3) was found in the fasted group and the largest (162 +/- 56 mm3) in the control diet group. Infarct volumes that were significantly smaller were found with the 1,3-butanediol diet (98 +/- 41 mm3) and with the triacetin/tributyrin diet (105 +/- 53 mm3). The volume of the infarct was directly related to the plasma glucose concentration before ischemia (n = 69, r = 0.47, p less than 0.01), but not to plasma lactate, ketone body, or acetate levels. It may be possible to develop a diet for patients with neurological injuries using noncarbohydrate calorie sources, such as 1,3-butanediol, triacetin, or tributyrin, that would supply systemic caloric and protein requirements without the adverse effect of conventional diets.Keywords
This publication has 19 references indexed in Scilit:
- The influence of ketosis on the metabolic response to skeletal traumaJournal of Surgical Research, 1988
- Protection against spinal cord ischemia with insulin-induced hypoglycemiaJournal of Neurosurgery, 1987
- Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarctionBrain Research, 1987
- Metabolic and Nutritional Sequelae in the Non-Steroid Treated Head Injury PatientNeurosurgery, 1985
- Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats.Stroke, 1985
- Protection of respiration of a crude mitochondrial preparation in cerebral ischaemia by control of blood glucose.Journal of Neurology, Neurosurgery & Psychiatry, 1985
- The metabolic response to severe head injuryJournal of Neurosurgery, 1984
- Effect of Glucose on Recovery of Energy Metabolism following Hypoxia—Oligemia in Mouse Brain: Dose-Dependence and Carbohydrate SpecificityJournal of Cerebral Blood Flow & Metabolism, 1983
- Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and NeurophysiologyJournal of Cerebral Blood Flow & Metabolism, 1981
- Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels.Stroke, 1980