Jasper9 wrote:This is a really interesting thread.
I am wondering what is the limiting factor.
- is the amount of glucose to go through the BBB limited by iron deposits to the extent that injesting additional glucose into the blood stream has no benefit?
In fact, is it logical to assume that if glucose is not absorbed correctly through the vascular system then the blood in veins may actually carry a higher sugar content than normal.
And what would be the affect of this on the endothelium? Cheerleader's endothial health report on CCSVI Alliance website says;
"Ingesting too much glucose in the form of simple sugars increases endothelial cell death and increases oxidative stress."
Is is another vicious circle?
(I'm actually hoping someone will tell me that the more glucose I have the better so I can go and eat cake! - but I don't think it will be as straightforward as that?)
Effects of unbalanced diets on cerebral glucose metabolism in the adult rat
From the Departments of Neurology (Drs. Al-Mudallal and Harik) and Neurological Surgery (Dr. Lust), Case Western Reserve University School of Medicine, Cleveland, OH; and the Neurology Service (Dr. Levin), VA Medical Center, and Department of Neurosciences, New Jersey School of Medicine and Dentistry, Newark, NJ.
Supported in part by USPHS grants HL 35617 and AM 30066 and by the Research Service of the Department of Veterans Administration.
Received December 6, 1994. Accepted in final form March 28, 1995.
Address correspondence and reprint requests to Dr. Sami I. Harik, Department of Neurology, University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 500, Little Rock, AR 72205.
We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In preliminary experiments, we found that moderate ketosis could not be achieved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blood beta-hydroxybutyrate (0.4 mM) and acetoacetate (0.2 mM), and a five- to 10-fold increase in their cerebral beta-hydroxybutyrate level. Cerebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentrations of glucose 6-phosphate. These findings indicate that long-term moderate ketonemia does not significantly alter brain glucose phosphorylation. However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS dysfunction.
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