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Vitamin C and Carbohydrate Metabolism

mantq

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Feb 22, 2022
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Eastern Europe
How does Vitamin C influence carbohydrate metabolism? Is more Vitamin C needed (perhaps supplementation), whenever higher carbohydrate intake is on the higher side?
Thank you for any relevant information!
 

mantq

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Thread starter
Joined
Feb 22, 2022
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15
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Eastern Europe
"Insulin promotes vitamin C uptake at the cellular level. Most know insulin as an escort for glucose into the cells. The problem lies when blood sugar rises. High blood sugar inhibits uptake of Vitamin C."
 

aliml

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Apr 17, 2017
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566

The Glucose-Ascorbate Antogonism Theory​

The glucose-ascorbate antagonism (GAA) theory was first proposed by John Ely as early as the 1970s [3]. The theory postulates that given the structural similarity between glucose and vitamin C, the two molecules compete for same transport system to enter cells [10]. It has been shown that cellular uptake of both AA and DHAA may be competitively antagonized by elevated glucose levels. Specifically, AA uptake by the small intestine enterocytes was shown to be inhibited by elevated glucose concentration [9]. DHAA transport into cells was shown to be impaired by high blood glucose concentration in most cell types including adipocytes, erythrocytes, granulosa cells, neutrophils, osteoblasts and smooth muscle cells [10].

A potential limitation of the GAA theory pertains to the lack of in vivo studies in animals and in humans. Diabetes, however, can be regarded as a natural model to study interaction between blood glucose and vitamin C in vivo in humans. Studies with diabetic patients are in line with the GAA therory. Two studies in type 2 diabetes [79,80] indicated that in spite of similar dietary intake of vitamin C, patients have decreased levels of plasma AA as compared to normal controls. Furthermore, serum level of AA inversely correlated with glucose levels [80] and in another study with glycated hemoglobin of diabetic patients [81]. Diabetes is also known to be associated with impaired renal reabsorption of AA [82] which likely contributes to the low level of AA in patients.

Uptake of glucose and DHAA also share the feature of insulin-dependency on the GLUT4 glucose transporter primarily found in muscle and adipose tissue [83]. In type 1 diabetes, deficiency of insulin has been shown to impair DHAA uptake of lymphoblasts [84]. Such a decreased DHAA uptake, through impaired AA accumulation, may lead to compromized immune system function in type 1 diabetes patients [84]. The effect of glucose seems to be immediate on intracellular AA given that intravenous glucose administration results in a prompt decrease in the AA concentration of leukocytes [85]. Also consistently with the GAA theory, blood level of vitamin C is inversely related with obesity [86] a correlate of increased carbohydrate intake.

Controlling hyperglycemia has also been suggested as an adjunct to cancer therapy [87]. Hyperglycemia in cancer patients is known to be associated with reduced intracellular AA concentration. Such a decrease results in impaired actions of AA, including a decreased activity of the hexose monophosphate shunt, a patway important in optimal immune cell functioning [87]. In cardiovascular disease, the association of high blood glucose and low AA concentration is also consistent with the GAA mechanism, and may plausibly explain functional impairments such as lipid peroxidation and endothelial dysfunction which are known to contribute to the generation of atherosclerosis [87].

As an additional parallelism, the study by Johnstone et al. [88] compared the effect of two high protein diets: one with low (in fact ketogenic) and another with medium carbohydrate content. To the surprise of the investigators, higher concentration of blood vitamin C was found on the low carbohydrate diet. Yet, the difference was explained by other factors.

AA is known to have a role in scavenging reactive oxygen species within the mitochondria. Reactive oxygen species within the mitochondria have been suggested to have a role in the development of degenerative disorders including cancer [89]. Given the fact that carbohydrate based Western type nutrition is associated with increased production of reactive oxygen species in the mitochondria [89], it is plausible to speculate that the need for AA
would be decreased when on a low carbohydrate diet.

In human brush border membrane vesicles evaluated ex vivo, AA uptake is competitively antagonized by glucose [9] coming abundantly from carbohydrate based diets may explain why according to a metaanalysis dietary intake and plasma level of AA were only moderately correlated [38]. Importantly, estimation of AA intake in this study relied on plant sources only. Negligation of animal sources of vitamin C is typical in the case of the other dietary studies too. This fact together with the loose association between the intake estimate and blood level indicate that plants are not ideal sources of vitamin C. Additionally, flavonoids abundantly found in fruits and vegetables were also shown to inhibit vitamin C uptake by enterocytes [90]. We are not aware of studies assessing the relation between animal sources of vitamin C and blood level of it. The striking dissociation between epidemiological and intervention studies, as revealed in this review for mortality, cardiovascular disease and cancer, may be regarded as an indication that vitamin C taken as a supplement may not be an optimal way to obtain this nutrient.

 
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