evidence that it isn’t high serum glucose
that drives the pathologies and thus justifies the tight management of serum sugar,
but rather supportive of low ascorbate and defective collagen that is driving
those pathologies. It is the cholesterol
myth all over again only this time it is blood sugar.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC508256/ J Clin Invest. 1997 Aug
15; 100(4): 839–846.
in ortho-tyrosine and methionine sulfoxide in human skin collagen is not
accelerated in diabetes. Evidence against a generalized increase in oxidative
stress in diabetes.
glycoxidation products Nepsilon-(carboxymethyl)lysine and pentosidine increase
in skin collagen with age and at an accelerated rate in diabetes. Their age-adjusted
concentrations in skin collagen are correlated with the severity of diabetic complications.
To determine the relative roles of increased glycation and/or oxidation in the
accelerated formation of glycoxidation products in diabetes, we measured levels
of amino acid oxidation products, distinct from glycoxidative modifications of
amino acids, as independent indicators of oxidative stress and damage to collagen
in aging and diabetes. We show that ortho-tyrosine and methionine sulfoxide are
formed in concert with Nepsilon-(carboxymethyl)lysine and pentosidine during glycoxidation
of collagen in vitro, and that they also increase with age in human skin collagen.
The age-adjusted levels of these oxidized amino acids in collagen was the same
in diabetic and nondiabetic subjects, arguing that diabetes
per se does not cause an increase in
oxidative stress or damage to extracellular matrix proteins. These results provide evidence for
an age-dependent increase in oxidative damage to collagen and support previous
conclusions that the increase in glycoxidation products in skin collagen in diabetes
can be explained by the increase in glycemia alone, without invoking a generalized,
diabetes-dependent increase in oxidative stress.
ascorbate role in production of collagen, and this is likely more of an issue
that oxidative stress.
http://care.diabetesjournals.org/content/diacare/27/10/2491.full.pdf Diabetes Care, Vol. 27, Oct. 2004
Plasma Vitamin C Levels in Type 2 Diabetic
Patients With and Without Diabetes Complications
Diabetes has been considered to be associated with oxidative
stress. It has been suggested that increased free radicals and decline of
antioxidant defense mechanisms induce diabetic micro- and macrovascular
complications (1–3). Vitamin C is one of the major antioxidants and is detected
in various blood components (4). However, measurements of vitamin C levels have
shown inconsistent results, and the interpretation of vitamin C levels in
diabetes as an antioxidant biomarker has not been clarified (5–8). In this
study, we investigated the lymphocyte and plasma vitamin C levels in type 2
diabetic patients with and without diabetes complications.
Increased oxidative stress in diabetes could contribute to depletion of antioxidants
such as vitamin C (2,3). In this report, we demonstrated that the lymphocyte
vitamin C level is significantly lower in type 2 diabetic patients, but we
could not observe such an association in plasma vitamin C levels. The plasma
concentration of vitamin C is considered to be strongly correlated with transient
consumption of foods such as fruit, supplements, and vegetables (4).
— The lymphocyte vitamin C level
in diabetic patients was significantly lower than in control subjects (18 4.5 vs. 28 7.9
nmol/mg protein, P
the plasma vitamin C level was not different (59 19
vs. 53 18 mol/l, P 0.17) (Fig. 1A and B). There were
no significant linear correlations between the lymphocyte and plasma vitamin C
levels in diabetic patients (r 0.011, P 0.95) as well as in control subjects (r
0.14, P 0.35). The lymphocyte vitamin C level in diabetic patients with
complications was significantly lower than in those without complications (17 3.3 vs. 21 5.4
nmol/mg protein, P 0.011) (Fig. 1C), whereas the plasma vitamin C level was not
different (59 18 vs. 59 21 mol/l,
P 0.97). CONCL
Testing for levels [Laboratory testing reflects recent dietary intake, not storage--jk].
tests use dichlorophenolindophenol, a redox indicator, to measure the levels of vitamin C in the urine and in serum or blood plasma. However these reflect recent dietary intake
rather than the level of vitamin C in body stores. Reverse phase high performance
liquid chromatography is used for determining the storage levels of vitamin C within lymphocytes and tissue. It has been observed that while serum or blood plasma levels follow the circadian rhythm or short term dietary changes, those within tissues themselves are more
stable and give a better view of the availability of ascorbate within the organism.
However, very few hospital laboratories are
adequately equipped and trained to carry out such detailed analyses, and require
samples to be analyzed in specialized laboratories. https://en.wikipedia.org/wiki/Vitamin_C#Deficiency