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jeudi 27 août 2015

High carb diet linked to high non fasting TG

Look at table 3!
And the link is: fructose metabolism in a positive balance of calories.

Hudgins, L. C., M. Hellerstein, C. Seidman, R. Neese, J. Diakun, and J. Hirsch. 1996. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J. Clin. Invest. 97: 2081– 2091.

Hudgins, L. C., C. E. Seidman, J. Diakun, and J. Hirsch. 1998. Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar. Am. J. Clin. Nutr. 67: 631–639.

 Hellerstein, M .K. 1996. Regulation of hepatic de novo lipogenesis in humans. Annu. Rev. Nutr. 16: 523–557.

From the study of fructose metabolism quoted supra:

4. Atherosclerosis

It appears that high fructose intake can create an unfavorable lipid profile in blood via DNL [94]. The main product of DNL is palmitic acid [95], a fatty acid specifically shown to increase the risk of atherosclerosis [96]. Fatty acids formed by DNL will mainly be packed in VLDLs delivered into the bloodstream. This may, in turn, increase the level of low-density lipoproteins (LDLs) in the blood. In several studies, fructose has to a greater extent than glucose increased blood levels of triglycerides [51, 65, 97, 98] and LDLs [65, 99103]. Aeberli et al. [104] showed that fructose increased the small dense LDLs, the type of LDLs that may in particular be linked to cardiovascular risk [105]. The level of high-density lipoproteins (HDLs) in blood does not seem to be affected by fructose [100, 101]. In most studies, an intake of fructose >100 g/day has been necessary to observe the adverse effects on lipid profiles [51, 65, 85, 98, 100, 106108]. However, in a recent study by Aeberli et al. [109], a daily intake of about 77 g fructose and 34 g glucose for 3 weeks resulted in increased levels of total cholesterol and LDLs in the blood of healthy young men, compared with a daily intake of approximately 109 g glucose and 28 g fructose over the same time period. The fact that both groups also ingested an unknown amount of starch and the fact that food intake was not controlled reduce the solidity of these results. Maersk et al. [90] found that intake of 50 g fructose per day together with 50 g glucose could have a negative effect on blood triglyceride level. The lack of a control group ingesting glucose makes it difficult to conclude that this is an effect of fructose. Conversely, Lowndes et al. [110] found no negative effect on lipid profile in overweight or obese individuals consuming HFCS or sucrose incorporated in a eucaloric diet for ten weeks at levels corresponding to the 25th and 50th percentiles of adult fructose consumption. Using the current knowledge, it does not appear that the consumption of moderate amounts of fructose (<50 d="" g="" i="" nbsp="">alone will result in an unfavorable blood lipid profile [86, 111].

Due to the insignificant levels of fructose in peripheral blood, as described above, only glucose has the potential to be a substrate for DNL in adipose tissue. Although DNL in adipose tissue seems to be small as earlier discussed, glucose will, because of its presence in blood and by raising blood insulin level, probably to a higher extent than fructose, stimulate DNL in adipose tissue. Intake of glucose, in amounts that exceed the total capacity for glycogen storage and glucose oxidation, may thus increase DNL in adipose tissue more than the same amount of fructose. While fat formed in the liver has to be transported as lipoproteins in blood, this is avoided if the fat is formed directly in adipose tissue. Considering known negative health effects of lipoprotein residues, DNL occurring in adipose tissue may be preferable compared with DNL in the liver. This may illustrate a metabolic difference between glucose and fructose when consuming large amounts of sugars.

Another possible difference between fructose and glucose on risk factors for atherosclerosis is the effect of these sugars on blood uric acid level. Increased uric acid level has been associated with atherosclerosis in epidemiological studies, but the causality is uncertain [112114]. Fructose appears to increase uric acid levels in the blood to a higher extent than glucose, especially at high intakes and when consumed as excess energy [86, 115, 116]. Intake of 0.5 g fructose/kg body weight is the lowest quantity shown to result in uric acid formation [117]. An increased blood level of uric acid can theoretically lead to elevated blood pressure because uric acid inhibits an enzyme in the endothelial cells of the arteries called endothelial nitric oxide synthase (eNOS). Activated eNOS leads to increased production of nitric oxide (NO), an important vasodilator. Thus, inhibition of eNOS may lead to vasoconstriction. Although only 0.5 g fructose/kg body weight has been shown to give uric acid formation and increased uric acid level theoretically could increase blood pressure, results from studies of the effect of fructose on blood pressure are very inconsistent [65, 72, 118, 119]. An average intake of fructose does not seem to lead to increased blood pressure [111, 120, 121]. The lack of causal link between uric acid level and atherosclerosis makes it difficult to draw conclusions on this effect of fructose."
Figure 1
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