Hyperglycemia/Glycation increases damaging AGEs
Why the hyperglycemia?
Excess dietary sugars and refined carbohydrates increases blood glucose - usually accompanied by prolonged high insulin levels.
Excess consumption of high fructose corn syrup (HFCS) - in processed foods, sodas etc;
Insulin resistance as in Type 2 diabetes - further increases blood sugar;
Advanced Gycation Endproducts (AGEs) do damage
GLYCATION of sugar molecules lead to Advanced Glycation Endproducts (AGEs) - some of which are implicated in age-related chronic diseases including CVD
- Glycation is another mechanism that causes significant damage and inflammation - this is the haphazard process (without the controlling action of an enzyme) of adding sugar molecules (i.e. glucose, fructose, galactose) to lipid molecules or proteins, to form a glycolipid or glycoprotein, and harmful by-products, aptly called AGEs (Advanced Glycation Endproducts).
AGEs can be formed outside or inside of the body:
- Exogenously - AGEs are typically formed when sugars are cooked with proteins or fats. Also, food manufacturers add AGEs to foods as flavor enhancers and colorants to improve appearance;
- Endogenously - glycations occur mainly in the bloodstream to some of the absorbed simple sugars, i.e. glucose, fructose and galactose.
AGEs can directly damage biomolecules, such as the endothelium, connective tissue collagen, elastin and fibrinogen (E.g. in blood vessel walls)
- Glucose and fructose glycate and so inactivate the enzyme glutathione reductase, responsible for maintaining the body's major cell-protecting antioxidant enzyme Glutathione (GSH) - Glucose, glucose 6-phosphate and fructose all displayed a time-dependent inhibition of glutathione reductase activity, suggesting that these sugars glycate this enzyme. (Blakytny et al, 1992)
• Fructose and galactose have about 10 TIMES the glycation activity of glucose. With the common practice of using high fructose corn syrup (HFCS) in many processed foods, fructose has become an excessive component in today's Western diet; (Bunn & Higgins, 1991)
- Cholesterol and fat is damaged by glycation - Increased amount and duration of glucose in the blood allows more glycation to occur, inflicting damage on tissues via lipid oxidation. (Bucal, 1993)
- Hyperglycemia is positively correlated with arterial disease in many diverse populations
• Hyperglycemia increases glyco-oxidation - which increases the formation of oxidized LDL, and its accumulation in the artery wall;
• Circulating AGEs bind LDL cholesterol and increase its accumulation in arterial wall - glycation of LDL cholesterol increases the proportion of lipoproteins that are taken up via inflammatory cells and decreases the proportion taken up by liver cells (hepatocytes) via classical LDL receptors, thus contributing to atherosclerosis by increasing accumulation of LDL cholesterol in the artery wall.
Organs and tissues NOT dependent on INSULIN for their absorption of glucose are more susceptible to damage from periods of hyperglycemia than other organs - i.e. kidneys, blood vessels, peripheral nerves and lenses of the eye.
Glycated sugar creates inflammation, which activates defensive immune system macrophages:
- Scavenger cells with special receptors for AGEs, called RAGEs - again how aptly named is that!? - these RAGEs “get mad” and bind to the AGEs to remove them.
Blakytny R, Harding JJ, (1992) Glycation (non-enzymic glycosylation) inactivates glutathione reductase. Biochem J.
Bucal R et al. (1993) Lipid advanced glycosylation: pathway for lipid oxidation in vivo.
Bunn and Higgins, (1991)
Chronic low-level inflammation (CLII) involved in almost all health problems
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