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Carnosine and diabetes

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Diabetes Mellitus is a disease in which the level of glucose or sugar in the blood is too high.

Glucose comes from the food we eat. Insulin is a hormone that helps glucose get into the cells to give them energy.

In type1 diabetes, the body does not make insulin.

In type 2 diabetes, the more common type, the body does not make or use insulin well. Without enough insulin, glucose stays in the blood.

Diabetes mellitus is not a single disorder; it is a series of metabolic conditions associated with hyperglycemia and caused by disturbances in insulin secretion and/or insulin action. Exposure to chronic hyperglycaemia can lead to microvascular complications in the retina, kidneys or peripheral nervous system. Studies show that people who are diabetic or prediabetic have low concentrations (63% below normal) of carnosine in their muscle and brain cells. Obese individuals who have been given L-carnosine show a drop in blood sugar levels. Oxidative stress has been identified as a common mechanism of cellular damage and dysfunction in a wide range ofrange of diseases, including diabetes (Giacco & Brownlee, 2010; Miceli, Pampalone, Frazziano, Grasso, Rizzarelli, Ricordi, & Conaldi, 2018).

Current understanding of the metabolic changes associated with the development of insulin resistance has focused on the role of oxidative stress and its interaction with inflammatory processes at both levels: tissue and organism. Obesity-related oxidative stress is an important factor contributing to the development of insulin resistance in both adipocytes and myocytes. In addition, oxidative stress is associated with mitochondrial dysfunction and this is thought to play a role in the metabolic defects associated with oxidative stress.

Among the various effects of oxidative stress, protein carbonylation has been identified as a potential mechanism underlying mitochondrial dysfunction.

Carnosine EXTRA is a dietary supplement that protects cells from oxidative stress by various mechanisms, including antioxidant and anticarbonylating effects at the mitochondrial level. There is no doubt that HbA1c is familiar to all diabetics. It is a glycosylated hemoglobin that provides information about blood glucose levels over the past few months.

Recent studies show that the most important effect of carnosine is probably the antiglycation effect (Houjeghani, Kheirouri, Faraji, & Jafarabadi, 2018). Diabetes intensifies the process of glycation, which is one of the reasons (but not the only one) that the arteries of diabetics are prone to thickening of the walls and further to the development of atherosclerosis. The incidence of atherosclerosis in diabetic patients is three times higher than in those who do not suffer from the disease, as is the incidence of myocardial infarction and cerebrovascular disorders. L-carnosine controls blood sugar levels via H3-receptors in the autonomic (autonomic) nervous system.

Animal tests have shown that pregnant mice deficient in carnosine are much more likely to give birth to offspring with diabetes. This is explained by the effect of carnosine, which improves glucose tolerance in the fetus. In this way, carnosine may be important for mothers with diabetes because it reduces the risk that their children will suffer from the disease. Supplementation with carnosine protects a person from diabetic nephropathy. Studies conducted on rats by a team of Japanese scientists have shown the possibility of using L-carnosine to lower blood glucose levels by regulating the activity of autonomic nerves. L-carnosine has an antiglycaemic effect and inhibits secondary complications associated with diabetes.

In addition to stabilizing blood sugar in diabetics, carnosine also protects against many complications of diabetes, such as organ failure, hearing loss, osteoporosis, eye problems, heart damage, and more. People with diabetes often have peripheral neuropathy – a condition in which the nerves in the body’s extremities (hands, feet and arms) are damaged. Carnosine can prevent the pain associated with this condition. L-carnosine is suitable for all types of diabetes because it reduces the risk of diabetes complications such as cardiac and cerebrovascular disease, atherosclerosis, kidney and eye complications (Kianpour & Yousefi, 2019)

What is glycation (non-enzymatic glycosylation)?

Every second, a process called glycation (glycosylation) takes place in our body. This reaction can be described as the binding of protein molecules to sugar (glucose) molecules and the subsequent formation of damaged, non-functional structures. This process of glycation changes the structure of proteins and reduces their biological activity.

Glycation proteins accumulated in the affected tissues are clear indicators of the disorder. Many diseases that are associated with aging, such as diabetes, atherosclerosis, cataracts, and some neurological diseases, can at least be attributed to glycation. L-carnosine prevents glycation and plays an important role in removing glycation proteins. So-called carnosylation, the process of adjusting carnosine to denatured molecules, allows the removal of glycation proteins from cells. Glycation, known in biochemistry as the Maillard reaction between protein and glucose, is thought to be an important factor in aging, complications caused by diabetes, and possibly in malignant tumors. Glucose is the “food” for glycation, the malicious binding of protein/glucose is accompanied by the formation of free radicals, leading to “AGEs” (Advanced Glycation End-products). When “AGEs” form, they interact with neighboring proteins to form pathological key linkages (cross-links) that cause tissue hardening and stiffening. It is a subject of current debate that in fact no other molecule has such an important and potentially toxic effect on proteins as “AGEs”.

Diabetics build up enormous amounts of “AGEs”, significantly earlier in life compared to healthy people, and this process completely disrupts organs that depend on flexibility to function. It is proven that glycation processes alone lead to “hardening” of the arteries in diabetics. “AGEs” trigger a series of destructive processes when they bind to related cellular structures. One result is the formation of 50 times more free radicals. Therefore, diabetes is in fact a disease of accelerated aging and a source of “AGEs”, in this case, particularly affected arteries, the lens and retina of the eye, peripheral nerves, and kidneys. Preventing glycation means mitigating the damage accompanied by inflammatory and degenerative changes. Diabetic rats that were not treated with glycation inhibitors showed twice as much renal damageglomeruli caused by “AGEs” compared to the control group that was treated with these inhibitors. Supplementation with glycation inhibitors may allow the prevention of many of the aberrations that accompany the aging process.

Due to the fact that carnosine structurally encompasses the sites that glycation attacks, carnosine must be sacrificed in order to protect their target.

Carnosine also promotes proteolytic pathways, removing damaged, unnecessary and often harmful proteins (Menini, Iacobini, Fantauzzi & Pugliese, 2020). . Therefore, L-carnosine with its antiglycation effect is useful in the prevention and treatment of complications caused by diabetes such as cataract, neuropathy, arteriosclerosis and renal failure. Researcher J. Vinson (University of Granton, PA, USA) studied the ability of carnosine to inhibit protein glycation and AGE formation. The results of this study showed that carnosine is indeed an important antioxidant in vivo. Although the mechanism of inhibition is still unclear, carnosine has been shown to be an antioxidant and/or to bind to sugars. As a consequence, the formation of AGE and Amadora products is inhibited. Vinson suggested that carnosine can be used as a drug to reduce the rate of glycation in cells.

Giacco, F. and Brownlee, M. (2010). Oxidative stress and diabetic complications. Circulation Research, 107(9), 1058-1070. Miceli, V., Pampalone, M., Frazziano, G., Grasso, G., Rizzarelli, E., Ricordi, C., … & Conaldi, P. G. (2018). Carnosine protects pancreatic beta cells and islets from oxidative stress damage. Molecular and Cellular Endocrinology, 474, 105-118. Houjeghani, S., Kheirouri, S., Faraji, E., & Jafarabadi, M. A. (2018). L-carnosine supplementation attenuated fasting glucose, triglycerides, advanced glycation end products, and tumor necrosis factor-α levels in patients with diabetes mellitus 2. Type 2 diabetes: a double-blind, placebo-controlled, randomized clinical trial. Nutrition Research, 49, 96-106. Kianpour, M., & Yousefi, R. (2019). Carnosine prevents various structural damages induced by methylglyoxal in lens crystallins. Cell Biochemistry and Biophysics, 77(4), 343-355. Menini, S., Iacobini, C., Fantauzzi, C. B., & Pugliese, G. (2020). L-carnosine and its derivatives as novel therapeutic agents for the prevention and treatment of vascular complications of diabetes. Current medicinal chemistry, 27(11), 1744-1763.

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