The hectic lifestyle makes us eat bakery products while waiting for the tram, and to eat lunch usually only after work, when due to the hunger that has accumulated during the day, we eat more than we planned.
Large oscillations vs high blood glucose concentration
The concentration of glucose in the blood of every person fluctuates throughout the day – after a meal it rises sharply, and between meals it is low. However, these oscillations are monitored only by patients suffering from type 2 diabetes mellitus. Studies have shown that fluctuations in glucose concentration in diabetics are associated with increased oxidative stress, inflammation, and micro- and macrovascular damage, and the latest research links it to the progression of atherosclerosis. Interestingly, the oscillation of blood glucose concentration has a greater impact on cardiovascular complications than the constantly high concentration of glucose in the blood. An additional problem is that people without diabetes rarely think about the effect a sudden increase in glucose can have on their body. So, what happens to our proteins when we suddenly expose them to a high concentration of glucose?
Vicious cycle of glycation
Once digested in the oral cavity and small intestine, monosaccharide carbohydrate units, such as glucose and fructose, go into the bloodstream where they are subject to the glycation process. Non-enzymatic glycation is the process by which sugars are linked to the amino groups of proteins by covalent bonds. This process is partly oxidative, so it is often called glycooxidation. The final products of glycation (AGE) are formed by polymerization of many intermediate products, and since there is no enzyme to remove them, this metabolic waste is stored in the body. In a state of oxidative stress, there is an increased production of free radicals, reactive oxygen species that stimulate new glucose molecules to glycation, and so we enter a vicious cycle.
Sugary drinks and obesity
Fructose increases the concentration of enzymes involved in a process called de novo lipogenesis, in which the synthesis of fatty acids and triglycerides from non-lipid precursors takes place. If the process is very active, non-alcoholic fatty liver occurs because a large amount of lipids accumulates in the liver. Interestingly, high concentrations of fructose promote de novo lipogenesis much more powerful than a fat-rich diet, which raises the question of whether increased consumption of sugary drinks actually has a higher role in the pathogenesis of obesity than we think.
Ageing because of glucose?
In addition to inflammation in the body, new scientific research links accumulation of AGE with aging. Research on the species C. elegans shows that a young individual, grown in conditions of high glucose concentration, lives about 2 days shorter than an individual grown on a nutrient medium with a glucose concentration that is sufficient for survival. Aging is also favored by glycation of extracellular proteins, which favors the cross-linking of collagen and elastic fibers, which causes the skin to lose elasticity and become stiff.
What to do?
Can we stop the damaging impact of a sudden rise in blood glucose? Of course we can! Several studies have shown that physical activity increases the production of antioxidant enzymes and reduces the formation of AGE. In addition, it is important to prevent glucose spades from happening at all. What we can do is consume more smaller meals throughout the day instead of a few large ones and include fiber in the daily menu, preferably at the beginning of the meal. We can practice mild physical activity after eating to encourage muscles to “burn” some glucose. In addition to feeling hungry less often, we will not feel a sudden drop in energy and drowsiness for an hour or two after a meal. We’ll also be thanked by our skin, which we will keep youthful for a long time to come.
Translated by: Asja Fajtović
Literature
2. Gugliucci A. Formation of fructose-mediated advanced glycation end products and their roles in metabolic and inflammatory diseases. Advances in nutrition, 2017, 8(1), 54-62.
3. Softic S, Cohen DE, Kahn CR. Role of dietary fructose and hepatic de novo lipogenesis in fatty liver disease. Digestive diseases and sciences, 2016, 61(5), 1282-1293.