The second theory is one known as carbohydrates hypothesis or in.sulin theory. Calorific value does not matter in this case. According to theory, carbohydrates are fattening, because they strongly affect in.sulin, while fats are not fattening, as they do not cause the release of in.sulin to blood. When storing the energy in fat tissue, in.sulin causes the energy imbalance which results in obesity, causing reduced physical activity and increased appetite.
In this theory, the most important is the glycemic index (GI) and glycemic load (GL) of consumed food, which contain carbohydrates. Diseases like type 1 and 2 diabetes are also crucial.
The example of something which has high glycemic index is a sugar contained in sweetened beverages or refined sugar (sucrose), which is made up of glucose and fructose. Sucrose quickly enters the bloodstream and increases the glucose level. Healthy organism reacts immediately with excretion of in.sulin, that helps to utilize the glucose as fuel in cells, and the excess is stored as glycogen in liver and muscles, thanks to which the glucose level goes back to the appropriate state. Sometimes this process may not work like these, especially when we consume glucose-fructose syrup or concentrated fruit juices, so the sugar with a high proportion of fructose (glucose-fructose syrup is usually made of 55% fructose, 45% glucose). These are carbohydrates with the very high GI. Burning process of these sugars in cells and storing it as glycogen may not be optimal.
Mechanism of the problem is located in specific properties of refined sugar and high-fructose corn syrup, more precisely how the fructose is metabolized. If we eat 100 calories of glucose (e.g., in bread, potatoes), they will be metabolized in a different way than fructose. So, calories are the same, but metabolic consequences are entirely different.
Fructose contained in sucrose or HFCS (High-Fructose Corn Syrup) is metabolized mainly by the liver to glycogen in a complicated process, which can be easily disturbed if there is a lack of the necessary co-factors, whereas glucose in sugar or starch is metabolized by all human cells. When eating simple sugar (fructose and glucose), we endanger our liver for greater effort in opposite to consumption of the same calorie amount from starch (only glucose). If we additionally consume liquid sugar, e.g., in fruit juice or soda, fructose and glucose will “hit” our liver faster, if we have eaten apples instead.
Using the energy consumed with food may happen on the fly, in line with demands of an organism, or storing sugars (glycogen in liver and muscles) and fat (triglycerides in fat cells). Some glycogen and fat supplies are crucial for proper functioning of an organism, and fat tissue does additional functions like shielding inner organs or give comfort (like fat tissue in buttocks provides seating). Problems with fat tissue (if we treat it as a problem) may occur when it increases. There is no problem with the excess of glycogen, as its ability to be stored is limited by muscle and liver mass. Muscles store glucose in the form of glycogen as 2% of muscle tissue mass, and as 10% of the liver mass. So, it turns out that the amount of muscle and fat tissue have a significant impact on body weight, especially the relation between the amount of muscle tissue and white adipose tissue (white fat). As mentioned before, white fat is not metabolically active and when its contribution in body weight increases, the RMR (Resting Metabolic Rate) decreases.
Even if we are bodybuilders, muscle tissue is not growing as fast as the white fat. Brown adipose tissue (brown fat), in contrast, is decreasing when we get older because of a warm environment. Fat tissue cells can increase their space even 1000 times to store fat. There are many fat cells in the human organism, and that is why it is easy to gain weight quickly.
Obesity is the excessive accumulation of fat tissue. The in.sulin theory and fat storing were described in detail many years ago. In.sulin stimulates the enzyme which inserts fat in fat cells, and this is not the only role of it. In.sulin is a crucial hormone which stores other nutrients, e.g., protein in muscles, and it converts glucose into glycogen, which is then stored in muscles and liver. A liver can store up to 150g of glycogen, and muscles of adult man up to 300g. In.sulin is produced by pancreas beta cells, together with its antagonist – glucagon, which is produced by pancreas alpha cells and plays the key role in nutrients management “stuffing” them in various body parts and obtaining them as fuel or building material.
When we eat and have plenty of in.sulin in the blood, it is the time when “storing mode” dominates and fat is transported from blood to fat cells. When some time passes, and we do not eat, in.sulin level decreases, and glucagon may “show up” and release fat cells from fat cells to the bloodstream.
Optimal metabolism of an adult human with proper body weight needs 200g of glucose and 160g of fatty acids. Glucose can be obtained directly from food, from supplies in muscle and liver cells, or as the result of gluconeogenesis.
Fats in the organism may be subject to two processes – burning and synthesis. We should focus primarily on burning.
A triglyceride is a primary chemical which serves as fat fuel. It can circulate in the bloodstream independently. Also, it can be a part of lipid fractions of blood plasma, like cholesterol VLDL (very-low-density lipoprotein), LDL (low-density lipoprotein), HDL (high-density lipoprotein). Finally, it can be stored in fat cells.
The first phase of burning triglyceride molecule happens mostly in fat tissue, and it applies to bloodstream triglycerides and those released from fat tissue. It is based on the breakdown of triglyceride molecule into glycerol and 3 fatty acids. The latter get to the blood, from which they are collected to be burned.
Conversion of fatty acids into energy is called beta-oxidation, and it happens inside metabolically active cells, more precisely in the mitochondrial matrix. The process in order to go problem-free needs micro-nutrients like biotin, magnesium, zinc, manganese, vitamins B2, B3, B6, B12, vitamin C, iron, methionine, and lysine amino acids. What is more, beta-oxidation of fatty acids needs carnitine (it is not needed by short-chain fatty acids like coconut oil or butter). The organism produces carnitine on its own, if it has components, or it can be obtained as a food supplement. Using fat as fuel to produce energy in mitochondria can happen when in.sulin level is low, and with mentioned above substances. Healthy organism and proper nutrition these conditions are easily fulfilled. However, it often happens that not everything functions in an optimal way, when we take fat burning under consideration. If any co-factor is absent, fatty acids cannot be broken down, and they will stay stored in the waist and abdomen fat cells.
In.sulin resistance is one of the examples. We must take under consideration not only fat but also glucose, which in excess resides in the circulatory system. In.sulin resistance of cells happens when resistant cells “do not open” (with in.sulin) to receive glucose. In this situation, the pancreas produces more in.sulin, up to the level when it overcomes the in.sulin resistance. Only then, glucose may get inside call and convert to energy in mitochondria. Supplying cells with glucose differs organism with in.sulin resistance, as it happens with consistently increased in.sulin level (conditions which foster storing of fat). The problem would not be so dangerous if all cell types became in.sulin resistant at the same time. Unfortunately, it does not happen. Different cells become resistant at a different time. The first cell type that usually becomes resistant is liver cells. The probable cause of this might be food and drinks with a high dose of fructose. The pace at which the liver must do its work has an additional impact on the way it metabolizes fructose and glucose. It is crucial especially in the case of fructose, as when it gets to the liver fast, and in large quantities, it will be converted to fat in the majority which can lead to non-alcoholic fatty liver disease. The disease may result in in.sulin resistance of the liver, which is considered as the fundamental problem of obese people.
In.sulin resistance of liver is a problem for sugar management in the organism, as the liver is the primary storage of processed sugar – glycogen.
Stored glycogen is released to the bloodstream as glucose, with the help of glucagon (the hormone produced by pancreatic alpha cells). A slight increasing of in.sulin level stops the production in the healthy organism. However, when liver cells become resistant (for in.sulin), more and more of in.sulin is needed to shut off the mechanism of sugar production inside a liver.
For most of the people, fat cells become in.sulin resistant later than a liver. When the concentration of in.sulin in blood raises to overcome the resistance of the liver and stop the production of glucose, the excess of in.sulin in blood impacts fat cells. Then, fat cells receive the order to store fat, so most of the fat from food will be stored inside them. Because of in.sulin resistance, bloodstream in.sulin level never decreases, so the glucagon cannot be secreted to release fat from fat cells, and then it cannot be transported to metabolically active cells to undergo beta-oxidation and be converted to energy.
To summarize, in.sulin not only stores fat in fat cells. Its increased level blocks secreting of glucagon, which impairs the releasing of fat from fat cells, so it cannot be used as energy source. Therefore, we feel tired and hungry, even though we have significant fuel supplies stored in fat cells.
The situation looks entirely different in the case of type 1 diabetes, as pancreatic beta cells do not produce in.sulin. Then, a liver releases large amounts of sugar to blood, which negatively affects the organism. The absence of in.sulin impairs the ability to store triglycerides in fat cells, and glycogen in muscles and liver. Most of type 1 diabetics, before diagnosis, strongly lose weight, despite eating much.
Today, when this dangerous disease is diagnosed, one who is suffering from type 1 diabetes takes in.sulin, which gives a chance for proper management of sugars and fats in the organism. Why only a chance? It is tough to keep the correct glucose and in.sulin levels in the blood. High in.sulin level causes the bloodstream fat to be stored in fat cells, and then it cannot be used as energy. In the past, when there was no possibility to produce in.sulin outside the human organism, people who have type 1 diabetes lost weight, which led to death. Today, they often take too much in.sulin, which results in gaining weight.