There are many queries that we have received in our Genetic Counseling service on the genetic analysis of OBESITY and DIABETES, which is why I have decided to write this article as the second part of “What is nutrigenetics?”.
To analyze the degree of genetic predisposition to obesity, there are several genes involved that we can group into several categories:
Central intake control
The genes involved in this group are those related to the control of appetite and satiety and there are three (MC4R, FTO, BDNF). The existence of certain genotypes in these genes can cause your intake control to be irregular. Simply put, the more genetypes that provide this irregularity you have, the more you want to eat than “normal” you will have or it will take longer to get satiated, which will cause you to eat more than you need to “get full”. In addition, these genotypes tend to produce a greater appetite for calorically dense foods.
Regulation of thermogenesis
Food thermogenesis is the energy (calories) your body needs to digest, absorb, and metabolize food. For example, when we say that a food makes us feel “very heavy” or “it is difficult to digest” it really means that a lot of energy is needed to be digested. Foods with a lot of fiber need more energy to be digested, absorbed and metabolized.
In this group there are six associated genes (UCP1, UCP3, ADRB2, ADRB3, PPARG, ACE), which when they have certain genotypes, means that your body has problems carrying out the processes of digestion, absorption and metabolism of food, so they stay longer in the digestive tract and take in more energy than “normal” from those foods. For example, if we should obtain 30 kcal from a food X, your body obtains 45 kcal; those extra 15 kcal are not used by the body and accumulate as fat. In addition, the PPARG gene is associated with an ancestral genotype not adapted to habitual eating habits, which causes it to not assimilate processed foods well.
The inflammatory process of the adipose tissue is related to an alteration of the immune system that what it does is inflame the adipocytes (the cells of the adipose tissue) increasing their size, and consequently, increasing the total fat mass in a chronic way. So physical activity is very important in this case to “burn” fat mass. The existence of this inflammation also means that it will cost more to “burn” that fat, that is, it takes more exercise than “normal” to burn the same amount of energy as a person who does not have this type of inflammation.
Why is this happening? Because a person who does not have this inflammation of the adipose tissue can have the same number of adipocytes as you, but since they are not inflamed, they take up less space than in your body.
Four genes are associated with this process (IL1B, IL1RN, IL6, TNFa).
Insulin resistance and predisposition to type II diabetes
To know the genetic predisposition to this disease there are five associated genes (FABP2, ADIPOQ, IRS1, IL6, PPARG). As I have previously commented, the PPARG gene, having the ancestral genotype where processed foods are not assimilated well, is also related to insulin resistance.
There are genotypes in these five genes that are related to insulin resistance or a malfunction of the same that creates an increase in blood glucose that can cause type II diabetes.
With this information, there are more tools to avoid the dreaded rebound effect when you follow a diet in which you lose weight and you can more effectively combat those bad habits that cause fat to be stored (especially visceral fat) and to develop. obesity and diabetes.