What internal factors cause obesity? The increase in fat synthesis due to calorie intake exceeding calorie expenditure is the material basis of obesity. Obesity is caused by internal factors in the human body that disrupt fat metabolism.
Which intrinsic factors cause obesity
1. Genetic factors
The onset of simple obesity in humans has a certain genetic background. Mayer et al. reported that if one parent is obese, the obesity rate of their children is about 50%; Both parents are obese, and the obesity rate of their children has increased to 80%. Human obesity is generally considered to be a polygenic inheritance, and genetics plays a susceptible role in its onset. The formation of obesity is also related to the interaction of lifestyle, feeding behavior, preferences, insulin response, and social psychological factors.
2. Neuropsychiatric factors
It is known that there are two pairs of neural nuclei related to feeding behavior in the hypothalamus of humans and various animals. One pair is the contralateral ventral nucleus (VMH), also known as the satiety center; The other pair is the lateral ventral nucleus (LHA), also known as the hunger center. When the satiety center is excited, there is a sense of fullness and refusal to eat, and when it is disrupted, the appetite increases significantly; When the hunger center is excited, there is a strong appetite, and when it is disrupted, there is loss of appetite and refusal to eat. The two regulate and constrain each other, and are in a dynamic equilibrium state under physiological conditions, regulating appetite within a normal range and maintaining normal weight. When lesions occur in the hypothalamus, regardless of the sequelae of inflammation (such as meningitis, encephalitis), trauma, tumors, or other pathological changes, such as damage to the ventromedial nucleus, the function of the ventromedial nucleus is relatively overactive, leading to overeating and obesity. On the contrary, when the ventral lateral nucleus is destroyed, the function of the ventral medial nucleus becomes relatively overactive and anorexia occurs, leading to emaciation. In addition, this area has close anatomical connections with higher-level neural tissues, which can also regulate the feeding center to a certain extent. The blood-brain barrier in the hypothalamus is relatively weak, and this anatomical feature makes it easy for various bioactive factors in the blood to migrate to this area, thereby affecting feeding behavior. These factors include: glucose, free fatty acids, norepinephrine, dopamine, serotonin, insulin, etc. Psychological factors often affect appetite, and the function of the feeding center is constrained by the mental state. When the mind is excessively tense and the sympathetic nervous system is excited or the adrenergic nervous system is stimulated (especially when alpha receptors are dominant), appetite is suppressed; When the vagus nerve is excited and insulin secretion increases, appetite often becomes hyperactive. The ventromedial nucleus is the sympathetic nervous center, and the ventromedial nucleus is the parasympathetic nervous center, both of which play important roles in the pathogenesis of this disease.
3. Hyperinsulinemia
In recent years, the role of hyperinsulinemia in the pathogenesis of obesity has attracted attention. Obesity often coexists with hyperinsulinemia, but it is generally believed to be caused by hyperinsulinemia. The insulin release of obese individuals with hyperinsulinemia is about three times that of normal individuals.
Insulin has a significant promoting effect on fat accumulation. Some people believe that insulin can be used as an indicator of overall fat mass and, to some extent, as a monitoring factor for obesity. Some people believe that there is a significant positive correlation between plasma insulin concentration and overall fat mass.
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