A comprehensive explanation of the breakdown and metabolism of body fat and the pathogenesis of obesity.

36. How is body fat broken down and metabolized?

Except for the brain and mature red blood cells, all other tissues and cells in the human body can oxidize and utilize fat, mainly by utilizing fatty acids mobilized from fat stores, and also by utilizing their own fat.

The liver and kidneys contain a relatively high amount of glycerol kinase, which allows them to utilize glycerol from fats.

Fat is first hydrolyzed into glycerol and fatty acids.

Glycerol is broken down into α-glycerol phosphate by glycerol kinase, and then further broken down into dihydroxyacetone phosphate by α-glycerol phosphate dehydrogenase, which then enters glycolysis to produce lactic acid.

Fatty acids undergo oxidative decomposition into β-oxidation.

The main processes are dehydrogenation and carbon chain degradation.

With the participation of lipids (ATP), acyl-CoA synthase in the endoplasmic reticulum or outer mitochondrial membrane is used to generate acyl-CoA, which is then transferred into the mitochondrial basement membrane for dehydrogenation and degradation.

In the endoplasmic reticulum or mitochondria of cells in tissues such as the liver and brain, there are enzyme systems that oxidize fatty acids into α-hydroxy acids. In the brain, α-hydroxy acids are dehydrogenated into α-keto acids, which are then oxidized and decarboxylated into a one-carbon fatty acid (RCOOH). This is the α-oxidation of fatty acids.

The oxidase activity of fatty acids in the endoplasmic network of cells in tissues such as the liver and kidneys, with its terminal CH₃ oxidation, is called W monoxide oxidation.

37. Will a person gain weight if they synthesize less fat?

The synthesis of body fat is influenced by many factors, such as nutrition, hormones, genetics, and related drugs.

These factors mainly affect the activity of some enzymes during fat synthesis, preventing fat cells and the liver from synthesizing fat.

To maintain stable blood glucose levels, the liver synthesizes most of the glucose into glycogen, which is then stored in the liver, as blood glucose concentration rises after meals.

When fasting, liver glycogen is immediately broken down into glucose, which enters the bloodstream and raises blood sugar levels.

Liver function plays an important role in lipid metabolism. Phospholipids, cholesterol, and cholesterol esters in plasma are synthesized in the liver. The liver oxidizes fatty acids to produce ketone bodies. If the synthesis of phospholipids or proteins is insufficient, fat will accumulate in the liver and be stored in adipose tissue.

Nutrition, hormones, and drugs can control the synthesis of fatty acid synthases and can regulate it in a long-term and sustained manner.

Weight loss drugs can be produced using high-tech bioengineering techniques that affect the enzyme system in the synthesis of fat and fatty acids, thereby reducing fat synthesis in fat cells and the liver, and thus can definitely lead to weight loss.

38. What is the pathogenesis of obesity?

From the perspective of modern medicine, the pathogenesis of obesity is related to various factors such as genetics, family history of obesity, diet and exercise, endocrine disorders, and metabolic disturbances caused by physiological factors.

Genetic factors play a role. According to statistics, if an infant is overweight before the age of 5 and his parents have normal weight, the probability of him becoming obese as an adult is about 8%; if one parent is obese, the probability of their child becoming obese as an adult is 40%; and if both parents are obese, the probability of their offspring becoming obese is 60% to 80%.

Endocrine disorders are often associated with secondary obesity, such as increased insulin secretion, hypopituitarism, and hypothyroidism.

Dietary factors, including (1) excessive food intake, (2) high energy and high fat intake, and (3) different ways of eating, can all lead to obesity.

The obesity rate among cooks can reach 60.4%.

Obesity rates among workers in food, confectionery, biscuit factories, and breweries can reach 44.8%, while the obesity rate among workers in other types of factories is only around 15%.

Physiological factors include the decline of physiological functions in men after middle age and in women after menopause, as well as reduced physical activity and chronic disease treatment, resulting in less energy expenditure and insufficient nutrition.

For example, the postpartum weight gain rate is 40.9%, and the premenopausal weight gain rate is 35.7%.

Therefore, as we age, our energy metabolism slows down, and when we consume more than we need to burn, it is converted into fat and deposited in our bodies, leading to obesity.

39. What is the relationship between thyroid function and obesity?

From a medical perspective, hypothyroidism is often mentioned in the differential diagnosis of obesity.

The thyroid gland is an important endocrine gland in the human body. The thyroid hormone secreted by the thyroid gland promotes the breakdown and metabolism of fat in the human body, increases the oxygen consumption, heat production and adenosine triphosphate synthesis in many tissues, and at the same time promotes the synthesis of proteins, ribonucleic acid and deoxyribonucleic acid in many tissue cells, thereby promoting human growth and development.

Hypothyroidism, caused by any reason, can reduce tissue catabolism, decrease heat production, and reduce the production of proteins and nucleic acids. This leads to the accumulation of some metabolic products in the tissues, especially substances called mucin and mucopolysaccharides, which can be widely deposited in various tissues and organs, including subcutaneous tissue, causing myxedema.

Patients may experience weight gain, especially noticeable swelling in the face, eyelids, and anterior tibial region.

This type of myxedema differs from obesity-related edema, which leaves pitting marks when pressed. Generally, it leaves no marks after pressing, and the skin has reduced elasticity and becomes rough.

Patients may also experience clinical symptoms of hypometabolism, such as chills, slowed reaction, slower speech, and significant memory loss.

Although hypothyroidism can cause weight gain, it is not necessarily obesity. It is important to distinguish between the two to avoid delaying diagnosis and treatment.