Classification and degrees of obesity
Assessment of excess body weight relies on several criteria. The main tool is the body mass index (BMI), which is calculated as the ratio of body weight in kilograms to the square of height in meters.
There are four main classification criteria:
- By the degree of body weight increase (BMI): Normal corresponds to values of 18.5–24.9. Grade 1 is recorded at 25–29.9 (overweight). Grade 2 covers the range of 30–39.9 (obesity). Grade 3 is diagnosed with a BMI of 40 and above (morbid obesity).
- By fat tissue localization: General and local obesity are distinguished. The latter is divided into the male type (android, with fat accumulation on the abdomen, chest, and back) and the female type (gynoid, with excess fat on the thighs and buttocks).
- By tissue morphology: The process can proceed through an increase in cell size (hypertrophic), an increase in their number (hyperplastic), or combine both pathways (mixed).
- By origin: Primary (synonym — hypothalamic) and secondary (symptomatic) obesity are distinguished.
Cellular mechanisms and body weight assessment
Morphological remodeling of adipose tissue determines the clinical course of the disease and the choice of therapeutic tactics.
- Hypertrophic obesity develops due to an increase in the mass and volume of existing adipocytes.
- Hyperplastic obesity is associated with the predominance of cell division and an increase in their total number. This variant is characterized by high resistance to conservative treatment methods and, in severe cases, requires surgical intervention.
- Hyperplastic-hypertrophic (mixed) obesity combines both mechanisms and is often observed in childhood.
To assess ideal body weight, along with BMI, the classic Broca index is used, which is calculated as the difference between height in centimeters and the number 100.
Pathogenesis: hypothalamic variant and lipostat
The development of the pathology is based on three main mechanisms: neurogenic, endocrine, and metabolic. A key role in neurogenic genesis is played by the hypothalamic variant, associated with the damage to neurons in specific hypothalamic nuclei (ventromedial, paraventricular, and posterolateral ventral).
The most important link in pathogenesis is a disruption in the “Leptin — Neuropeptide Y” (lipostat) loop, which sets the intensity level of energy metabolism:
- Normally, adipose tissue produces the hormone leptin, which inhibits the synthesis of neuropeptide Y (NPY) in the posterolateral ventral nucleus of the hypothalamus, reducing the feeling of hunger.
- In pathology, leptin resistance or a gene mutation develops, causing NPY synthesis to increase, creating constant hunger, enhancing appetite, and depressing the body's energy expenditure.
Pathogenetic significance and complications
The disease is chronic with periods of exacerbations, leading to early disability and increased overall mortality, affecting children and adolescents as well. The resulting disorders are divided into several groups:
- Somatic and autonomic: Vegetovascular dystonia, GI motility disorders (constipation, tendency toward irritable bowel syndrome), and respiratory failure caused by high standing of the diaphragm.
- Metabolic disorders: Insulin resistance, arterial hypertension, and diabetes mellitus.
- Impact on the central nervous system and development: In children, due to limited physical activity, higher nervous activity (HNA) processes are impaired.
- Sexual development in children: Girls show early appearance of secondary sexual characteristics and menstrual cycle irregularities; boys may experience either accelerated or delayed puberty.
Briefly: answers to topical questions
What are the endocrine and metabolic mechanisms of obesity pathogenesis?
The endocrine mechanism of obesity pathogenesis in the provided sources includes leptin, hypothyroid, adrenal, and insulin variants; the sexual (hypogonadal) mechanism is also mentioned in the source. The adrenal mechanism is caused by the excessive influence of glucocorticoids: activation of gluconeogenesis → hyperglycemia → increased glucose transport into adipocytes → activation of glycolysis in adipocytes → inhibition of lipolysis → obesity. The insulin mechanism reduces to the activation of lipogenesis in adipocytes under the influence of insulin. The hypothyroid mechanism is associated with a decrease in basal metabolism and lipolysis due to a deficiency of thyroid hormones. The sexual (hypogonadal) mechanism is associated with a decrease in the lipolytic effect of sex hormones. The metabolic mechanism is mentioned among the main mechanisms of obesity development, however, its detailed description is absent in the provided materials.
Which specific endocrine diseases lead to the development of secondary (symptomatic) obesity?
The sources include the following in the development of secondary (symptomatic) endocrine obesity:
- diseases of the hypothalamo-pituitary system;
- adrenal diseases, including hypercorticism and Cushing's syndrome;
- hypothyroid obesity;
- hypoovarian obesity.
What is the role of brown adipose tissue in the regulation of energy metabolism and the pathogenesis of obesity?
Brown adipose tissue plays a key role in the regulation of energy metabolism through non-shivering thermogenesis. In the mitochondria of this tissue, oxidation processes are uncoupled from phosphorylation due to the protein thermogenin (UCP-1), so energy is dissipated as heat rather than stored as ATP. This mechanism is especially important for maintaining thermal balance in newborns. The direct impact of brown adipose tissue dysfunction on the pathogenesis of obesity is not described in the sources.
The lipostat regulates appetite: fat releases leptin (inhibits hunger), and the hypothalamus produces neuropeptide Y (stimulates hunger). A failure of this pair leads to pathology.
Class and exam questions
What are the degrees of obesity according to the body mass index?
Three degrees are distinguished: Grade I corresponds to a BMI of 25–29.9 (overweight), Grade II to a BMI of 30–39.9 (obesity), and Grade III is diagnosed at a BMI of 40 and above (morbid obesity).
What is the difference between hypertrophic and hyperplastic obesity?
Hypertrophic obesity develops due to an increase in the size and mass of adipocytes. Hyperplastic obesity develops due to an increase in the total number of fat cells; it is less amenable to conservative treatment.
How does the «Leptin — Neuropeptide Y» loop work normally?
Excess adipose tissue releases leptin, which inhibits the production of neuropeptide Y in the hypothalamus, reducing appetite and the feeling of hunger, limiting further mass accumulation.
What are the main causes of hypothalamic obesity?
The cause is damage to neurons in the hypothalamic nuclei (e.g., ventromedial or posterolateral ventral) as a result of traumatic brain injuries, encephalitis, or tumors.
What else to study on this topic
- Endocrine and metabolic mechanisms of obesity development
- The role of insulin resistance in the formation of metabolic syndrome
- Pathogenetic features of sexual development in children with obesity
- Secondary (symptomatic) forms of obesity and their etiology
- The effect of high standing of the diaphragm on external respiration parameters
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