Diagnostic Criteria and Epidemiology
In an adult weighing 70 kilograms, the normal fat tissue depot is approximately 10–11 kilograms. The physiological increase in the number of fat cells continues from birth until roughly 22–25 years of age, after which their number stabilizes. However, the problem of pathological lipid accumulation is extremely widespread, being detected in nearly 50% of individuals over 50 years of age.
The main diagnostic tool is the body mass index (BMI). It is calculated by dividing weight (in kilograms) by the square of height (in meters).
Interpretation of BMI Results:
- 20–24.9 kg/m² — physiological norm.
- 25–29.9 kg/m² — overweight.
- Greater than 30 kg/m² — diagnosed obesity.
Cellular Mechanisms of Adipose Tissue Expansion
The pathological enlargement of the fat depot occurs in two consecutive stages:
- Hypertrophy. Initially, there is a simple increase in the size of existing fat cells. Adipocytes actively store lipids and stretch.
- Hyperplasia. When the volumetric reserve of existing cells is exhausted, a differentiation process is triggered. Precursor cells (preadipocytes) transform into new, additional adipocytes to accommodate the continuously incoming fats.
Genetics: The ob Gene and Leptin
A key role in the genetic control of body weight is played by the ob gene (obese gene), which is present in both humans and animals. The product of this gene's expression is a 145-amino-acid protein called leptin (from the Greek leptos — thin).
Leptin is synthesized directly by fat cells and secreted into the bloodstream, acting as a hormone that strictly controls adipose tissue mass.
Five different mutations of the leptin gene have been described in medical practice. This genetic phenotype is characterized by:
- Increased lipid deposition in fat depots.
- Polyphagia (excessive, uncontrolled food intake).
- Low physical activity.
- Rapid development of type 2 diabetes mellitus.
Biochemical pathogenesis develops via two scenarios:
- Absolute deficiency (ob gene defect): Leptin concentration in the blood drops to a minimum. The central nervous system perceives this as a critical signal of extreme energy reserve depletion. In response, mechanisms to increase appetite are activated, inevitably leading to weight gain.
- Leptin resistance: Fat cells synthesize the hormone in adequate or even excessive amounts, but the sensitivity of cellular receptors to leptin is sharply reduced. Protective weight-loss mechanisms are triggered only at extremely high blood concentrations of the hormone.
Endocrine Role of Adipocytes and Metabolic Syndrome
Modern biochemistry classifies adipocytes not only as energy storage depots but also as fully functional secretory cells. They continuously release hormones (including leptin) and cytokines. In obesity, this delicate secretory balance is disrupted, provoking insulin resistance in peripheral tissues and, consequently, diabetes mellitus.
Pathological increases in adipose tissue mass often become the root cause of metabolic syndrome — a severe complex of interrelated conditions. Its structure includes:
- Obesity.
- Type 2 diabetes mellitus.
- Hypertension.
- Atherosclerosis.
Blood chemistry panels in metabolic syndrome consistently show high concentrations of fatty acids, cholesterol, and other lipid fractions.
Note: Primary obesity should be differentiated from secondary obesity, which develops as a consequence of another underlying condition, most commonly of endocrine origin (e.g., uncompensated hypothyroidism).