Diagnostic criteria and epidemiology
In an adult with a body weight of 70 kilograms, the normal amount of fat tissue in storage depots 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 the age of 50.
The primary diagnostic tool is the body mass index (BMI). It is calculated by dividing weight (in kilograms) by height squared (in meters).
Interpretation of BMI results:
- 20–24.9 kg/m² — physiological norm.
- 25–29.9 kg/m² — overweight.
- Over 30 kg/m² — diagnosed obesity.
Cellular mechanisms of adipose tissue growth
The process of the pathological increase in fat depot volume occurs in two sequential stages:
- Hypertrophy. At the initial stage, there is a simple increase in the size of pre-existing fat cells. Adipocytes actively store lipids and stretch.
- Hyperplasia. When the volume reserve of existing cells is exhausted, the differentiation process is triggered. Precursor cells (preadipocytes) transform into new, additional adipocytes to accommodate the continuously incoming fats.
Genetics: the ob gene and the hormone leptin
A key role in the genetic control of body weight is played by the ob gene (from obese gene), which is present in both humans and animals. The product of this gene's expression is a protein consisting of 145 amino acids — leptin (from the Greek leptos — thin).
Leptin is synthesized directly by fat cells and secreted into the bloodstream, functioning as a hormone that strictly controls adipose tissue mass.
Medical practice describes five distinct mutations of the leptin gene. This genetic phenotype is characterized by:
- Increased lipid deposition in depots.
- Polyphagia (excessive, uncontrolled food intake).
- Low physical activity.
- Rapid development of type 2 diabetes mellitus.
Biochemical pathogenesis develops according to two scenarios:
- Absolute deficiency (ob gene defect): The concentration of leptin 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 sufficient or even excessive amounts, yet the sensitivity of cellular receptors to leptin is sharply reduced. Protective mechanisms for weight loss are triggered only at extremely high concentrations of the hormone in the blood.
Endocrine role of adipocytes and metabolic syndrome
Modern biochemistry classifies adipocytes not only as energy storage depots, but also as full-fledged secretory cells. They continuously release hormones (including leptin) and cytokines. In obesity, this delicate secretory balance is disrupted, provoking the development of peripheral tissue insulin resistance and, consequently, diabetes mellitus.
The pathological increase in adipose tissue mass frequently becomes the primary cause of metabolic syndrome — a severe complex of interrelated disorders. Its structure includes:
- Obesity.
- Type 2 diabetes mellitus.
- Hypertension.
- Atherosclerosis.
Biochemical blood analysis in metabolic syndrome consistently shows 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 an endocrine profile (e.g., in uncompensated hypothyroidism).
Briefly: answers to topical questions
What specific hormones and cytokines do adipocytes secrete besides leptin?
Aside from leptin, the sources explicitly name adiponectin, which is produced by visceral adipocytes. Leptin and adiponectin regulate appetite, fat composition, insulin sensitivity, and inflammation.
It is also noted that adipose tissue, acting as an endocrine organ, produces cytokines, adipokines, fatty acids, and reactive oxygen species (ROS). These pro-inflammatory mediators exert a negative impact on joint tissues, provoking and maintaining low-grade "metainflammation".
Specific names of cytokines are not listed in the cited sources.
BMI thresholds are easy to remember using the rule of fives: up to 25 is normal, the next 5 units (up to 30) are simply overweight, and anything above 30 is already obesity.
Class and exam questions
What is leptin resistance?
This is a pathological state in which adipocytes secrete a sufficient amount of leptin, but tissue receptors lose their sensitivity to it. Due to this high perception threshold, the body fails to receive the signal of satiety and adequate fat reserves.
How does the structure of adipose tissue change in obesity?
First, hypertrophy occurs—existing adipocytes increase in size. Then, when their volume reaches its limit, hyperplasia begins—preadipocytes transform into new fat cells.
What blood changes are characteristic of metabolic syndrome?
In metabolic syndrome, the blood concentrations of fatty acids, free cholesterol, and total lipids significantly increase.
What else to study on this topic
- Mechanisms of preadipocyte differentiation during adipose tissue hyperplasia
- Biochemical structure of leptin and its interaction with receptors
- Pathogenesis of insulin resistance in cytokine imbalance
- Differences between primary nutritional obesity and secondary obesity
- Impact of polyphagia on the development of type 2 diabetes mellitus
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