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Appetite Regulation and Adipokines

Regulatio appetitus et adipokina

For medical students2 min readUpdated 2026-10-10

Feeding behavior is governed by the integration of neural and humoral signals within the hypothalamus. A key role in this process is played by adipokines—biologically active substances produced by adipose tissue that determine the body's energy balance.

Regulation CenterThe hypothalamus integrates hunger and satiety signals.

Satiety HormonesLeptin and adiponectin are the primary metabolic regulators.

Hunger StimulatorGhrelin is produced in the GI tract and increases appetite.

PathologyAdipokine imbalance leads to insulin resistance.

Hypothalamic Control

Feeding behavior is shaped within hypothalamic nuclei, which receive impulses from peripheral nerve terminals.

Appetite Stimulators: GABA, dopamine, β-endorphin, enkephalins.
Appetite Inhibitors: Serotonin, norepinephrine, cholecystokinin, somatostatin.

Of particular importance is neuropeptide Y (NPY), which stimulates the sensation of hunger. Normally, leptin suppresses its synthesis, but when hypothalamic sensitivity to leptin decreases, NPY is disinhibited, provoking overeating.

Key Adipokines

Adipose tissue is not merely an energy depot, but an active endocrine organ:

Leptin: Synthesized by adipocytes, it decreases appetite and increases energy expenditure. Its level is proportional to fat mass.
Adiponectin: Increases tissue sensitivity to insulin. Its concentration drops in obesity.
Resistin: An insulin antagonist that inhibits cellular glucose uptake.
Ghrelin: Produced in the stomach and intestines, it is a potent hunger stimulator.

Pathophysiology of Obesity

Obesity is often associated with impaired regulatory loops:

Leptin Deficiency: Absolute or relative leptin deficiency leads to a constant sensation of hunger.
Centrogenic Mechanism: Psychogenic factors where food intake becomes a mechanism of pleasure, activating behavioral reward systems.
Metabolic Shifts: Adipokine imbalance in children and adults promotes the development of insulin resistance and disrupts free fatty acid metabolism.

Mnemonic

Leptin LEANs out appetite (decreases appetite); Ghrelin GRABs food (stimulates hunger).

Frequently asked questions

In which specific hypothalamic nuclei are the hunger and satiety centers localized?

The satiety center is localized in neurons of the ventromedial hypothalamic nucleus. The specific nuclei forming the hunger center are not detailed in the provided materials. In general, afferent impulses from peripheral nerve terminals are integrated within hypothalamic nuclei, leading to the production of mediators that stimulate appetite (GABA, dopamine) or inhibit it (serotonin, cholecystokinin).

Which biologically active substances are classified as adipokines?

The main adipokines include the following biologically active substances:

Leptin — decreases appetite and increases the body's energy expenditure;
Adiponectin — correlates with tissue sensitivity to insulin;
Resistin — a cysteine-rich protein functioning as an insulin antagonist;
Ghrelin — regulates energy balance and directly stimulates appetite.

What gastrointestinal hormones, besides ghrelin and cholecystokinin, participate in forming the sensation of satiety?

The provided sources do not list a verified set of GI hormones participating in satiety formation other than cholecystokinin. It is confirmed that:

Cholecystokinin acts as an appetite inhibitor and establishes the feeling of fullness;
Somatostatin is also listed as an appetite inhibitor that produces satiety;
Incretins (GLP-1 and glucose-dependent insulinotropic polypeptide) are gut hormones released by the small intestine in response to food intake that potentiate glucose-stimulated insulin secretion, though their direct role in satiety is not specified in the sources.

What are the main pathogenetic mechanisms for the development of obesity?

The main pathogenetic mechanisms of obesity development include:

Centrogenic mechanism — related to psychiatric disorders and a persistent drive to consume food;
Leptin mechanism — arising from absolute or relative leptin deficiency;
Insulin mechanism — caused by an increase in number or hypersensitization of insulin receptors, which activates lipogenesis;
Hypothyroid mechanism — developing due to insufficient thyroid hormone action, which suppresses metabolism and lipolysis.

Why doesn't leptin help with weight loss in obesity?

In obesity, a decrease in hypothalamic sensitivity to leptin (leptin resistance) frequently develops. As a result, the 'satiety signal' is not perceived, and the synthesis of hunger-stimulating neuropeptide Y is not suppressed.

What is the difference between the actions of leptin and resistin?

Leptin promotes appetite suppression and energy expenditure, whereas resistin acts as an insulin antagonist and impairs normal cellular glucose uptake.

How does ghrelin level change throughout the day?

Ghrelin levels are higher while fasting, which stimulates foraging and feeding behavior. Following a meal, its concentration decreases, contributing to the sensation of satiety.

Go deeper

Pulsatile pattern of leptin secretion and its nocturnal peak.
Role of leptin as a growth factor (angiogenesis, cell proliferation).
Impact of adiponectin on the development of type 2 diabetes mellitus.
Genetic aspects of ghrelin gene mutations.
Interrelationship between adipocyte differentiation and resistin synthesis.