How Leptin Controls Appetite?
Leptin is a hormone with many functions. It is mostly known for its role in enhancing satiety and prolonging starvation. It is synthesized from adipocytes and is controlled by the concentration of fat mass. The fat-loving peptide’s role in inhibiting hunger is maintained solely by the concentration of fat cells. Leptin has two main action points on the hypothalamus.
The first is its action in the lateral hypothalamus, which suppresses hunger and feeding. The second is its action in the medial hypothalamus, which stimulates satiety. Both functions are crucial in appetite regulation.
What Stimulates Leptin Secretion?
The increasing number of fat storage cells triggers the secretion of leptin. Your body converts excess glucose into triglycerides in a process called lipogenesis when there is a spike of sugar in your bloodstream. The created fat mass is stored in fatty cells called lipocytes contained in the adipose tissue. When the concentration of these fat cells increases, leptin synthesis commences. Hormonal Harmony (HB-5) contains Leptin hormone which sends a signal to the hypothalamus to indicating that there are enough fat reserves. Its effect on the hypothalamus also suppresses appetite and enhances satiety.
Other biomolecules also stimulate the secretion of leptin. For instance, insulin not only signals leptin’s release but also prompts its synthesis in mature adipocytes. While the exact mechanism of insulin’s role in leptin secretion remains unknown, the two hormones work hand in hand in regulating energy balance after a meal.
Insulin is vital in enhancing lipogenesis. The continued synthesis of the fat mass sustains the synthesis of leptin. Aside from insulin, estrogen also stimulates the secretion of leptin. Both hormones work together in energy expenditure, appetite reduction, and reproduction.
There are also negative feedbacks pathways that stimulate the release of the fat-loving peptide. For instance, when ghrelin, serotonin, and glucocorticoids are inhibited, leptin is secreted. These hormones have an opposite effect to the starvation hormone. They stimulate hunger.
Action on the Hypothalamus In the lateral hypothalamus, leptin binds to receptors in the satiety and feeding centers to suppress appetite. It also stimulates certain neuroendocrine functions vital in glucose homeostasis. Excess glucose is converted to glycogen and stored in the liver, and the rest is converted into fatty acid and stored in the adipose tissue.
The process sustains the release of the hunger hormone. After a meal, glucose levels increase in the blood triggering the release of insulin. The presences of insulin and leptin inhibit the release of glucocorticoids. Leptin also inhibits serotonin, an appetite stimulator, outside of the hypothalamus.
Additionally, the action of leptin on the lateral hypothalamus affects the mesolimbic dopamine pathways to suppress your desire for food. Leptin’s effect in the ventromedial nucleus of the hypothalamus is energy expenditure. The brain maintains the hormone’s function in energy storage for its long-term fuel reserves.
When the levels of adipose cells reduce, leptin concentration also goes down. Appetite Suppression Leptin acts in response to body fat mass. When your fat mass levels drop, leptin is inhibited, and ghrelin, the primary hormone that stimulates hunger, is released. The action of ghrelin is sustained until fatty acids increase. The degree of leptin’s secretion is dependant on the concentration of adipocytes.
The more fat cells available, the higher the stimuli of leptin secretion. In other words, the brain interprets high levels of leptin as satiety and maintains a no hunger state. For this reason, leptin is rightly called a fat reporter instead of an appetite suppressant. Leptin’s Appetite Effects in Obesity Obese individuals have a higher fat mass. As a result, leptin is constantly synthesized and released in the blood. The impact of this condition is leptin resistance.
Conclusion on How Leptin Hormone Works
The hormone’s continuous release interferes with its function in regulating appetite and glucose homeostasis. The increase also triggers insulin resistance. The condition inhibits the body’s ability to use stored energy. The reason why obesity always causes insulin resistance partially stems from leptin’s out-of-control levels.
Thus, high concentrations of leptin results in uncontrolled hunger and poor energy regulation. The role of leptin in energy expenditure also sustains appetite suppression. Together with insulin and estrogen, leptin inhibits feelings of hunger and uphold fat storage and energy use. Overall, leptin’s secretion is a signal for starvation mode.
The brain interprets its presence as an abundance of energy that requires expulsion. The hormone is an appetite inhibitor. The only exemption to the rule is extremely high concentrations of mature fat cells.
