Leptin, often called the “satiety hormone,” is an adipokine (signaling molecule produced by fat cells) whose main function is to regulate energy and fat stores. In a metabolically healthy person, a temporary increase in caloric intake (such as after a big meal) corresponds to an increase in leptin production. This prompts the hypothalamus to send signals that promote satiety, which cues one to stop eating.
Leptin was the first adipokine to be discovered (in 1994) and changed how scientists view fat tissue. Fat stores were previously thought to be inert tissue that did not cause any direct harm. Upon the discovery of leptin and its related genes, scientists learned that excess adipose tissue is actually metabolically active, releasing several hormones (adipokines) and inflammatory enzymes. Consequently, it is now considered an endocrine organ.
Although leptin suppresses appetite, one can become leptin resistant, feeling hungry even when one consuming enough calories to maintain metabolic requirements. In a way that is analogous to insulin resistance, leptin resistance occurs in obesity: the higher the fat stores, the more leptin produced. In fact, leptin varies exponentially (as opposed to linearly) with adipose tissue. This means that changes in fat mass profoundly affect leptin levels. Over time, as leptin increasingly circulates in blood, the brain eventually becomes resistant to its effects. As a result, one becomes inclined to overeat, unable to experience satiety and therefore feeling hungry even when leptin levels are high! This is referred to as leptin resistance.
An increase in leptin (in the short term) follows an increase in caloric intake. This promotes satiety and signals one to stop eating. However, in the long term, a chronic increase in leptin can be attributed to excess body fat, estrogen (endogenous and exogenous), insulin (leptin is released dose-dependently in response to insulin), stress, and some steroid medications such as dexamethasone.
Loss of fat tissue, reduction in caloric intake via dieting and fasting, testosterone (which is anabolic – this increases appetite), and ghrelin (the hunger hormone) are all factors that lower leptin. Sleep deprivation, which upregulates appetite, is a reason why sleep loss is linked to cravings, and also impacts levels.
Factors that impact leptin sensitivity include:
- High Fructose Corn Syrup (this blocks leptin receptors)
- High Triglyceride levels block leptin’s ability to reach the hypothalamus
- Estrogen deficiency: the leptin-estrogen link may cause menstrual cravings
- Lectins in grains bind to leptin receptors, inducing leptin resistance
Leptin receptors are found in several tissues besides the hypothalamus, including endothelial, muscle, placental, and liver cells. Although its appetite-regulating effects are well established, it is known to play a role in fertility and puberty; however, its other functions are not fully understood.
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