Protein product of obesity gene synthesized and secreted by adipocytes.

Regulates food, intake, and energy expenditure through effects in the CNS.

An adipokine produced in subcutaneous and visceral adipose tissue.

Leptin is a hormone produced by fat cells and acts as a long-term internal measure of energy state. 

The storage of excess triglycerides leads to the expansion of lipid droplets during feeding, and as a result, adipocytes  secrete leptin into the circulation.

Leptin, is made predominantly by adipose cells and enterocytes in the small intestine, 

The type I cytokine leptin produced mainly by adipocytes.

Leptin does not induce satiety, but low leptin levels signal low energy stores and starvation.

When leptin levels are low, energy expenditure is reduced and hunger is increased.

After crossing the blood brain barrier, leptin inhibits orexigenic neurons in the hypothalamus, by binding to the long form of leptin receptor, which is present on the surface of these neurons.

Leptin has the effect of increasing energy expenditure and decreasing food intake.

As circulating leptin levels increase, the hormone becomes less effective at inhibiting orexigenic neurons.

Leptin resistance is present with obesity such  that exaggerates administration does not lead to appetite suppression or weight loss, except in persons with a rare leptin deficiency.

Leptin reduces appetite in response to feeding, but obese people develop a resistance to leptin. 

Genetic deficiency of leptin or its receptor fools the brain into thinking that stores are absent, resulting in extreme hunger and obesity.

Congenital leptin deficiency is an autosomal recessive disorder in which loss of function variants in the leptin gene result in the complete absence of leptin, causing severe early onset obesity.

There are 38 known variants in the lepton receptor gene that causes severe, early on said, obesity, and type two diabetes.

A key product of the obese gene.

The dose-response relationship for leptin ranges from low levels seen in fasting to normal levels seem in fed, non-obese individuals.

The role of leptin in maintaining energy balance is asymmetric: low levels promote restoration of fat stores, where as high levels weakly resist obesity.

Leads to suppression of appetite and reduction of food intake.
Acquired leptin resistance due to obesity, is characterized by increased levels of serum leptin.
increased high leptin levels that persist lead to partial antagonism and reduced bioactivity.

When sufficient food  has been consumed and leptin is high, then the satiety center is stimulated and sends impulses that inhibit the feeding center. 

The more adipose tissues present the more leptin is produced.

This overproduction of leptin will cause the hypothalamus to become resistant to leptin and so, although the adipose cells are producing leptin, the body will not understand that it should stop eating, and will produce a perpetual cycle for those that are obese.

Leptin, an appetite-regulating hormone, is not triggered following consumption of fructose.

In some this may create an unsatisfying feeling after consumption which might promote binge behavior that culminates in an increased blood triglyceride level arising from fructose conversion by the liver.

Leptin resistance occurs with obesity as reflected by elevated concentrations with higher fat mass.

Has an active role in cytokine adipokine metabolism, and may be involved in the development of cardiovascular disease and frailty.

A signal of the energy state of the body.

Leptin is a mediator between muscle mass and adipose tissue.

Exerts its function as a satiety signal in the hypothalamus.

Signals long-term calorie intake and fat stores to the hypothalamus and modifies food consumption and energy expenditure.

Leptin-sensitive neurons in the hypothalamus regulate appetite and body weight. 

Levels increase in obesity and decrease with fasting.

Obese people tend to have raised levels of the hormone leptin, which is secreted by adipose tissue and under normal circumstances increases ventilation. 

May have beneficial effects on brain development and function.

Maybe partially mediated via the release of pro-inflammatory cytokines such as TNF, iIL-1 and IL-6.

May mediate structural and functional changes in the hippocampus and improve memory function.

Concentrations are strongly associated with female sex.

Body mass index correlates well with leptin concentrations as does skinfold-thickness measurements.

Most obese persons have hyperleptinemia proportionate to body fat.

Increased serum levels associated with psoriasis.

Leptin expression is enhanced in the skin of patients with active psoriasis, as it induces pro inflammatory response in dermal fibroblasts, keratinocytes, and leptin deficiency ameliorates psoriasis.

Higher baseline concentrations are associated with reduced incidence of dementia and Alzheimer’s disease (Lieb W).

Leptin elevation is noted in older men with higher risk of cardiovascular death.

High leptin levels may be a biomarker for cardiovascular mortality in men, particularly in those with obesity.

Considered a component of the metabolic syndrome which may be associated with increased risk of death.

Leptin, an adipokine promotes inflammation in keratinocytes and dermal fibroblasts and probably accounts for the fact that obesity  adversely affects the course of psoriasis.

Leptin and insulin act to decrease hyperphosphorylation of tau, the primary component of the neurofibrillary tangle, the second major histopathological finding in Alzheimer’s disease.

Increases apolipoprotein E dependent beta-amyloid uptake into brain cells and reduce brain extracellular concentrations of beta amyloid, a major component neuritic plaques that are the hallmark of AD.

Congenital leptin deficiency associated with early onset of extreme obesity, marked hyperphagia, metabolic and hormonal abnormalities.

Congenital leptin deficiency associated with undetectable or very low levels of leptin in the circulation.

Elevated levels predictive of cardiovascular mortality, only in men (Batsis JA et al).

During infection by a pathogen, leptin synthesis changes and a reduction in food intake occurs.

This is to decrease the likelihood of ingesting another pathogen as well as preserving receptors critical for pathogen sensing, from sensing pathogenic nutrients instead.

Metreleptin is the pharmacologic substitute for leptin.

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