LEPR

SNP Table

variant	genotype	frequency	risk allele
rs1137100
rs1805094
rs4655802
rs1805134
rs10889549
rs11590603
rs12402567
rs17412368
rs17412403
rs17412682
rs17412723
rs2025803
rs2025805
rs61779815
rs6698653
rs7513047
rs7524834
rs7542824
rs9661436
rs10749753

22829 associated SNPs in total

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Summary Blog Articles GHR Function Frequently Asked Questions

Summary

The LEPR gene codes for the leptin receptor [R].

Leptin is one of the two major hormones that control how much food you eat. When leptin binds to its receptor, it promotes a feeling of fullness that encourages you to stop eating [R].

Leptin is mainly released by fat tissue. Leptin levels tend to decrease when there's less fat tissue [R].

LEPR variants are linked to many conditions, including [R, R, R]:

Weight gain and obesity
Diabetes
Heart disease

Protein names

leptin receptor [Source:HGNC Symbol;Acc:HGNC:6554]

Found in These Blog Articles

A Gene That Controls Hunger and Satiety (LEPR)

LEPR encodes the receptor for leptin, a hormone that lets us know when we’ve had enough to eat. What is its role in obesity?

GHR Function

The leptin receptor is turned on (activated) by a hormone called leptin that attaches (binds) to the receptor, fitting into it like a key into a lock. Normally, the body's fat cells release leptin in proportion to their size. As fat cells become larger, they produce more leptin. This rise in leptin indicates that fat stores are increasing. In the hypothalamus, the binding of leptin to its receptor triggers a series of chemical signals that affect hunger and help produce a feeling of fullness (satiety).

More Information

LEPR encodes the protein for the leptin receptor, which is involved in regulating body weight. When leptin binds to its receptor, it triggers a series of chemical signals that affect hunger and helps you feel full (R).

Leptin receptor deficiency is associated with excessive hunger and weight gain (R).

At least 18 LEPR gene mutations that cause leptin receptor deficiency have been identified; this disorder is associated with excessive hunger, massive weight gain, and reduced production of hormones that direct sexual development (hypogonadotropic hypogonadism). Some of the mutations result in less receptor protein getting to the cell surface where leptin binding takes place. The receptors that get to the cell surface may bind to leptin, but their signaling function is impaired. The resulting shortage of leptin signaling disrupts normal feelings of hunger and satiety, leading to extreme weight gain. Because hypogonadotropic hypogonadism occurs in leptin receptor deficiency, researchers suggest that leptin receptor signaling is also involved in regulating the body's response to hormones that control sexual development, and that this response is affected by LEPR gene mutations. However, the mechanism of this effect is unknown.

The LEPR gene provides instructions for making a protein called the leptin receptor, which is involved in the regulation of body weight. The leptin receptor protein is found on the surface of cells in many organs and tissues of the body, including a part of the brain called the hypothalamus. The hypothalamus controls hunger and thirst as well as other functions such as sleep, moods, and body temperature. It also regulates the release of many hormones that have functions throughout the body. The leptin receptor is turned on (activated) by a hormone called leptin that attaches (binds) to the receptor, fitting into it like a key into a lock. Normally, the body's fat cells release leptin in proportion to their size. As fat cells become larger, they produce more leptin. This rise in leptin indicates that fat stores are increasing. In the hypothalamus, the binding of leptin to its receptor triggers a series of chemical signals that affect hunger and help produce a feeling of fullness (satiety).

Frequently Asked Questions

Why Are Alleles for This SNP Different Elsewhere? Major vs. Reference Allele Is My Variant Good or Bad? SNP vs. Mutation

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