Hormone leptin (the "satiety hormone"), is a hormone made by fat cells that regulates the amount of fat stored in the body. This is done by adjusting both the sensation of hunger, and adjust energy expenditure. Hunger is inhibited (satiety) when the amount of fat stored reaches a certain level. Leptin is secreted and then circulate throughout the body, eventually activating leptin receptors in the arcuate nucleus of the hypothalamus. Increased energy expenditure either by signaling to the brain, and directly through leptin receptors on peripheral target. Effect of leptin is in contrast to ghrelin, "hunger hormone". Ghrelin is a receptor on brain cells is the same as the leptin receptor, so that these cells receive competing signals of satiety and hunger. Leptin and ghrelin, along with many other hormones, participate in the complex process of energy homeostasis.
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| Leptin PDB rendering based on 1ax8. |
In 1994, the ob gene isolated, Friedman reported the discovery of the gene. At the suggestion of Roger Guillemin, Friedman named this new hormone "leptin" (lepto, the Greek word for thin). Leptin is the first cell-derived hormones fat to be found. Subsequent research confirms that the db gene encodes the leptin receptor and is expressed in the hypothalamus, the brain region known to regulate hunger and weight gain.
Recognition of scientific progress
Coleman and Friedman has received many awards acknowledging their role in the discovery of leptin, Including the Gairdner Foundation International Award (2005), the Shaw Prize (2009), the Lasker Award, the BBVA Prize and the King Faisal International Prize
The discovery of leptin was also documented in a series of books including Fat: Fight the Obesity Epidemic by Robert Pool, The Hungry Gene by Ellen Ruppel Shell, and Rethinking Thin: The New Science of Weight Loss and Diet Myths and Realities by Gina Kolata Fat:. Fight the Obesity Epidemic and Rethinking Thin: The New Science of Weight Loss and the Myths
Site synthesis
Leptin is produced mainly in adipocytes of white adipose tissue. It is also produced by brown adipose tissue, placenta (syncytiotrophoblasts), ovaries, skeletal muscle, stomach (lower part of fundic glands), mammary epithelial cells, bone marrow, pituitary, liver, gastric chief cells and P / cell D1.
Variations in blood levels of physiological
Leptin circulates in the blood in free form and bound to the protein. Leptin levels vary exponentially, not linearly, with fat mass. Leptin levels in the blood is higher between midnight and early morning, possibly suppress appetite at night. The diurnal rhythm of blood leptin levels can be modified by meal-time.
Under certain conditions
In humans, there are examples where it looks Leptin strictly separate from the role of communication between the nutritional status of the body and the brain and is no longer correlated with the level of body fat:
- Decreased leptin levels after short-term fasting (24-72 hours), even when the changes in fat mass was not observed. Leptin plays an important role in the adaptive response to starvation. In obese patients with obstructive sleep apnea, leptin levels increased, but decreased after the administration of continuous positive airway pressure. In non-obese individuals, however, deep sleep (ie, 8-12 hours of uninterrupted sleep) may increase leptin levels to normal.
- Leptin levels decreased with sleep deprivation. However, recent research suggests that sleep deprivation is associated with higher levels of leptin.
- Leptin levels increased perceived emotional stress.
- Leptin levels decreased or increased by an increase in testosterone or estrogen levels, respectively.
- Leptin levels are chronically reduced by physical exercise.
- Leptin levels increase with dexamethasone.
- Leptin levels increased by insulin.
- Leptin levels are increased in obesity paradox.
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| A comparison of a mouse unable to produce leptin, resulting in obesity (left), and a normal mouse (right) |
Effects
Central (hypothalamic) Effect: Two white mice either with the same size ears, black eyes, and a pink nose: The body of the mouse on the left, however, is about three times the width of a normal sized mouse on the right.
Comparison of mouse unable to produce leptin, thus obesity (left), and a normal mouse (right) Leptin works on receptors in the hypothalamus, where it inhibits hunger
Effects of peripheral
In the outskirts of leptin are modulators of energy expenditure, metabolic modulators between fetus and mother, permissive factor in puberty, driving the immune cells, activators of beta islet cells, and growth factors. Furthermore, interacting with other hormones and energy regulators. Insulin, glucagon, growth factors such as insulin, growth hormone, glucocorticoids, cytokines, and metabolites
Circulatory system
The role of leptin receptor / leptin in modulating T cell activity in the immune system was shown in experiments with rats. It modulates the immune response to atherosclerosis, obesity is a predisposing factor.
Reproductive System
Ovulation cycleLeptin is required for male and female fertility. Ovulatory cycles in women associated with energy balance (positive or negative depending on whether women or weight loss) and energy flux (how much energy is consumed and expended) over the energy status (fat content). When the energy balance is highly negative (meaning women starving) or energy flux is very high (meaning women exercising at extreme levels, but still consume enough calories), ovarian cycle stops and females stop menstruating. Only if women have a very low body fat percentage sense energy status affect menstruation. Leptin levels outside the ideal range can have a negative effect on egg quality and outcomes during in vitro fertilization.
GestationThe placenta produces leptin. Leptin levels increase during pregnancy and after childbirth fall. Leptin is also expressed in the fetal membranes and uterine tissue. Uterine contractions inhibited by leptin. Leptin plays a role in hyperemesis gravidarum (severe morning sickness of pregnancy),LactationImmunoreactive leptin has been found in human breast milk; and leptin from mother's milk have been found in the blood of infant mammals.PubertyLeptin along with kisspeptin control the onset of puberty. High levels of leptin, as usually observed in obese women, can trigger a cascade of neuroendocrine lead to early menarche. This in turn can lead to shorter stature as estrogen secretion begins at the time of menarche and cause premature epiphyseal closure.
Bone
Leptin's ability to regulate bone mass was first recognized in 2000. Leptin may affect bone metabolism through direct signals from the brain. Leptin decreases cancellous bone, but increased the cortical bone. a mechanism to increase bone size, bone and thus resilience, to cope with increasing body weight. There is potential for the treatment of diseases of bone formation by leptin.
Brain
Leptin deficiency has been shown to alter brain proteins and nerve function obese rats can be restored by leptin injection. In humans, low circulating plasma leptin have been associated with cognitive changes associated with anorexia, depression, and HIV.
The immune system
Factors influencing acute leptin levels are also factors that affect other markers of inflammation, eg, testosterone, sleep, emotional stress, caloric restriction, and body fat levels. While it is well established that leptin is involved in the regulation of the inflammatory response,
Both in terms of structure and function, the role of leptin in response stres.konsentrasi Increased leptin associated with increased white blood cell count in men and women.
Similar to what was observed in chronic inflammation, chronically elevated leptin levels are associated with obesity, overeating, and related inflammatory diseases, including hypertension, metabolic syndrome, and cardiovascular disease. However, while leptin is associated with body fat mass, the size of individual fat cells, and acts overeating, it is interesting that it is not affected by exercise.
ObesityAlthough leptin reduces appetite as a circulating signal, obese people generally show higher circulating leptin concentrations than individuals with normal weight for a higher percentage of their body fat. These people show resistance to leptin, similar to insulin resistance in type 2 diabetes, with elevated levels failed to control hunger and modulate their weight. Leptin is known to interact with amylin, a hormone involved in gastric emptying and creates a feeling of fullness. When both leptin and amylin given to obese, leptin-resistant mice, sustained weight loss seen. Because the apparent ability to reverse leptin reisistance, amylin has been suggested as a possible therapy for obesity. It has been suggested that the primary role of leptin is to act as a hunger signal when a low level, to help keep fat reserves to survive during times of famine, rather than a signal of satiety to prevent overeating. allows energy to be stored efficiently when food is abundant would be advantageous in populations where food can often be scarce.
Weight lossWeight loss diet that decreased circulating levels of leptin. This decrease causes a reversible decrease in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increased muscle efficiency and parasympathetic tone. The result is that someone who has lost weight have a lower rate of basal metabolism than individuals at the same weight who has never lost weight; The leptin-mediated changes, homeostatic response intended to reduce energy expenditure and increase the weight back. Many of these changes are reversed by peripheral administration of recombinant leptin to restore the pre-diet levels.The decrease in circulating levels of leptin are also changes in brain activity in regions involved in the control regulation, emotional, and cognitive appetite reversed by administration of leptin.http://www.google.com
References:
id.wikipedia.org/wiki/Leptin
en.wikipedia.org/wiki/Leptin
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