Leptin is produced mainly in white adipose (fat) tissue, and a very small amount in brown adipose (fat) tissue. It has been determined that it is an effective obesity-preventing factor. It is also released from the placenta.
It is found in the blood free and bound to protein. Its free form is responsible for its activity. In obese individuals, most of the leptin in the serum is in free form. Leptin binding protein regulates the half-life and biological activity of leptin. Its life span is about 25 minutes in humans. Leptin is largely excreted by the kidneys. Although the blood plasma concentration of leptin is not constant, it changes throughout the day. Studies performed to determine the amount of leptin at different times of the day have shown variability. While it was reported that it peaked after midnight and decreased to the lowest levels towards sunrise, in another study, it was reported that it was highest at night, peaked between midnight and early morning, and decreased to the lowest levels in the afternoon.
It is stated that it has an appetite-reducing effect during night sleep, and its increase at night may be due to the effect of food intake and hyperinsulinemia (high insulin in the blood) throughout the day. in the central nervous system and other tissues (lung, kidney, liver, heart, endocrine (hormone-secreting) part of the pancreas, adrenal (adrenal) glands, uterus (uterus), ovary (ovary), testis, (male gland), hematopoietic (blood forming) cells interact with receptors in skeletal muscle. The main site of action of leptin receptors is the hypothalamus (an area in the brain). Control of appetite, reproduction, and growth is in this area.
(1) Leptin is found in adipose (fat) tissue. It stimulates lipolysis (fat breakdown) and prevents insulin release from beta cells.
- Sympathetic nervous system activation
- Increases energy expenditure.
- Leptin inhibits feeding via hypothalamic receptors and decreases body weight by increasing thermogenesis (heat production).
- Leptin concentration in weight while it decreases with weight loss, it increases after weight gain. The region that manages the hormone system) plays an important role in the regulation of functions and insulin resistance. Growth hormone affects the regulation of thyroid, adrenal (adrenal gland) system, immune system functions. It takes part in the regulation of gastrointestinal system functions(1).
Obesity, diabetes and infertility occur in cases of deficiency or resistance of leptin due to its functions related to appetite, blood sugar balance and reproduction.
It also has strong effects on fatty acid metabolism and endocrine (hormone) axis.
It has been shown to increase the use of fats as an energy source by increasing the use of oxygen.
Leptin, by increasing the capacity of fatty acid oxidation and triacylglyserol (storage fat) stores, it deeply affects skeletal muscle fatty acid metabolism.(2)
Body weight is the most important factor regulating leptin secretion. There is a direct proportion.
Small changes in body weight cause large changes in serum leptin level. This situation explains that leptin secretion varies depending on factors other than stored fat mass
One of the factors determining leptin level is gender. In addition to higher leptin blood levels in women due to the high fat content and different distribution, the suppression of leptin level by testosterone in men is a factor that plays a role in this situation.(1)
The most important determinant of leptin level in women is BMI (body mass). index) while it is waist circumference in men.(2)
The effects of leptin and leptin deficiency Blood samples taken from mice and obese people were examined for the purpose of research, and blood leptin levels were found to be high in obese people. Elevations in leptin levels vary in proportion to the fat mass. In this case, the concept called leptin resistance has emerged. It is not known for sure whether it plays a role or not.
Abesity (obesity) developing as a result of leptin mutation has been found in very few of the hundreds of studies. Defects in the carriers (there is a selective barrier) and at the receptor level in the central nervous system cause resistance to leptin. .
As a result of the studies, it is thought that the mutation occurring in the currently known leptin or its receptors rarely causes obesity and this is not the cause of obesity in the entire obese population.(1)
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