Leptin is a hormone secreted by adipose tissue. It is generally believed that it will participate in the regulation of sugar, fat and energy metabolism after entering the blood circulation, prompting the body to reduce food intake, increase energy release, inhibit the synthesis of fat leptin cells, and then achieve the purpose of losing weight. Scientists' research last year showed that taking leptin in infancy may fix the brain's response to appetite, so as not to overeat for life. People made this discovery in experiments on mice.
According to Professor Cauthorn, in fact, human breast milk also contains this substance. Milk containing additives will only increase the amount of things that already exist. However, this research is still in the primary stage, and it will take at least 10 years to finally develop baby food that can prevent obesity.
Professor Cauthorn's plan has caused great controversy in the scientific community, and people are most concerned about its safety, such as dosage and side effects. In addition, some critics believe that this also involves ethical issues. They believe that obesity is a disease brought by modern society, and people need to examine and change their lifestyle to avoid getting sick, not just looking for an artificial compound that can solve the problem quickly. [Edit this paragraph] Leptin-Overview 1994, American scholars cloned the obesity gene product of mice and humans for the first time, and its main function is to regulate energy balance and weight. The increase of human plasma leptin level is directly proportional to body fat weight, and the mutation of leptin and its receptor gene can lead to morbid obesity. In a 24-week study, subcutaneous injection of leptin every day can reduce weight to varying degrees. In recent years, it has been found that the ability of leptin transport to the brain in obese patients is reduced, which leads to leptin resistance in obese individuals. Therefore, some researchers are working on the research of small molecular analogues of leptin that can cross the blood-brain barrier to develop potential obesity treatment drugs. At present, the substances acting on leptin receptor are mostly synthetic short peptides, and small molecular compounds have not been reported.
Obesity has become a major factor endangering human health, and scientists have done a lot of research to find ways to repel the "enemy". British media reported on 23rd that Professor Mike Cauthorn, director of Crowley Experimental Center of Buckingham University in England, suggested adding a hormone called leptin to baby food, especially baby milk, so that babies would not have to worry about getting fat for life after eating this food.
Leptin is a hormone secreted by adipose tissue. It was generally believed that it will participate in the regulation of sugar, fat and energy metabolism after entering the blood circulation, prompting the body to reduce food intake, increase energy release, inhibit the synthesis of fat cells, and then achieve the purpose of losing weight. Scientists' research last year showed that taking leptin in infancy may fix the brain's response to appetite, so as not to overeat for life.
People made this discovery in experiments on mice. According to Professor Cauthorn, in fact, human breast milk also contains this substance. Milk containing additives will only increase the amount of things that already exist. However, this research is still in the primary stage, and it will take at least 10 years to finally develop baby food that can prevent obesity.
Professor Cauthorn's plan has caused great controversy in the scientific community, and people are most concerned about its safety, such as dosage and side effects. In addition, some critics believe that this also involves ethical issues. They believe that obesity is a disease brought by modern society, and people need to examine and change their lifestyle to avoid getting sick, not just looking for an artificial compound that can solve the problem quickly.
The latest research shows that obesity has become the main health and social burden facing Europe, and the trend of childhood obesity is particularly worrying. Britain has one of the highest rates of childhood obesity in Europe, with overweight children accounting for about 30%. [Edit this paragraph] The increase of leptin-leptin level leads to leptin resistance, which has a negative impact on myocardial muscle strength. The level of leptin in plasma is usually positively correlated with the changes of body weight, especially the adipose tissue in the body. Clinically, the serum leptin levels of obese patients are often different. Because the normal physiological function of leptin is mainly mediated by leptin receptor, the increase of leptin level in obesity directly leads to the feedback reduction of leptin receptor level or the obstruction of signal transduction after leptin receptor, which is called leptin resistance.
The emergence of leptin resistance is directly caused by the increase of circulating leptin level. To make a very appropriate analogy, the status of leptin resistance in obesity is similar to that of insulin resistance in type 2 diabetes. Leptin at physiological level can cause vasodilation and has no obvious effect on myocardial function, while leptin at pathological level can promote the production of a large number of oxidative free radicals, which in turn has obvious negative effects on myocardial muscle strength. There is evidence that the negative inotropic effect of leptin at pathological level may be realized by activating endothelin receptor (ET- 1 receptor) and its downstream reduced coenzyme II (NAPDH) oxidase. The activation of NAPDH oxidase directly produces a large number of superoxide anions. These results have been confirmed in the db/db mouse model with leptin excess. [Edit this paragraph] The decrease of leptin-leptin level leads to the loss of leptin's regulatory effect on heart function at physiological level, which leads to myocardial hypertrophy and low heart function, which is contrary to the increase of leptin level. The decrease of leptin level can also directly lead to the loss of leptin signal transduction, which leads to the loss of leptin's regulatory effect on heart function at physiological level. The author's laboratory has made an in-depth study on ob/ob obese mice with hereditary leptin deficiency. The results showed that low leptin level resulted in obvious obesity (twice the weight of wild-type mice), myocardial hypertrophy, decreased myocardial contractility, slow contraction/relaxation rate, prolonged relaxation time, calcium regulation of myocardial cells and other cardiac dysfunction in mice. Interestingly, leptin supplementation can significantly improve myocardial hypertrophy and cardiac dysfunction caused by leptin deficiency, while significantly inhibiting weight gain.
Further research results show that low leptin level directly leads to the decrease of insulin sensitivity. In 2007, the author's laboratory changed the structure of chromium complex, an insulin sensitizer, and obtained a new chromium amino acid complex (patented in the United States). We use this complex to sensitize obese leptin deficiency in obese mice. After oral administration of [45 μ g/(kg/d)] for 6 months, the myocardial function of OB/OB mice was obviously improved, and the disorder of intracellular calcium regulation was corrected, which was consistent with the improvement of myocardial insulin sensitivity. From this point of view, whether the leptin level is increased or decreased, it will lead to the disorder of leptin regulating energy and fat metabolism, thus contributing to obesity and eventually leading to type 2 diabetes. However, high-fat diet or overnutrition can lead to a sharp increase in leptin levels, and the resulting leptin resistance prevents leptin from promoting fat and energy metabolism and its related appetite suppression.