Now is proved beyond doubt that overweight individuals are prone for several diseases and suffer form morbidities. About 80 percent of the most common diseases are linked to obesity and a sedentary lifestyle.
Obese people are at an increased risk for cardiovascular diseases, vascular diseases, hypertension, diabetes and cancer. Weight loss and physical activity help to counteract this. Women who lose weight lower their breast cancer risk. Regular physical activity lowers the risk of developing breast, colorectal and cervical cancers.
Combination of physical activity and calorie restriction keeps in a more favourable relation of the two hormone levels that play a crucial role in energy metabolism and immune modulation. Leptin and adiponection are two important hormones in this respect, apart from a number of hormones produced from adipose tissue.
In an interventional study, it has been seen that leptin production considerably decreased, most noticeably (up to 40 percent) in the diet+exercise group; whereas adiponectin production increased most in women who were on a reduced calorie diet only.
The more was the weight loss, the more was the increase in adiponectin levels and the more decrease in leptin levels. Some of these participants reached a 20 percent increase in adiponectin levels and their leptin decreased by more than 50 percent.
Leptin production appears to be influenced by mere changes of body composition, because in the exercise intervention group, participants gained muscle mass also without losing weight.
The health-promoting effect of adiponectin is regarded as established by numerous studies now. Lower leptin levels, on the other hand, offer less growth incentives for tumour cells.
Adipose tissue is no longer considered to be solely an energy storage, but responsible for important endocrine functions, which are primarily mediated by a network of various soluble factors derived from fat cells, called adipocytokines.
Leptin, adiponectin, and resistin are produced by the adipose tissue. The protein leptin, a satiety hormone, regulates appetite and energy balance of the body.
In addition to their responsibility to influence energy homoeostasis, new studies have identified important pathways linking metabolism with the immune system, and demonstrating a modulatory role of adipocytokines in immune function.
Epidemiological studies show that obesity represents a significant risk factor for the development of cancer, although the exact mechanism of this relationship remains to be determined. There is a possible role of adipocytokines on the proliferation of tumour cells and locomotion of tumour cells or metastasis.
A key molecule in obesity is leptin, a 16 kDa peptide hormone predominantly produced by white adipose tissue. Circulating leptin is actively transported through the blood-brain barrier and acts on the hypothalamic satiety center to decrease food intake. The main function of leptin in the human body is the regulation of energy expenditure and control of appetite.
Lack of leptin in mice results in obesity and many associated metabolic complications such as insulin resistance. Serum level of leptin reflects the amount of energy stored in the adipose tissue and is in proportion to body fat mass, i.e. increased in obese and decreased after several months of pronounced weight loss.
Adiponectin is a 30 kDa protein secreted exclusively by white adipocytes. Serum levels of adiponectin are markedly decreased in individuals with visceral obesity and states of insulin resistance, such as type 2 diabetes mellitus and atherosclerosis.
In contrast to leptin, adiponectin seems to have several beneficial and protective effects. Although its role has not been definitely established, adiponectin was shown to have anti-inflammatory, vasculoprotective, and anti-diabetic effects.
Adiponectin increases the body's sensitivity to insulin including stimulation of glucose uptake in skeletal muscle and suppression of glucose production in liver, and affects the lipid metabolism by decreasing tissue fatty acid content and serum lipids.
Interestingly, levels of adiponectin in obese individuals have shown to be decreased even though it comes primarily from adipose tissue.
Increased resistin concentrations might cause insulin resistance and thus could link obesity with type II diabetes. Ghrelin is produced in the stomach. In addition to its role in long-term regulation of energy metabolism, it is involved in the short-term regulation of feeding.
Ghrelin is produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas; also known as the appetite-regulating hormone or growth hormone secretagogue or motilin-related peptide.
Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. In some bariatric procedures, the level of ghrelin is reduced in patients, thus causing satiation before it would normally occur.
The combined effect of calorie restriction and exercise may be beneficial in keeping a balance among the hormones, mainly from adipose tissue and disrupt the link between overweight and cancer.
Related articles
 |
| Two mice; the mouse on the left has more fat stores than the mouse on the right. (Photo credit: Wikipedia) |
Combination of physical activity and calorie restriction keeps in a more favourable relation of the two hormone levels that play a crucial role in energy metabolism and immune modulation. Leptin and adiponection are two important hormones in this respect, apart from a number of hormones produced from adipose tissue.
In an interventional study, it has been seen that leptin production considerably decreased, most noticeably (up to 40 percent) in the diet+exercise group; whereas adiponectin production increased most in women who were on a reduced calorie diet only.
The more was the weight loss, the more was the increase in adiponectin levels and the more decrease in leptin levels. Some of these participants reached a 20 percent increase in adiponectin levels and their leptin decreased by more than 50 percent.
Leptin production appears to be influenced by mere changes of body composition, because in the exercise intervention group, participants gained muscle mass also without losing weight.
The health-promoting effect of adiponectin is regarded as established by numerous studies now. Lower leptin levels, on the other hand, offer less growth incentives for tumour cells.
Adipose tissue is no longer considered to be solely an energy storage, but responsible for important endocrine functions, which are primarily mediated by a network of various soluble factors derived from fat cells, called adipocytokines.
Leptin, adiponectin, and resistin are produced by the adipose tissue. The protein leptin, a satiety hormone, regulates appetite and energy balance of the body.
In addition to their responsibility to influence energy homoeostasis, new studies have identified important pathways linking metabolism with the immune system, and demonstrating a modulatory role of adipocytokines in immune function.
Epidemiological studies show that obesity represents a significant risk factor for the development of cancer, although the exact mechanism of this relationship remains to be determined. There is a possible role of adipocytokines on the proliferation of tumour cells and locomotion of tumour cells or metastasis.
A key molecule in obesity is leptin, a 16 kDa peptide hormone predominantly produced by white adipose tissue. Circulating leptin is actively transported through the blood-brain barrier and acts on the hypothalamic satiety center to decrease food intake. The main function of leptin in the human body is the regulation of energy expenditure and control of appetite.
Lack of leptin in mice results in obesity and many associated metabolic complications such as insulin resistance. Serum level of leptin reflects the amount of energy stored in the adipose tissue and is in proportion to body fat mass, i.e. increased in obese and decreased after several months of pronounced weight loss.
Adiponectin is a 30 kDa protein secreted exclusively by white adipocytes. Serum levels of adiponectin are markedly decreased in individuals with visceral obesity and states of insulin resistance, such as type 2 diabetes mellitus and atherosclerosis.
In contrast to leptin, adiponectin seems to have several beneficial and protective effects. Although its role has not been definitely established, adiponectin was shown to have anti-inflammatory, vasculoprotective, and anti-diabetic effects.
Adiponectin increases the body's sensitivity to insulin including stimulation of glucose uptake in skeletal muscle and suppression of glucose production in liver, and affects the lipid metabolism by decreasing tissue fatty acid content and serum lipids.
Interestingly, levels of adiponectin in obese individuals have shown to be decreased even though it comes primarily from adipose tissue.
Increased resistin concentrations might cause insulin resistance and thus could link obesity with type II diabetes. Ghrelin is produced in the stomach. In addition to its role in long-term regulation of energy metabolism, it is involved in the short-term regulation of feeding.
Ghrelin is produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas; also known as the appetite-regulating hormone or growth hormone secretagogue or motilin-related peptide.
Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. In some bariatric procedures, the level of ghrelin is reduced in patients, thus causing satiation before it would normally occur.
The combined effect of calorie restriction and exercise may be beneficial in keeping a balance among the hormones, mainly from adipose tissue and disrupt the link between overweight and cancer.
Related articles
...
Click here to Subscribe news feed from "Clinicianonnet; so that you do not miss out anything that can be valuable to you !!
...
Posts
