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Glycogen metabolism

The role of hormones in energy metabolism -

RANKL regulates metabolism by binding with RANK on the cell membrane. In addition, MAT can also secrete the adipokines leptin and adiponectin.

Leptin and adiponectin combine with ADIPOR and OBR on the cell membrane of peripheral tissue, regulating cellular sugar metabolism.

They also act on the central nervous system, leading to reduced food intake and energy consumption. Leptin, which is encoded by the obesity gene Ob and secreted primarily by WAT, is directly related to obesity.

Mutations of the leptin gene lead to obesity. At present, the regulatory mechanism of leptin on energy metabolism has been clearly studied. It was recently discovered that MAT also expresses leptin.

Additionally, leptin expressed in bone MAT can directly act on leptin receptors in bone and affect bone growth by activating FGF23 and regulating the secretion of osteocalcin. There is a complex relationship between bone and energy metabolism.

The main action of circulating endocrine factors is not limited to regulating energy metabolism but affects bone metabolism and remodeling. Insulin is an important hormone regulating energy metabolism in the human body, and its receptor exists in almost all cells.

Insulin promotes glycogen, fat, and protein synthesis by binding to IRs and ultimately lowers blood sugar. demonstrated in mice that when osteoblasts lack IR, osteoporosis can easily develop after birth. However, it may also lead to bone fragility by increasing cortical osteoporosis or other bone structural defects.

The regulation of bone by insulin can affect whole-body energy metabolism. Insulin can promote osteoblast differentiation and glucose uptake by increasing the expression of Glut4 on the cell membrane.

The absence of this pathway will lead to peripheral insulin resistance, which is mainly manifested by an increase in systemic insulin levels and a decrease in insulin sensitivity.

However, no significant phenotypes were found in skeletal muscle cells and adipocytes. Therefore, the decrease in insulin absorption by bone may lead to systemic insulin resistance, which proves the influence of insulin and bone on whole-body energy metabolism from another aspect.

Vitamin D is a steroid hormone that plays a vital role in maintaining bone metabolism and calcium homeostasis. On the other hand, when the serum calcium level declines, VDR in osteoblasts can enhance bone resorption, thereby mobilizing bone calcium into the blood to maintain serum calcium homeostasis.

The relationship between vitamin D and metabolic diseases such as obesity, diabetes, and NAFLD is a trend in research. Adipocytes are the main storage sites of vitamin D and express active vitamin D and VDR.

Vitamin D supplementation can reduce the risk of elevated blood glucose and insulin resistance. Parathyroid hormone PTH can directly affect bone and kidney to regulate calcium and phosphorus metabolism.

One of the key mechanisms of PTH in regulating calcium homeostasis is stimulating bone remodeling. It not only promotes bone resorption and mobilizes bone calcium into blood but also promotes osteogenesis and ameliorates osteoporosis. PTH1R is expressed on the surface of osteoblasts and many bone cells.

In addition to regulating systemic calcium and phosphorus metabolism, PTH also has some effects on energy metabolism, which may be related to the level of vitamin D. It was found that the level of blood sugar increased significantly after parathyroidectomy and decreased after PTH administration, while the secretion of insulin remained unchanged.

also demonstrated that PTH could reduce the blood sugar level in obese type 2 diabetic rats without changing the serum insulin level. One piece of evidence is that the insulin sensitivity index is negatively correlated with plasma PTH levels. PTH induces lipolysis of adipocytes by activating the cAMP-PKA pathway, leading to increased serum cholesterol and triglyceride concentrations in mice.

In addition to reproductive function, estrogen also regulates bone metabolism and energy metabolism. Lack of estrogen increases the risk of metabolic syndromes such as obesity and type 2 diabetes mellitus. In the central nervous system, activation of ERs in the ventromedial hypothalamus and arcuate nucleus can control dietary intake.

Postmenopausal estrogen deficiency can lead to osteoporosis, which is due to estrogen inducing osteoclast apoptosis through ERs and protecting bone through the inflammatory mediators RANKL and Scl. It has been known for a long time that skeletal health is closely related to the overall metabolism of the individual.

For example, people with diabetes have a greater risk of developing osteoporosis than normal individuals, , and a low body mass index causes bone loss. Later, through the discovery of osteocalcin, the first bone-derived factor that regulates energy metabolism, researchers found that bone could also regulate energy metabolism throughout the body.

Some findings showed that bone-derived factors, such as Lcn2 secreted by osteoblasts and adiponectin and leptin secreted by MAT, could cross the blood—brain barrier and act on the central nervous system, which is one of the discoveries in recent years.

Further study on bone-derived factors and their interactions will help to understand the fundamentals of the central nervous system for energy balance. Bone-derived exosomes are also a new research area in recent years and have been found to regulate bone itself and other tissues.

The effect of bone-derived factors on the regulation of energy metabolism-related organs is complicated. This may be due to the different distributions and proportions of receptors on the surfaces of other cells so that these factors have more than one regulatory pathway.

Moreover, sometimes the results of experiments on animals and cell cultures in vitro may be different from those obtained from human subjects, indicating that the human body has a more complex internal environment, which impacts the results.

Bone-derived factors may be affected by a variety of factors in the processes involved in secretion, circulation and function, including genetic background diversity, age and health status of the human body. For example, decarboxylation of OCN is vitamin K dependent, so the vitamin K concentration in the human body will affect the physiological function of osteocalcin.

One of the key points in studying the regulation of bone-derived factors on energy metabolism is to confirm whether the change in the levels of those factors is the cause but not the result of altered energy metabolism.

Because of the close relationship between bone metabolism and whole-body energy metabolism, the levels of factors secreted by bone are likely to be determinants of energy homeostasis and metabolism.

Second, it is of interest to determine whether those factors that play a crucial role in other tissues and organs are from bone. This could be easily determined for some factors, such as osteocalcin and FGF23, which are mostly secreted by bone cells. For other factors expressed in multiple tissues and organs, most of them need to be assessed through genetic engineering techniques by using animal models Table 2.

However, at present, not all bone-derived factors may possess the necessary gene-specific knockout animal models applicable to energy metabolism regulation experiments, such as BMP and OPN. Another reason is that although some autocrine factors in bone cannot be secreted into the blood circulation to act on other organs, they can indirectly affect systemic metabolism by regulating bone metabolism, which should not be ignored.

In view of the complex regulation of whole-body energy metabolism by bone, the clinical application of bone-derived factors will become one of the future research directions. For example, studying the role of bone-derived factors in aging, which is a severe problem facing society, may explain some diseases.

In the process of human aging, bone metabolism and whole-body metabolism are continually changing. Aging may lead to metabolic disorders and affect bone metabolism.

Macroscopically, the aging of bone is characterized by osteoporosis and a decrease in organic and inorganic components. At the same time, its significance is marked by a decrease in bone cells and the transformation of BMSCs into MAT and osteoblasts. Bone is an important motor organ, so exercise can have a significant impact on bone metabolism.

Therefore, exercise therapy may be used to treat or prevent metabolic diseases, especially those related to aging, in the future Fig. The network relationship between bone and whole-body energy metabolism.

Aging is one of the main causes of bone and whole-body metabolism disorder, and exercise training can alleviate it. Changes in bone metabolism will affect multiple organs and tissues, including the brain a potential research direction in the future , and lead to metabolic diseases.

Metabolic diseases, as well as changes in circulating endocrine factors, can in turn affect bone. On the other hand, bone-derived factors can also be used as autocrine factors to regulate their own metabolic state.

The next question is whether we can use bone-derived factors as a marker for the diagnosis or as a new target for the treatment of metabolic diseases and their related complications.

This conjecture has been verified by some research. For example, OPG has been found to be a potential marker for the diagnosis of diabetes in postmenopausal women, and experiments have explored whether regulating the proportion of OPG-RANKL-RANK signaling can interfere with the process of cardiovascular complications noted in patients with diabetes.

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Cortisol is a steroid hormone produced by the adrenal glands in response to stress. It plays a crucial role in the metabolism of carbohydrates, proteins, and fats. Cortisol promotes the breakdown of proteins in muscle cells to release amino acids for gluconeogenesis, the production of glucose from non-carbohydrate sources.

It also promotes the breakdown of fats in adipose tissue and the release of fatty acids for energy production. Thyroid hormones, produced by the thyroid gland, play a critical role in the regulation of metabolism. They increase the metabolic rate by promoting the production of ATP, the energy currency of cells.

Thyroid hormones also increase the activity of enzymes involved in carbohydrate, protein, and fat metabolism. Leptin is another hormone that plays a crucial role in the regulation of metabolism. It is produced by adipose tissue and is involved in the regulation of energy balance.

Leptin suppresses appetite and increases energy expenditure, promoting weight loss. Ghrelin is a hormone produced by the stomach that stimulates appetite and promotes food intake. It also plays a role in the regulation of energy balance by promoting the release of growth hormone, which increases the breakdown of fats for energy production.

Adiponectin is a hormone produced by adipose tissue that regulates glucose and lipid metabolism. Adiponectin increases insulin sensitivity, promoting glucose uptake by cells for energy production.

It also promotes the breakdown of fats in adipose tissue and the utilization of fatty acids for energy production. In conclusion, hormones play a crucial role in the control of metabolism.

Insulin and glucagon regulate glucose levels in the blood, while cortisol promotes the breakdown of proteins and fats for energy production.

Weight management is a common Polyphenols and bone health for women and men of all ages. Natural fat blocker rkle hormones that also play a critical role Diabetic foot care resources roe weight management enwrgy cortisol, insulin, progesterone, and thyroid hormone triiodothyronine T3. Hormoens an imbalance occurs, it can Te related to metabolidm, Natural fat blocker, illness or stress. Hormones produced by the ovaries, such as estrogen and progesterone, may regulate where fat sits on the body and help determine whether your metabolic engine will use sugar or fat. When a hormone imbalance occurs, women may find they develop extra fat around the middle. Exercise is an essential component to controlling weight, is vital for health, and may reduce some of the problems associated with hormone imbalances. You cannot change fat placement, but you can increase activity to alter your gut flora, change how you extract calories from food and reduce fat storage. University of Missouri-Columbia, USA. You Natural energy sources also merabolism for this editor rolee PubMed Google Scholar. Part of the book series: Advances in Experimental Medicine and Biology AEMB, volume This is a preview of subscription content, log in via an institution to check for access. David M. Klachko, Ralph R. Anderson, Murray Heimberg.