Where is adipose tissue

A number of different hormones are released from adipose tissue and these are responsible for different functions within the body. Examples of these are:. Both too much and too little adipose tissue can have severe health implications. More commonly, too much adipose tissue leads to obesity, mainly from too much visceral fat.

Obesity leads to a number of serious health problems. Obesity increases the risk of developing type 2 diabetes as it causes the body to become resistant to insulin. This resistance results in high levels of blood sugar, which is bad for health. Obesity also increases the chance of developing high blood pressure, high cholesterol levels and an increased tendency for blood to clot. All of these raise the risk of heart attacks and stroke. In eating disorders such as anorexia nervosa , the patient does not eat enough food to maintain their adipose tissues levels.

This means that they can lose a dangerous amount of body weight. About Contact Events News. Search Search. You and Your Hormones. Students Teachers Patients Browse. Human body. Home Glands Adipose tissue. Adipose tissue Adipose tissue body fat is crucial for health. Along with fat cells, adipose tissue contains numerous nerve cells and blood vessels, storing and releasing energy to fuel the body and releasing important hormones vital to the body's needs.

Alternative names for adipose tissue Fat; body fat Where is my adipose tissue? Multiple lines of evidence suggest that ATMs influence angiogenesis in adipose tissues — In mouse models, ATM depletion through the use of clodronate liposomes reduces blood vessel structures in adipose tissues In addition, macrophages recruited into the tip of the gonadal adipose tissue promote angiogenesis during tissue outgrowth Extracellular matrix ECM remodeling, including the degradation of the connective tissue and basement membrane proteins, is necessary during the early stage of angiogenesis , Remodeling of ECM is also associated with the modulation of adipogenesis during adipose tissue expansion.

Adipocyte differentiation is regulated by the deposition of collagen, a major protein component of ECM In addition, it has been proposed that adipose tissue fibrosis in obese subjects caused by excess deposition of collagen, including type VI, leads to adipose tissue inflammation by triggering the infiltration of immune cells, such as macrophages, neutrophils, and lymphocytes 87 , , Pathological remodeling of ECM may also reduce the number of adipose tissue capillaries in obese and insulin-resistant subjects Certain subtypes of collagen appear crucial for adipose tissue fibrosis-mediated inflammation and metabolic dysfunction in obesity , Deletion of collagen VI in obese mice improves metabolic parameters and inflammatory profiles even though overall collagen content of the adipose tissue is not altered However, it remains to be determined whether MMPs secreted from ATMs prevent collagen deposition linked to adipose tissue fibrosis.

Accumulation of ATMs is a key factor aggravating inflammatory responses in adipose tissues 2 — 4. However, recruited ATMs in obese adipose tissues may also play a protective role by enhancing angiogenesis in response to local hypoxia.

Hypoxia is one of the most potent microenvironmental factors for macrophage recruitment into adipose tissues , and recruited macrophages are the predominant producers of pro-angiogenic factors in response to hypoxia In mouse obese adipose tissues, ATM depletion decreases the expression level of platelet-derived growth factor PDGF , an angiogenic factor that mediates endothelial cell tube formation and capillary maturation by pericyte recruitment Therefore, it has been speculated that ATMs may counteract hypoxia by promoting angiogenesis through production of angiogenic factors.

However, recent elucidation of ATM-mediated angiogenesis in the obese adipose tissue still needs to be confirmed in vivo.

Another potential physiological role of ATMs in obesity is the clearance of dead or damaged adipocytes and fragmented cellular contents. In DIO mice, perilipin-negative adipocytes show features of necrosis-like death, such as plasma membrane rupture, dilated endoplasmic reticulum, and cell debris 80 , Most of the recruited ATMs in obese adipose tissues are present near perilipin-negative adipocytes, forming CLSs 80 , These CLS macrophages are multinucleated giant cells that surround residual adipocyte lipids, implying that CLS macrophages scavenge free lipids released from dead adipocytes to the interstitium It was recently shown that depletion of mannose-binding lectin, which stimulates the phagocytic capacity of ATM, increases the numbers of CLSs in the adipose tissue of DIO mice, and decreases dead adipocyte clearance Thus, it is likely that macrophage recruitment into the obese adipose tissue is involved in the clearance of dead adipocytes via phagocytosis.

Furthermore, it has been suggested that ATMs could mediate the removal of extracellular lipids from adipose tissues This phenomenon could contribute to the prevention of lipotoxicity by buffering local extracellular FFA elevations in the adipose tissue. In obesity, however, lipid-loaded ATMs resembling foam cells have been suggested to have pro-inflammatory characteristics , that contribute to insulin resistance.

In both mice with adipocyte-targeted activation of caspase-8 and fat-transplanted mice, adipocyte death facilitates the recruitment of M1 and M2 macrophages , It is possible that M1 macrophages phagocytize dead adipocytes, whereas M2 macrophages reconstruct ECM and resolve the activation of M1 macrophages after removal of dead adipocytes.

These complementary functions of M1 and M2 macrophages may minimize tissue damage through tight regulation of phagocytosis and tissue repair. However, in obesity, the balance between M1 and M2 ATMs appears to be shifted by a greater increase in M1 macrophage number 2 — 4. Enhanced M1 polarization of ATMs in obese adipose tissues may interrupt the normal process of dead cell clearance, whereas further stimulating a pro-inflammatory response.

Also, chronic cold exposure leads to the remodeling of BAT and SAT, resulting in a dramatic increase in the metabolic rate, mitochondrial biogenesis, and fatty acid oxidation Emerging evidence suggests that M2 ATMs mediate thermogenic adipose tissue remodeling in response to cold exposure — In accordance with this notion, ATM depletion suppresses the cold-induced increase in thermogenic gene expression, lipolysis, and energy expenditure. In addition, blockage of M2 polarization by inhibition of IL-4 signaling diminishes adaptive thermogenesis and attenuates the generation of UCPpositive beige adipocytes in SAT.

Together, these results indicate that ATM-associated adipose tissue remodeling is intimately involved in the modulation of adipose tissue function as well as adipose tissue growth and expansion in changing environments. We have focused on the physiological and pathological roles of the adipose tissue and its remodeling in regulating whole-body energy metabolism by sensing the nutritional status and crosstalk between adipocytes and stromal vascular cells. During adipose tissue expansion, numerous cellular responses are dynamically altered.

Modulation of ECM remodeling and angiogenesis may promote differentiation of de novo adipocytes, preventing the formation of hypertrophic adipocytes by providing additional capacity to store extra lipids.

Recruited ATMs probably act to remove dead adipocytes and repair damaged adipose tissue for healthy adipose tissue remodeling. Adipose tissue remodeling is modulated by the inflammatory responses of multiple immune cell types, including macrophages and lymphocytes.

However, in obesity, chronic excessive energy storage in the adipose tissue initiates pathological remodeling, which triggers pro-inflammatory responses of immune cells. Furthermore, tissue remodeling, including angiogenesis and tissue repair for healthy expansion of the adipose tissue, is hindered by inflammatory and metabolic stress.

Thus, resolving uncontrolled pro-inflammatory responses during adipose tissue remodeling is important for maintaining a metabolically healthy status. Adipose tissue remodeling is a complex but well-orchestrated mechanism modulated by multiple adipose tissue cell types that allow adaptation to external environmental changes.

A deeper mechanistic understanding of adipose tissue remodeling could facilitate the development of therapeutic approaches against obesity-induced metabolic diseases. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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