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Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders.

Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB - Front Endocrinol (Lausanne) (2016)

Bottom Line: In response to changes in the nutritional status, the adipose tissue undergoes dynamic remodeling, including quantitative and qualitative alterations in adipose tissue-resident cells.A growing body of evidence indicates that adipose tissue remodeling in obesity is closely associated with adipose tissue function.This review will discuss current mechanistic understandings of adipose tissue remodeling processes in adaptive energy homeostasis and pathological remodeling of adipose tissue in connection with immune response.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, National Creative Research Initiatives Center for Adipose Tissue Remodeling, Institute of Molecular Biology and Genetics, Seoul National University , Seoul , South Korea.

ABSTRACT
The adipose tissue is a central metabolic organ in the regulation of whole-body energy homeostasis. The white adipose tissue functions as a key energy reservoir for other organs, whereas the brown adipose tissue accumulates lipids for cold-induced adaptive thermogenesis. Adipose tissues secrete various hormones, cytokines, and metabolites (termed as adipokines) that control systemic energy balance by regulating appetitive signals from the central nerve system as well as metabolic activity in peripheral tissues. In response to changes in the nutritional status, the adipose tissue undergoes dynamic remodeling, including quantitative and qualitative alterations in adipose tissue-resident cells. A growing body of evidence indicates that adipose tissue remodeling in obesity is closely associated with adipose tissue function. Changes in the number and size of the adipocytes affect the microenvironment of expanded fat tissues, accompanied by alterations in adipokine secretion, adipocyte death, local hypoxia, and fatty acid fluxes. Concurrently, stromal vascular cells in the adipose tissue, including immune cells, are involved in numerous adaptive processes, such as dead adipocyte clearance, adipogenesis, and angiogenesis, all of which are dysregulated in obese adipose tissue remodeling. Chronic overnutrition triggers uncontrolled inflammatory responses, leading to systemic low-grade inflammation and metabolic disorders, such as insulin resistance. This review will discuss current mechanistic understandings of adipose tissue remodeling processes in adaptive energy homeostasis and pathological remodeling of adipose tissue in connection with immune response.

No MeSH data available.


Related in: MedlinePlus

Balance of immune responses in the regulation of adipose tissue function. Lean adipose tissue harbors various anti-inflammatory immune cells, such as eosinophils, M2 macrophages, Th2 cells, iNKT cells, and Treg cells. These immune cells help in maintaining insulin sensitivity and store extra energy in the form of TGs. In obese adipose tissue, the numbers of pro-inflammatory immune cells, including neutrophils, M1 macrophages, mast cells, Th1 cells, and CD8 T cells, are greatly elevated. Simultaneously reduced number of anti-inflammatory immune cells accelerates pro-inflammatory response and adipose tissue dysfunction.
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Figure 4: Balance of immune responses in the regulation of adipose tissue function. Lean adipose tissue harbors various anti-inflammatory immune cells, such as eosinophils, M2 macrophages, Th2 cells, iNKT cells, and Treg cells. These immune cells help in maintaining insulin sensitivity and store extra energy in the form of TGs. In obese adipose tissue, the numbers of pro-inflammatory immune cells, including neutrophils, M1 macrophages, mast cells, Th1 cells, and CD8 T cells, are greatly elevated. Simultaneously reduced number of anti-inflammatory immune cells accelerates pro-inflammatory response and adipose tissue dysfunction.

Mentions: Immune cells residing in the adipose tissue actively secrete numerous pro- and anti-inflammatory cytokines (2–4). Anti-inflammatory cytokines help in maintaining insulin sensitivity in the lean adipose tissue, while accumulation of pro-inflammatory cytokines in obesity leads to insulin resistance (2–4) (Figure 4). In addition, pro-inflammatory cytokines stimulate lipolysis in adipocytes, leading to lipotoxicity in other tissues (2, 3). In C57BL/6 mice, an inflammatory response was specifically induced in the adipose tissue but not in other metabolic tissues by a brief (1 week) high-fat diet (HFD) (130). During long-term HFD, however, pro-inflammatory responses were also greatly enhanced in other metabolic tissues, including the liver and muscles (130). This report proposes that inflammatory responses because of excess energy intake are primarily initiated in adipose tissues and that chronic inflammation of adipose tissues subsequently induces inflammation in other metabolic organs, such as the liver, muscle, and pancreas. Therefore, it is likely that inflammation is a causal factor for widespread systemic insulin resistance in obesity.


Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders.

Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB - Front Endocrinol (Lausanne) (2016)

Balance of immune responses in the regulation of adipose tissue function. Lean adipose tissue harbors various anti-inflammatory immune cells, such as eosinophils, M2 macrophages, Th2 cells, iNKT cells, and Treg cells. These immune cells help in maintaining insulin sensitivity and store extra energy in the form of TGs. In obese adipose tissue, the numbers of pro-inflammatory immune cells, including neutrophils, M1 macrophages, mast cells, Th1 cells, and CD8 T cells, are greatly elevated. Simultaneously reduced number of anti-inflammatory immune cells accelerates pro-inflammatory response and adipose tissue dysfunction.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4829583&req=5

Figure 4: Balance of immune responses in the regulation of adipose tissue function. Lean adipose tissue harbors various anti-inflammatory immune cells, such as eosinophils, M2 macrophages, Th2 cells, iNKT cells, and Treg cells. These immune cells help in maintaining insulin sensitivity and store extra energy in the form of TGs. In obese adipose tissue, the numbers of pro-inflammatory immune cells, including neutrophils, M1 macrophages, mast cells, Th1 cells, and CD8 T cells, are greatly elevated. Simultaneously reduced number of anti-inflammatory immune cells accelerates pro-inflammatory response and adipose tissue dysfunction.
Mentions: Immune cells residing in the adipose tissue actively secrete numerous pro- and anti-inflammatory cytokines (2–4). Anti-inflammatory cytokines help in maintaining insulin sensitivity in the lean adipose tissue, while accumulation of pro-inflammatory cytokines in obesity leads to insulin resistance (2–4) (Figure 4). In addition, pro-inflammatory cytokines stimulate lipolysis in adipocytes, leading to lipotoxicity in other tissues (2, 3). In C57BL/6 mice, an inflammatory response was specifically induced in the adipose tissue but not in other metabolic tissues by a brief (1 week) high-fat diet (HFD) (130). During long-term HFD, however, pro-inflammatory responses were also greatly enhanced in other metabolic tissues, including the liver and muscles (130). This report proposes that inflammatory responses because of excess energy intake are primarily initiated in adipose tissues and that chronic inflammation of adipose tissues subsequently induces inflammation in other metabolic organs, such as the liver, muscle, and pancreas. Therefore, it is likely that inflammation is a causal factor for widespread systemic insulin resistance in obesity.

Bottom Line: In response to changes in the nutritional status, the adipose tissue undergoes dynamic remodeling, including quantitative and qualitative alterations in adipose tissue-resident cells.A growing body of evidence indicates that adipose tissue remodeling in obesity is closely associated with adipose tissue function.This review will discuss current mechanistic understandings of adipose tissue remodeling processes in adaptive energy homeostasis and pathological remodeling of adipose tissue in connection with immune response.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, National Creative Research Initiatives Center for Adipose Tissue Remodeling, Institute of Molecular Biology and Genetics, Seoul National University , Seoul , South Korea.

ABSTRACT
The adipose tissue is a central metabolic organ in the regulation of whole-body energy homeostasis. The white adipose tissue functions as a key energy reservoir for other organs, whereas the brown adipose tissue accumulates lipids for cold-induced adaptive thermogenesis. Adipose tissues secrete various hormones, cytokines, and metabolites (termed as adipokines) that control systemic energy balance by regulating appetitive signals from the central nerve system as well as metabolic activity in peripheral tissues. In response to changes in the nutritional status, the adipose tissue undergoes dynamic remodeling, including quantitative and qualitative alterations in adipose tissue-resident cells. A growing body of evidence indicates that adipose tissue remodeling in obesity is closely associated with adipose tissue function. Changes in the number and size of the adipocytes affect the microenvironment of expanded fat tissues, accompanied by alterations in adipokine secretion, adipocyte death, local hypoxia, and fatty acid fluxes. Concurrently, stromal vascular cells in the adipose tissue, including immune cells, are involved in numerous adaptive processes, such as dead adipocyte clearance, adipogenesis, and angiogenesis, all of which are dysregulated in obese adipose tissue remodeling. Chronic overnutrition triggers uncontrolled inflammatory responses, leading to systemic low-grade inflammation and metabolic disorders, such as insulin resistance. This review will discuss current mechanistic understandings of adipose tissue remodeling processes in adaptive energy homeostasis and pathological remodeling of adipose tissue in connection with immune response.

No MeSH data available.


Related in: MedlinePlus