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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

Invariant natural killer T (iNKT) cell-mediated regulation of anti-inflammatory response in the adipose tissue. Adipocytes secrete various inflammation-inducing factors including FFAs upon excess energy intake, such as HFD. In addition, antigen presentation by CD1d on adipocytes could activate iNKT cells, which rapidly secrete great quantities of cytokines, such as IL-4, IL-2, and IL-10. IL-4 produced by iNKT cells induces macrophage polarization into M2 type and arginase expression. IL-2 secretion by iNKT cells promotes Treg cell function in the adipose tissue. Activation of anti-inflammatory responses mediated by iNKT cells could play a crucial role in the suppression of excessive pro-inflammatory response in the adipose tissue upon HFD.
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Figure 5: Invariant natural killer T (iNKT) cell-mediated regulation of anti-inflammatory response in the adipose tissue. Adipocytes secrete various inflammation-inducing factors including FFAs upon excess energy intake, such as HFD. In addition, antigen presentation by CD1d on adipocytes could activate iNKT cells, which rapidly secrete great quantities of cytokines, such as IL-4, IL-2, and IL-10. IL-4 produced by iNKT cells induces macrophage polarization into M2 type and arginase expression. IL-2 secretion by iNKT cells promotes Treg cell function in the adipose tissue. Activation of anti-inflammatory responses mediated by iNKT cells could play a crucial role in the suppression of excessive pro-inflammatory response in the adipose tissue upon HFD.

Mentions: Beneficial roles of invariant natural killer T (iNKT) cells in adipose tissue inflammation and insulin sensitivity have recently been identified, which are associated with secretion of anti-inflammatory cytokines, such as IL-4 and IL-10 (Figure 5) (148–152). These iNKT cells have unique functional characteristics. For example, iNKT cells recognize the lipid antigen loaded on CD1d molecules of antigen-presenting cells, whereas CD4 and CD8 T cells recognize the peptide antigens loaded on MHC molecules (153). In addition, iNKT cells can rapidly secrete large quantities of cytokines after activation (153). The number of iNKT cells in adipose tissues is reduced in obese subjects (149, 150, 152). In short-term HFD-fed mice, adipose iNKT cell numbers are rapidly reduced concomitant with enhanced expression of iNKT cell activation markers (152). These results suggest that iNKT cells are involved in the early inflammatory response to metabolic stress in the adipose tissue. In addition, it has been shown that iNKT cell-deficient mice are more susceptible to adipose tissue inflammation and insulin resistance than wild-type mice (150, 152). Moreover, when iNKT cells are supplemented by adoptive transfer or activated by α-galactosylceramide treatment in murine models, body weight gain is reduced; glucose tolerance is improved; and anti-inflammatory cytokines, such as IL-4 and IL-10, are elevated in DIO (149, 150). Under HFD, the expression of the arginase gene is increased in wild type but not in iNKT cell-depleted mice, suggesting a crucial role of iNKT cells in M2 polarization (148). These data suggest that iNKT cells suppress adipose tissue inflammation and insulin resistance in DIO mice. It was recently suggested that iNKT cells in the adipose tissue possess a unique tissue-resident property, unlike iNKT cells in other tissues. Moreover, iNKT cells can regulate the functions of regulatory T (Treg) cells via IL-2 production as well as those of M2 macrophages via IL-10 production in the adipose tissue (154). Further, CD1d molecules that present lipid antigens to iNKT cells are highly expressed in adipocytes that store large amounts of lipid metabolites (151, 152). Despite these recent findings, the roles of adipocyte CD1d under physiological and pathological conditions and the identity of the endogenous lipid antigens exclusively loaded on adipocyte CD1d remain to be elucidated.


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)

Invariant natural killer T (iNKT) cell-mediated regulation of anti-inflammatory response in the adipose tissue. Adipocytes secrete various inflammation-inducing factors including FFAs upon excess energy intake, such as HFD. In addition, antigen presentation by CD1d on adipocytes could activate iNKT cells, which rapidly secrete great quantities of cytokines, such as IL-4, IL-2, and IL-10. IL-4 produced by iNKT cells induces macrophage polarization into M2 type and arginase expression. IL-2 secretion by iNKT cells promotes Treg cell function in the adipose tissue. Activation of anti-inflammatory responses mediated by iNKT cells could play a crucial role in the suppression of excessive pro-inflammatory response in the adipose tissue upon HFD.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 5: Invariant natural killer T (iNKT) cell-mediated regulation of anti-inflammatory response in the adipose tissue. Adipocytes secrete various inflammation-inducing factors including FFAs upon excess energy intake, such as HFD. In addition, antigen presentation by CD1d on adipocytes could activate iNKT cells, which rapidly secrete great quantities of cytokines, such as IL-4, IL-2, and IL-10. IL-4 produced by iNKT cells induces macrophage polarization into M2 type and arginase expression. IL-2 secretion by iNKT cells promotes Treg cell function in the adipose tissue. Activation of anti-inflammatory responses mediated by iNKT cells could play a crucial role in the suppression of excessive pro-inflammatory response in the adipose tissue upon HFD.
Mentions: Beneficial roles of invariant natural killer T (iNKT) cells in adipose tissue inflammation and insulin sensitivity have recently been identified, which are associated with secretion of anti-inflammatory cytokines, such as IL-4 and IL-10 (Figure 5) (148–152). These iNKT cells have unique functional characteristics. For example, iNKT cells recognize the lipid antigen loaded on CD1d molecules of antigen-presenting cells, whereas CD4 and CD8 T cells recognize the peptide antigens loaded on MHC molecules (153). In addition, iNKT cells can rapidly secrete large quantities of cytokines after activation (153). The number of iNKT cells in adipose tissues is reduced in obese subjects (149, 150, 152). In short-term HFD-fed mice, adipose iNKT cell numbers are rapidly reduced concomitant with enhanced expression of iNKT cell activation markers (152). These results suggest that iNKT cells are involved in the early inflammatory response to metabolic stress in the adipose tissue. In addition, it has been shown that iNKT cell-deficient mice are more susceptible to adipose tissue inflammation and insulin resistance than wild-type mice (150, 152). Moreover, when iNKT cells are supplemented by adoptive transfer or activated by α-galactosylceramide treatment in murine models, body weight gain is reduced; glucose tolerance is improved; and anti-inflammatory cytokines, such as IL-4 and IL-10, are elevated in DIO (149, 150). Under HFD, the expression of the arginase gene is increased in wild type but not in iNKT cell-depleted mice, suggesting a crucial role of iNKT cells in M2 polarization (148). These data suggest that iNKT cells suppress adipose tissue inflammation and insulin resistance in DIO mice. It was recently suggested that iNKT cells in the adipose tissue possess a unique tissue-resident property, unlike iNKT cells in other tissues. Moreover, iNKT cells can regulate the functions of regulatory T (Treg) cells via IL-2 production as well as those of M2 macrophages via IL-10 production in the adipose tissue (154). Further, CD1d molecules that present lipid antigens to iNKT cells are highly expressed in adipocytes that store large amounts of lipid metabolites (151, 152). Despite these recent findings, the roles of adipocyte CD1d under physiological and pathological conditions and the identity of the endogenous lipid antigens exclusively loaded on adipocyte CD1d remain to be elucidated.

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