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Details for anatomical structure: adipose tissue

EndoNet ID: ENC00005

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Synonyms

adipose tissue, ,

Links to other resources

Cytomer cy0010718

Larger structures

    Substructures

      Secreted hormones

      • Hormone: free fatty acid

      • Hormone: leptin

        • The majority of Leptin is expressed in white adipose tissue while a small amount is present in brown adipose tissue. [1]

        Influenced by:

        • melanocortin-4 receptor
          in adipose_tissue
          • Leptin secretion and gene expression of differentiated rat adipocytes is inhibited by administration of alpha-MSH (alpha-melanocyte stimulating hormone), and this effect is antagonised by antagonist of melanocortin receptor MC4R (AgRP, agouti-related protein). [2]
        • PPARgamma1
          in adipose_tissue
          • Catecholamines (beta 2 adrenoreceptor), cAMP agonists, and peroxisome proliferator-activated receptor gamma (PPAR-gamma) inhibit leptin synthesis and secretion. [3]
        • beta-2 adrenoreceptor
          in adipose_tissue
          • Catecholamines (beta 2 adrenoreceptor), cAMP agonists, and peroxisome proliferator-activated receptor gamma (PPAR-gamma) inhibit leptin synthesis and secretion. [3]
        • galanin receptor 1
          in adipose_tissue
          • Galanin inhibits ob gene expression and leptin protein secretion in vitro and in vivo. [3]
          • Galanin-induced decrease in plasma level of leptin might be mediated by inhibiting leptin release from pre-existing intracellular pool. [3]
          • Inhibitory action of galanin probably involved in GalR1 signaling, galanin-repressed leptin production may be mediated by changes in intracellular cAMP level. [3]
        • leptin receptor
          in adipose_tissue
          • Leptin receptor is involved in regualting the circulating leptin concentration. [4]
          • Tonic suppression of leptin synthesis could be mediated by effects of leptin on the adipocyte leptin receptor acting in an autocrine fashion. [4]
        • leptin receptor isoform b
          in adipose_tissue
          • Isoform b from leptin receptor is responsible for mediating the autoregulation of leptin expression in adipose tissue. [4]
          • Leptin receptor mediated autocrine suppression by leptin on its own expression in adipose tissue is likely to play an important role in regulating plasma leptin concentration. [4]
        • TNFR1
          in adipose_tissue
          • Leptin secretion is regulated by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [5]
        • TNFR2
          in adipose_tissue
          • Leptin secretion is regulated by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [5]

      • Hormone: PAI-1

        • PAI-1, the major inhibitor of both urokinase- (u-PA) and tissue-type (t-PA) plasminogen activators, is a 50-kDa glycoprotein present in blood platelets and synthesized by endothelial cells, muscle cells and fibroblast cells. [6]
        • TNF-alpha, but not IL-6, stimulates plasminogen activator inhibitor-1 expression in human subcutaneous adipose tissue. [7]

      • Hormone: haptoglobin

        Influenced by:

        • PPARgamma1
          in adipose_tissue

      • Hormone: adipsin

        • Human adipsin is identical to complement factor D and is expressed at high levels in adipose tissue. [8]

      • Hormone: tissue factor

        • Tissue factor gene expression in the adipose tissues of obese mice. [9]

      • Hormone: TNF-alpha

        • Several inflammatory cytokines are now recognised to be expressed in, and secreted by, white adipocytes, the first to be identified being TNFα. [10]

      • Hormone: CRP

        • The gene encoding CRP is expressed in adipose tissue. [10]

      • Hormone: complement C3

        • Chylomicrons in vitro stimulate ASP production by adipocytes. [11]

      • Hormone: interleukin 6

        • Ten to thirty-five percent of the body's basal circulating IL-6 is derived from adipose tissue. [12]
        • IL-6 is expressed in, and secreted by, adipocytes. [10]

        Influenced by:

        • ACTH receptor
          in adipose_tissue
          • Melanocortins induce interleukin 6 gene expression and secretion through melanocortin receptor 2 and 5 in adipocytes. [13]
          • Function of melanocortins in regulating Il6 gene expression and production in adipocytes through membrane receptors which are called melanocortin receptors. Of the five melanocortin receptors, MC2R and MC5R are expressed during adipocyte differentiation. AlphaMSH in addition to ACTH function as a regulator of inflammation by regulating cytokine production. [13]
        • melanocortin receptor 5
          in adipose_tissue
          • Function of melanocortins in regulating Il6 gene expression and production in adipocytes through membrane receptors which are called melanocortin receptors. Of the five melanocortin receptors, MC2R and MC5R are expressed during adipocyte differentiation. AlphaMSH in addition to ACTH function as a regulator of inflammation by regulating cytokine production. 2306 [13]
          • Melanocortins induce interleukin 6 gene expression and secretion through melanocortin receptor 2 and 5 in adipocytes. 2306 [13]

      • Hormone: IL-1 beta

        • Several cytokines and related factors are synthesised in adipose tissue, including IL-1β. [10]

      • Hormone: MIF

      • Hormone: TGF-beta 1

        • Several cytokines and related factors are synthesised within adipose tissue, including TGF-β. [10]

      • Hormone: NGF

        • The target-derived neurotrophin, NGF, is synthesised by the main adipose tissue depots in both rodents and man, and is secreted from white adipocytes. [10]

      • Hormone: HIF1

        • Expression occurs in both the adipocytes and in the stromal vascular cells, and in the WAT of obese mice the level of the mRNA is markedly increased compared with lean siblings. [10]

      • Hormone: VEGF-165

        • Several angiogenic factors are secreted by adipocytes, including recognised angiogenic signals like VEGF, PAI-1 and leptin, as well as putative signals such as metallothionein and haptoglobin. [10]

      • Hormone: IL-8

        • IL-8 is produced and released from human adipose tissue and from isolated adipocytes in vitro, which may indicate that IL-8 from adipose tissue could be involved in some of the obesity-related complications. [14]

      • Hormone: IL-10

        • Secretion of IL-10 from human adipocytes. [10]

      • Hormone: RBP4

        • RBP4 is an adipocyte-derived 'signal' that may contribute to the pathogenesis of type 2 diabetes. [15]

      • Hormone: cholesteryl ester transfer protein

        • White adipose tissue also secretes important regulators of lipoprotein metabolism like lipoprotein lipase (LPL), apolipoprotein E (apoE) and cholesteryl ester transfer protein (CETP). [16]

      • Hormone: metallothionein

      • Hormone: metallothionein 2A

        • In human adipose tissue the metallothionein (MT-2A) gene is expressed both in adipocytes and in other cells of the tissue. [17]

      • Hormone: C-C motif chemokine 2

        • In obesity, MCP-1, a key chemokine in the process of macrophage accumulation, is overexpressed in adipose tissue. [18]

      • Hormone: RELMalpha

      • Hormone: angiopoietin-like protein 4

      • Hormone: angiotensinogen

      • Hormone: lipoprotein lipase

      • Hormone: APOE

      • Hormone: BMP9

      • Hormone: IGF-1

      • Hormone: LIF

      • Hormone: NOS

      • Hormone: resistin

      • Hormone: ghrelin

      • Hormone: eotaxin

        • Eotaxin is a secretory product of adipose tissue and its expression is reversibly increased in obesity. [19]

      • Hormone: sFRP-2

      • Hormone: IL-17D

      • Hormone: adiponectin

        • Adiponectin is a hormone secreted from adipose tissue, and serum levels are decreased with obesity and insulin resistance. [20]

        Influenced by:

        • ER-alpha
          in breast
          • Bisphenol A and estrogen suppress adiponectin release from human breast, subcutaneous, and visceral adipose tissue explants and mature adipocytes. [21]
          • Bisphenol A binds both estrogen receptors alpha and beta. [22]
        • ER-beta
          in breast
          • Bisphenol A and estrogen suppress adiponectin release from human breast, subcutaneous, and visceral adipose tissue explants and mature adipocytes. [21]
          • Bisphenol A binds both estrogen receptors alpha and beta. [22]

      • Hormone: GDF-3

      • Hormone: visfatin

      • Hormone: FABP4

        • Is released from adipocytes and abundantly present in human serum. [23]

      • Hormone: osteopontin

        • Osteopontin expression is strongly elevated in the adipose tissue (AT) of obese patients compared with lean subjects in both omental and sc AT. [24]

      • Hormone: apelin-13

      • Hormone: PGE2

      Receptors

      • Receptor: GL-R

        • Glucagon receptor is expressed in adipose tissue. The biochemical characterization of the rat adipocyte glucagon receptor indicates that it closely resembles the hepatic glucagon receptor. [25]

        Induced phenotype:

        • positive regulation of lipid catabolic process
          • Glucagon exerts thermogenic effects on rat BAT possibly via its lipolytic action. [26]
          • It is suggested that there is no major role of glucagon in the control of BAT thermogenesis after 1 week in the cold. [27]

      • Receptor: PPAR-alpha

        • PPARα is expressed at high levels in organs that carry out significant catabolism of fatty acids such as the brown adipose tissue, liver, heart, kidney, and intestine [28]

      • Receptor: PPARgamma1

        • PPARγ1 had the broadest tissue expression(...)PPARγ1 mRNA was found in the heart, large and small intestines, colon, kidney, pancreas, spleen and skeletal muscle. [29]
        • The peroxisome proliferation-activated receptor gamma (PPARγ)1 is a member of the nuclear receptor superfamily. It is expressed in many cell types, including adipocytes, epithelial cells, B- and T-cells, macrophages, endothelial cells, neutrophils, and smooth muscle cells [30]

        Induced phenotype:

        • regulation of fat cell differentiation
          • PPARγ expression is observed in adipose tissue in rodents. Its expression is induced early in differentiation of 3T3-L1 preadipocytes into adipocytes, and its overexpression in fibroblasts induces them to differentiate into adipocytes. [31]
        • negative regulation of transcription
          • Insulin decrease PPAR gamma mRNA expression. [32]
        • regulation of glucose homeostasis
          • PPAR-gamma is expressed in human fat, one tissue where most of the insulin-stimulated glucose uptake occurs. [33]

        Influences:

        • haptoglobin
        • resistin
          • PPAR-gamma agonists were initially reported to suppress resistin expression in murine adipocytes, although a second study suggested that PPAR-gamma agonists increase adipose tissue resistin mRNA levels. [34]
        • adiponectin
          • Adiponectin secretion is stimulated by exposure of adipocytes to PPAR-gamma agonists. [35]
        • leptin
          • Catecholamines (beta 2 adrenoreceptor), cAMP agonists, and peroxisome proliferator-activated receptor gamma (PPAR-gamma) inhibit leptin synthesis and secretion. [3]

      • Receptor: leptin receptor

        • Both, the long and the short isoforms of the leptin receptor, are present in adipose tissue. [36]

        Induced phenotype:

        • negative regulation of insulin receptor signaling pathway
          • Leptin inhibits insulin receptor signaling in cultured cells. [5]
        • regulation of glucose homeostasis
          • The ability of leptin to regulate insulin secretion from the pancreatic beta cells might contribute to the abnormalities in glucose homeostasis in obesity . [5]
        • negative regulation of gene expression
          • Leptin inhibits the expression of the reate-limiting enzyme for long chain fatty acid synthesis, acetyl CoA carboxylase, in cultured adipocytes. [37]
        • insulin resistance
          • The obesity-related increase of Leptin production positively correlated with increased insulin resistance. [38]
          • More direct measures of insulin sensitivity have indicated leptin as potential mediator of insulin resistance in obesity. [39]
        • hyperinsulinemia
          • The obesity-related increase of Leptin production is positively correlated with hyperinsulinemia. [38]
        • obesity
          • Elevated Leptin expression and increased pasma leptin levels are associated with obesity and are presumably part of an adipostat mechanism [5]

        Influences:

        • leptin
          • Leptin receptor is involved in regualting the circulating leptin concentration. [4]
          • Tonic suppression of leptin synthesis could be mediated by effects of leptin on the adipocyte leptin receptor acting in an autocrine fashion. [4]
        • insulin
          • Leptin has an important physiological role an inhibitor of insulin secretion and the failure of leptin to inhibit insulin secretion from the beta-cells may explain, in part, the development of hyperinsulinemia, insulin resistance, and the progression to non-insulin-dependent diabetes mellitus. [40]

      • Receptor: PPAR-gamma2

        Induced phenotype:

        • regulation of fat cell differentiation
          • PPARγ expression is observed in adipose tissue in rodents. Its expression is induced early in differentiation of 3T3-L1 preadipocytes into adipocytes, and its overexpression in fibroblasts induces them to differentiate into adipocytes. [31]

      • Receptor: angiotensin II type 1 receptor

        Induced phenotype:

        • differentiation of preadipocytes
          • The production of angiotensin II in conjunction with the angiotensin II type 1 receptor has been demonstrated to regulate the differentiation and the growth of adipocytes. [41]
        • positive regulation of lipid metabolic process
          • The expression of angiotensin II type 1 receptor in adipocytes participates in the lipid metabolism. [41]
        • regulation of lipid metabolic process
          • An angiotensin II AT1 receptor antagonist influences lipid metabolism in adipose tissue by promoting adipose tissue rearrangement and modulating adipokine expression and release. [42]
          • The activity of local renin-angiotensin system plays an important role in adipose tissue metabolism. [42]

      • Receptor: angiotensin receptor 2

        Influences:

        • NO
          • Activation of AT2 results in the production of NO and activation of several phosphatases, such as PTPase and PP2A, resulting in the inactivation of MAPK and changes in potassium and calcium current. [43]

      • Receptor: PPAR-gamma1

        Induced phenotype:

        • regulation of fat cell differentiation
          • PPARγ expression is observed in adipose tissue in rodents. Its expression is induced early in differentiation of 3T3-L1 preadipocytes into adipocytes, and its overexpression in fibroblasts induces them to differentiate into adipocytes. [31]

      • Receptor: thrombospondin receptor

        Induced phenotype:

        • transport of long-chain fatty acids
          • CD36 is a fatty acid translocase necessary for the transport of long-chain fatty acids. [44]

      • Receptor: beta-3 adrenoreceptor

        Induced phenotype:

        • positive regulation of lipid catabolic process
          • Beta-3 adrenoreceptor is located mainly in adipose tissue and is involved in the regulation of lipolysis and thermogenesis. [45]

      • Receptor: ACTH receptor

        Influences:

        • interleukin 6
          • Melanocortins induce interleukin 6 gene expression and secretion through melanocortin receptor 2 and 5 in adipocytes. [13]
          • Function of melanocortins in regulating Il6 gene expression and production in adipocytes through membrane receptors which are called melanocortin receptors. Of the five melanocortin receptors, MC2R and MC5R are expressed during adipocyte differentiation. AlphaMSH in addition to ACTH function as a regulator of inflammation by regulating cytokine production. [13]

      • Receptor: melanocortin receptor 5

        Influences:

        • interleukin 6
          • Function of melanocortins in regulating Il6 gene expression and production in adipocytes through membrane receptors which are called melanocortin receptors. Of the five melanocortin receptors, MC2R and MC5R are expressed during adipocyte differentiation. AlphaMSH in addition to ACTH function as a regulator of inflammation by regulating cytokine production. 2306 [13]
          • Melanocortins induce interleukin 6 gene expression and secretion through melanocortin receptor 2 and 5 in adipocytes. 2306 [13]

      • Receptor: melanocortin-4 receptor

        Influences:

        • leptin
          • Leptin secretion and gene expression of differentiated rat adipocytes is inhibited by administration of alpha-MSH (alpha-melanocyte stimulating hormone), and this effect is antagonised by antagonist of melanocortin receptor MC4R (AgRP, agouti-related protein). [2]

      • Receptor: beta-2 adrenoreceptor

        Influences:

        • leptin
          • Catecholamines (beta 2 adrenoreceptor), cAMP agonists, and peroxisome proliferator-activated receptor gamma (PPAR-gamma) inhibit leptin synthesis and secretion. [3]

      • Receptor: galanin receptor 1

        Induced phenotype:

        • regulation of feeding behavior
          • Galanin mRNA expressed in visceral adipose tissue may be involved in the regulation of feeding and energy balance after fasting. [3]

        Influences:

        • leptin
          • Galanin inhibits ob gene expression and leptin protein secretion in vitro and in vivo. [3]
          • Galanin-induced decrease in plasma level of leptin might be mediated by inhibiting leptin release from pre-existing intracellular pool. [3]
          • Inhibitory action of galanin probably involved in GalR1 signaling, galanin-repressed leptin production may be mediated by changes in intracellular cAMP level. [3]

      • Receptor: leptin receptor isoform b

        Influences:

        • leptin
          • Isoform b from leptin receptor is responsible for mediating the autoregulation of leptin expression in adipose tissue. [4]
          • Leptin receptor mediated autocrine suppression by leptin on its own expression in adipose tissue is likely to play an important role in regulating plasma leptin concentration. [4]

      • Receptor: TNFR1

        Induced phenotype:

        • negative regulation of insulin receptor signaling pathway
          • TNF-alpha inhibits insulin receptor signaling in cultured cells. [5]
          • TNF-α inhibits insulin signaling via stimulation of p55 TNFR and sphingomyelinase activity, which results in the production of an inhibitory form of insulin receptor substrate-1 . [46]
        • regulation of glucose homeostasis
          • The ability of TNF-alpha to regulate insulin secretion from the pancreatic beta cells might contribute to the abnormalities in glucose homeostasis in obesity . [5]
        • hyperinsulinemia
          • The obesity-related increase in TNF-alpha production is positively correlates with hyperinsulinemia. [47]
        • insulin resistance
          • The obesity-related increase in TNF-alpha production positively correlates with increased insulin resistance. [47]
          • More direct measures of insulin sensitivity have indicated TNF alpha as potential mediator of insulin resistance in obesity. [47]
        • negative regulation of gene expression
          • TNF-alpha inhibits expression of the rate-limiting enzyme for long chain fatty acid synthesis, acetyl CoA carboxylase, in cultured adipocytes. [48]
        • obesity
          • TNF-alpha can act directly on adipocytes to regulate the release of a preformed pool of leptin. Elevated adipose tissue expression of TNF-alpha that occurs in obesity may contribute to obesity-related hyperleptinemia. [5]
          • Leptin secretion is regulatd by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [5]

        Influences:

        • leptin
          • Leptin secretion is regulated by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [5]
        • insulin
          • TNF alpha regulates leptin release from adipocztes, therebz influencing insulin secretion. [5]
          • The ability of leptin and TNF/alpha to suppress insulin secretion from the pancreas beta cells might also contribute to the abnormalities in glucose homeostasis in obesity. [5]

      • Receptor: TNFR2

        Influences:

        • leptin
          • Leptin secretion is regulated by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [5]

      • Receptor: Sphingosine 1-phosphate receptor 1

      • Receptor: Sphingosine 1-phosphate receptor 2

        Induced phenotype:

        • promotion of mesenchymal cell differentiation
          • S1P2 appears to be, by pharmacological inhibition, the most important receptor for transmitting the myogenic signal brought about by S1P. [49]
          • S1P promotes differentiation of adipose tissue-derived mesenchymal stem cells towards smooth muscle cells, by enhancing the expression of myogenic marker proteins and by inducing the onset of ionic currents which are characteristic of myogenic phenotype. [49]

      • Receptor: PPAR beta/delta

        • A study with human tissues showed that PPARä was present in liver, intestine, kidney, abdominal adipose, and skeletal muscle, tissues that are all involved in aspects of lipid metabolism [29]

      • Receptor: ALK7

        • Expression of activin receptor-like kinase 7 (ALK7) was adipose tissue specific. [50]

        Induced phenotype:

        • regulation of adipose-tissue homeostasis
          • We propose that GDF3 regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the ALK7 receptor. [51]
      Reference