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Details for anatomical structure: fat cell

EndoNet ID: ENC00004

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Synonyms

fat cell, adipocyte, adipose cell, lipocyte, Adipozyt, Lipozyt

General information

fat-storage cell; differentiation between white unilocular fat cell and brown multilocular fat cell

Links to other resources

Cytomer cy0014559

Larger structures

  • circulatory_system__hematopoietic_system
  • immune_system
  • bone_marrow

Substructures

  • fat_cell_of_brown_fat

Secreted hormones

  • Hormone: IGF-1

  • Hormone: resistin

    • Elevated levels of the hormone resistin are proposed to cause insulin resistance and to serve as a link between obesity and type 2 diabetes. [1]
    • An examination of adipocytes from a patient with a genetic defect in PPAR-gamma failed to provide any support for the notion that human resistin expression is directly altered by PPAR-gamma action. [2]

    Influenced by:

    • PPARgamma1
      in adipose_tissue
      • 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. [2]

  • Hormone: SAA3

    • Expression and release of SAA3 occurs in murine adipocytes. [3]

  • Hormone: SAA

  • Hormone: complement factor B

  • Hormone: collagen VI alpha 3

    • Type VI collagen, while expressed by a number of other cell types, is abundantly produced and secreted by adipocytes. [4]

  • Hormone: free fatty acid

  • Hormone: tissue factor

    • Products secreted by adipocytes also include tissue factor. [5]

  • Hormone: adipsin

    • Adipose tissue is a major site of synthesis of human adipsin/complement factor D mRNA. [6]

  • Hormone: complement C3

    • Chylomicrons in vitro stimulate ASP production by adipocytes. [7]

  • Hormone: leptin

    Influenced by:

    • growth hormone receptor
      in fat_cell
    • insulin receptor
      in fat_cell
    • beta-1 adrenoreceptor
      in fat_cell
      • Catecholamines suppress leptin release from in vitro differentiated subcutaneous human adipocytes via b1- and b2-adrenergic receptors. [8]
    • beta-2 adrenoreceptor
      in fat_cell
      • Catecholamines suppress leptin release from in vitro differentiated subcutaneous human adipocytes via b1- and b2-adrenergic receptors. [8]

  • Hormone: MIF

  • Hormone: TNF-alpha

    • Several inflammatory cytokines are now recognised to be expressed in, and secreted by, white adipocytes, the first to be identified being TNF-alpha. [3]
    • Adipocyte TNF-alpha action strikingly ameliorates the insulin resistance of murine obesity, but inhibition of TNF-alpha has a negligible effect on the insulin resistance of obese humans, because TNF-alpha is expressed at much lower levels in human adipose tissue. [2]

  • Hormone: interleukin 6

    • IL-6 is expressed in, and secreted by, adipocytes. [3]

    Influenced by:

    • biliary glycoprotein 1
      in neutrophil_granulocyte
      • Evidence in mice suggests that biliary glycoprotein activation on murine dendritic cells causes IL-6 and IL-12 release. [9]

  • Hormone: TGF-beta 1

    • Several cytokines and related factors are synthesised within adipose tissue, including TGF-β. [3]

    Influenced by:

    • vasorin
      in smooth_muscle_cell
      • We found that vasorin directly binds to transforming growth factor (TGF)-β and attenuates TGF-β signaling in vitro. [10]

  • Hormone: adiponectin

    • Synthesized exclusively by adipocytes and secreted into plasma. [11]
    • Adiponectin, which is synthesised only in adipose tissue, appears to have an anti-inflammatory effect, inhibiting phagocytic activity and TNFα production in macrophages. [3]

    Influenced by:

    • PPARgamma1
      in adipose_tissue
      • Adiponectin secretion is stimulated by exposure of adipocytes to PPAR-gamma agonists. [12]

  • 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. [3]

  • 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. [3]

  • 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. [3]
    • Hypoxia leads to an induction of leptin and VEGF expression in adipocytes, raising the likelihood that a low oxygen tension leads to the stimulation of angiogenesis in adipose tissue through the HIF-1 pathway. [3]

    Influenced by:

    • insulin receptor
      in fat_cell
      • The ability of insulin to stimulate VEGF formation by adipocytes suggests that the elevated circulating levels of insulin in obesity promote angiogenesis in adipose tissue as well as the enhanced accumulation of fat in human adipocytes. [13]

  • 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]

    Influenced by:

    • insulin receptor
      in fat_cell
      • Insulin enhanced the formation of IL-8. [13]

  • Hormone: IL-10

    • Secretion of IL-10 from human adipocytes. [3]

  • Hormone: RBP4

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

  • Hormone: cholesteryl ester transfer protein

    • CETP is either present on the lipoprotein surface or secreted by the adipocyte. [16]

  • Hormone: metallothionein

    • Metallothionein is a low molecular-weight cysteine-rich, stress-response and metal-binding protein expressed in human adipose tissue. [17]

  • 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

  • Hormone: angiotensinogen

    • Esxpression is increased in obese state. [19]

  • Hormone: PGI2

  • Hormone: FGF-2

  • Hormone: PAI-1

    Influenced by:

    • beta-2 adrenoreceptor
      in fat_cell
      • Catecholamines are able to down-regulate PAI-1 expression and secretion in human adipocytes via beta-adrenergic receptors. [20]

  • Hormone: visfatin

  • Hormone: ANG-2

    Influenced by:

    • leptin receptor isoform b
      in fat_cell
      • Leptin induces Ang-2 and no VEGF in cultured adipocytes. [21]

  • Hormone: IGF-1A

    • Expression is increased in obese state. [19]

Receptors

  • Receptor: insulin receptor

    Influences:

    • VEGF-165
      • The ability of insulin to stimulate VEGF formation by adipocytes suggests that the elevated circulating levels of insulin in obesity promote angiogenesis in adipose tissue as well as the enhanced accumulation of fat in human adipocytes. [13]
    • IL-8
      • Insulin enhanced the formation of IL-8. [13]
    • leptin

  • Receptor: CaSR

    Induced phenotype:

    • regulation of lipid biosynthetic process
      • CaSR signaling could be plausible related to proliferation, differentiation, and metabolic activity of adipose cells. Activation of the receptor in the adipocyte is expected to trigger signaling cascades, that have been described in relevant phenomena in adipocyte metabolism such as adipogenesis and lipogenesis. [22]
    • inhibition of lipolysis
      • The CaSR displays an inhibitory effect on lipolysis by mediating intracellular cAMP and calcium levels causing the downregulation of downstream key enzymes of lipolysis (i.e. HSL and ATGL). [23]

  • Receptor: growth hormone receptor

    Influences:

    • leptin

  • Receptor: LXR-alpha

    Induced phenotype:

    • regulation of gene expression
      • Expression and ligand activation of LXRα has no significant effect on adipogenesis or lipid accumulation and does not modulate the adipogenic activity of PPARγ. The identification of novel LXR adipocyte target genes in cultured cells and in vivo points to an important role for LXR in the regulation of adipocyte gene expression and adipose tissue function distinct from PPARγ. [24]
    • regulation of lipid biosynthetic process
      • LXR activates the coordinate expression of major fatty acid biosynthetic genes (lipogenesis) and increased plasma triglyceride and phospholipid levels. [25]

  • Receptor: leptin receptor isoform b

    Influences:

    • ANG-2
      • Leptin induces Ang-2 and no VEGF in cultured adipocytes. [21]

  • Receptor: PPAR-gamma1

    Induced phenotype:

    • regulation of glucose homeostasis
      • PPAR-gamma is expressed in human fat, one tissue where most of the insulin-stimulated glucose uptake occurs. [26]

  • 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. [27]

  • Receptor: beta-2 adrenoreceptor

    Influences:

    • PAI-1
      • Catecholamines are able to down-regulate PAI-1 expression and secretion in human adipocytes via beta-adrenergic receptors. [20]
    • leptin
      • Catecholamines suppress leptin release from in vitro differentiated subcutaneous human adipocytes via b1- and b2-adrenergic receptors. [8]

  • Receptor: beta-1 adrenoreceptor

    Influences:

    • leptin
      • Catecholamines suppress leptin release from in vitro differentiated subcutaneous human adipocytes via b1- and b2-adrenergic receptors. [8]

  • Receptor: beta-3 adrenoreceptor

    Influences:

    • insulin
      • b3-Adrenergic receptors (b3-ARs) are expressed predominantly on white and brown adipocytes, and acute treatment of mice with CL 316,243, a potent and highly selective b3-AR agonist, produces a 2-fold increase in energy expenditure, a 50–100-fold increase in insulin levels, and a 40–50% reduction in food intake. [28]
      • CL-mediated effects on insulin levels and food intake and only minimally restored effects on oxygen consumption, indicating that any effect on insulin secretion and food intake, and a full stimulation of oxygen consumption required the presence of b3-ARs in white adipocytes. [28]

  • Receptor: leptin receptor

    Induced phenotype:

    • regulation of lipid metabolic process
      • Leptin receptor is the receptor for obesity factor leptin and is involved in the regulation of fat metabolism. [29]

  • Receptor: PPAR-gamma2

    Induced phenotype:

    • regulation of glucose homeostasis
      • PPAR-gamma is expressed in human fat, one tissue where most of the insulin-stimulated glucose uptake occurs. [26]
Reference