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Details for anatomical structure: liver

EndoNet ID: ENC00578

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Synonyms

liver, , Hepar

General information

The largest gland in the body of the vertebrates, exocrine, lying beneath the diaphragm in the right hypochondrium and upper part of the epigastrium; it is of irregular shape and weighs from 1 to 2 kg, it secretes the bile and is also of great importance in both carbohydrate and protein metabolism

Links to other resources

Cytomer cy0048368

Larger structures

  • parts_of_human_body
  • digestive_system

Substructures

  • B-lymphocyte
  • cell:plasma_cell
  • lymphoblast
  • hepatocyte
  • Kupffer_cell_stellate_cell_of_liver
  • smooth_muscle_cell
  • endothelial_cell
  • lipocyte_of_liver
  • sinusoidal_endothelial_cell
  • red_blood_cell
  • mast_cell
  • mesenchyme_cell
  • macrophage
  • fibroblast

Secreted hormones

  • Hormone: MSP

    • Hepatocyte growth factor-like protein (HGFL) is a liver-derived serum glycoprotein. [1]
  • Hormone: SAA1

    • SAA1 (Serum amyloid A1) protein is produced mainly in the liver and circulates in low levels in the blood.

    Influenced by:

    • IL-6R
      in hepatocyte
  • Hormone: FAM3A

  • Hormone: Serotransferrin

  • Hormone: FGF-23

  • Hormone: calcidiol

    • Prehormon wich is produced by hydroxylation of vitamin D3 (cholecalciferol) in the liver.
    • Calcidiol is then converted in the kidneys (by the enzyme 25(OH)D-1α-hydroxylase) into calcitriol (1,25-(OH)2D3), a secosteroid hormone that is the active form of vitamin D. It can also be converted into 24-hydroxycalcidiol in the kidneys via 24-hydroxylation.
  • Hormone: VLDL

  • Hormone: HDL

  • Hormone: chemerin

    • Abundant chemerin transcripts were found in liver, lung, pituitary, and ovary. [2]
    • Chemerin is secreted as a precursor of low biological activity, which upon proteolytic cleavage of its COOH-terminal domain, is converted into a potent and highly specific agonist of ChemR23, the chemerin receptor. [2]
  • Hormone: fetuin-B

    • This fetuin-B transcript could be detected in the liver and also at a lower level in the placenta. [3]

    Influenced by:

    • bile acid receptor
      in hepatocyte
      • FXR agonists induce fetuin-B expression in human primary hepatocytes. [4]

Receptors

  • Receptor: THRB1

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [5]
  • Receptor: CHRNA1-2

  • Receptor: PRLR

    Induced phenotype:

    • increase in bile secretion
      • Prolactin has been shown to increase bile secretion. [6]
    • stimulation of lipoprotein lipase activity
      • Prolactin has marked effects on lipid metabolism. PRL stimulates lipoprotein lipase activity in the liver. [7]
    • Factor XII activation
      • In terms of more specific protective effects, PRL induces the production of coagulation factor XII by the liver. [8]
  • Receptor: Sphingosine 1-phosphate receptor 3

    Induced phenotype:

    • hepatic stellate cell migration
      • S1P3 regulates migration and fibrogenic activation of HSCs. [9]
  • Receptor: Sphingosine 1-phosphate receptor 4

  • Receptor: Lysophosphatidic acid receptor 5

  • Receptor: G-protein coupled receptor 4

  • Receptor: G-protein coupled receptor 12

  • Receptor: Sphingosine 1-phosphate receptor 1

    Induced phenotype:

    • hepatic stellate cell migration
      • S1P1 regulates migration and fibrogenic activation of HSCs. [9]
  • Receptor: Sphingosine 1-phosphate receptor 2

  • Receptor: Psychosine receptor

    Induced phenotype:

    • negative regulation of oxidoreductase activity
      • Galactosylsphingosine, glucosylsphingosine and sphingosine all inhibited cytochrome c oxidase activity in mitochondria from rat liver. [10]
  • Receptor: AR

    Induced phenotype:

    • mediation of effects from thymus on liver
      • The thymus plays an important role in maintaining the drug-metabolizing enzyme activity, anti-oxidative ability and biomembrane integrity in the liver of rats. These effects are mediated by sex hormones. Androgen mainly mediates the regulation of the thymus on liver drug-metabolizing enzymes in male rats. [11]
  • Receptor: ER-alpha

    Induced phenotype:

    • mediation of effects from thymus on liver
      • The thymus plays an important role in maintaining the drug-metabolizing enzyme activity, anti-oxidative ability and biomembrane integrity in the liver of rats. These effects are mediated by sex hormones. Estrogen mainly mediates the effect of the thymus on liver anti-oxidative functions in female rats. [11]

    Influences:

    • CBG
      • Our results show that o,p′-DDD (mitotane) increases CBG expression and secretion by an ERα-dependent mechanism. [12]
  • Receptor: ER-beta

    Induced phenotype:

    • mediation of effects from thymus on liver
      • The thymus plays an important role in maintaining the drug-metabolizing enzyme activity, anti-oxidative ability and biomembrane integrity in the liver of rats. These effects are mediated by sex hormones. Estrogen mainly mediates the effect of the thymus on liver anti-oxidative functions in female rats. [11]
  • Receptor: 5-HT-2B

    Induced phenotype:

    • liver regeneration
      • 5-HT receptor subtype 2B mediates serotonin-dependent liver regeneration. [13]
  • Receptor: 5-HT-2A

  • Receptor: 5-HT-2A

    Induced phenotype:

    • liver regeneration
      • 5-HT receptor subtype 2A mediates serotonin-dependent liver regeneration. [13]
  • 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 [14]
Reference