Abstract
Obesity is a state of leptin resistance in which the membrane leptin receptor and the JAK-STAT pathway are blocked. This leads to increased intracellular concentrations of lipid metabolites, increased non-oxidative metabolism by adipocytes, and stimulation of the cell estrogen cycle. These factors are potentially oncogenic via the shared mitogen-activated protein kinase (MAPK), mitogen/extracellular signal-regulated kinase (MEK) and extracellular signal-regulated kinase (ERK) cellular pathways.
MeSH terms
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Adipocytes / metabolism
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Animals
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Enzyme Inhibitors / pharmacology
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Estrogens / metabolism*
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Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Humans
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Leptin / metabolism*
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Lipids / blood
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MAP Kinase Kinase Kinases / antagonists & inhibitors
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MAP Kinase Kinase Kinases / metabolism
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Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
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Mitogen-Activated Protein Kinase Kinases / metabolism
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Neoplasms / enzymology
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Neoplasms / metabolism*
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Obesity / enzymology
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Obesity / metabolism*
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Obesity / pathology
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Protein-Tyrosine Kinases / metabolism
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Receptors, Cell Surface / metabolism
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Receptors, Estrogen / metabolism
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Receptors, Leptin
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STAT Transcription Factors / metabolism
Substances
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Enzyme Inhibitors
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Estrogens
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LEPR protein, human
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Leptin
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Lipids
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Receptors, Cell Surface
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Receptors, Estrogen
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Receptors, Leptin
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STAT Transcription Factors
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Protein-Tyrosine Kinases
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Extracellular Signal-Regulated MAP Kinases
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MAP Kinase Kinase Kinases
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Mitogen-Activated Protein Kinase Kinases