Tags

Type your tag names separated by a space and hit enter

Adipose tissue as an endocrine organ.

Abstract

Adipose tissue plays a critical role in energy homeostasis, not only in storing triglycerides, but also responding to nutrient, neural, and hormonal signals and secreting adipokines that control feeding, thermogenesis, immunity, and neuroendocrine function. A rise in leptin signals satiety to the brain through receptors in hypothalamic and brainstem neurons. Leptin activates tyrosine kinase, Janus kinase 2, and signal transducer and activator of transcription 3, leading to increased levels of anorexigenic peptides, e.g., alpha-melanocyte stimulating hormone and cocaine- and amphetamine-regulated transcript, and inhibition of orexigenic peptides, e.g., neuropeptide Y and agouti-related peptide. Obesity is characterized by hyperleptinemia and hypothalamic leptin resistance, partly caused by induction of suppressor of cytokine signaling-3. Leptin falls rapidly during fasting and potently stimulates appetite, reduces thermogenesis, and mediates the inhibition of thyroid and reproductive hormones and activation of the hypothalamic-pituitary-adrenal axis. These actions are integrated by the paraventicular hypothalamic nucleus. Leptin also decreases glucose and stimulates lipolysis through central and peripheral pathways involving AMP-activated protein kinase (AMPK). Adiponectin is secreted exclusively by adipocytes and has been linked to glucose, lipid, and cardiovascular regulation. Obesity, diabetes, and atherosclerosis have been associated with reduced adiponectin levels, whereas adiponectin treatment reverses these abnormalities partly through activation of AMPK in liver and muscle. Administration of adiponectin in the brain recapitulates the peripheral actions to increase fatty acid oxidation and insulin sensitivity and reduce glucose. Although putative adiponectin receptors are widespread in peripheral organs and brain, it is uncertain whether adiponectin acts exclusively through these targets. As with leptin, adiponectin requires the central melanocortin pathway. Furthermore, adiponectin stimulates fatty acid oxidation and reduces glucose and lipids, at least in part, by activating AMPK in muscle and liver.

Links

  • FREE Publisher Full Text
  • Authors+Show Affiliations

    University of Pennsylvania School of Medicine, Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Philadelphia, PA 19104, USA. ahima@mail.med.upenn.edu

    Source

    Obesity (Silver Spring, Md.) 14 Suppl 5: 2006 Aug pg 242S-249S

    MeSH

    Adipocytes
    Adiponectin
    Adipose Tissue
    Animals
    Energy Metabolism
    Homeostasis
    Humans
    Leptin
    Signal Transduction

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural
    Review

    Language

    eng

    PubMed ID

    17021375

    Citation

    Ahima, Rexford S.. "Adipose Tissue as an Endocrine Organ." Obesity (Silver Spring, Md.), vol. 14 Suppl 5, 2006, 242S-249S.
    Ahima RS. Adipose tissue as an endocrine organ. Obesity (Silver Spring). 2006;14 Suppl 5:242S-249S.
    Ahima, R. S. (2006). Adipose tissue as an endocrine organ. Obesity (Silver Spring, Md.), 14 Suppl 5, 242S-249S.
    Ahima RS. Adipose Tissue as an Endocrine Organ. Obesity (Silver Spring). 2006;14 Suppl 5:242S-249S. PubMed PMID: 17021375.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Adipose tissue as an endocrine organ. A1 - Ahima,Rexford S, PY - 2006/10/6/pubmed PY - 2006/12/21/medline PY - 2006/10/6/entrez SP - 242S EP - 249S JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 14 Suppl 5 N2 - Adipose tissue plays a critical role in energy homeostasis, not only in storing triglycerides, but also responding to nutrient, neural, and hormonal signals and secreting adipokines that control feeding, thermogenesis, immunity, and neuroendocrine function. A rise in leptin signals satiety to the brain through receptors in hypothalamic and brainstem neurons. Leptin activates tyrosine kinase, Janus kinase 2, and signal transducer and activator of transcription 3, leading to increased levels of anorexigenic peptides, e.g., alpha-melanocyte stimulating hormone and cocaine- and amphetamine-regulated transcript, and inhibition of orexigenic peptides, e.g., neuropeptide Y and agouti-related peptide. Obesity is characterized by hyperleptinemia and hypothalamic leptin resistance, partly caused by induction of suppressor of cytokine signaling-3. Leptin falls rapidly during fasting and potently stimulates appetite, reduces thermogenesis, and mediates the inhibition of thyroid and reproductive hormones and activation of the hypothalamic-pituitary-adrenal axis. These actions are integrated by the paraventicular hypothalamic nucleus. Leptin also decreases glucose and stimulates lipolysis through central and peripheral pathways involving AMP-activated protein kinase (AMPK). Adiponectin is secreted exclusively by adipocytes and has been linked to glucose, lipid, and cardiovascular regulation. Obesity, diabetes, and atherosclerosis have been associated with reduced adiponectin levels, whereas adiponectin treatment reverses these abnormalities partly through activation of AMPK in liver and muscle. Administration of adiponectin in the brain recapitulates the peripheral actions to increase fatty acid oxidation and insulin sensitivity and reduce glucose. Although putative adiponectin receptors are widespread in peripheral organs and brain, it is uncertain whether adiponectin acts exclusively through these targets. As with leptin, adiponectin requires the central melanocortin pathway. Furthermore, adiponectin stimulates fatty acid oxidation and reduces glucose and lipids, at least in part, by activating AMPK in muscle and liver. SN - 1930-7381 UR - https://www.unboundmedicine.com/medline/citation/17021375/Adipose_tissue_as_an_endocrine_organ_ L2 - https://doi.org/10.1038/oby.2006.317 DB - PRIME DP - Unbound Medicine ER -