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Cited by 640

The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.

Adipose Tissue as an Endocrine Organ

Open access
Ahima, Rexford S.·2006·Obesity
DOI 10.1038/oby.2006.317
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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., α‐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.

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Metadata

Authors
Ahima, R. S.
Venue
Obesity
Publisher
Wiley
Published
2006-08
Volume
14
Issue
S8
Pages
242S-249S
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
DOI
10.1038/oby.2006.317
OpenAlex
W2158574701
Cited by
640
References
20
FWCI
30.32
Type
journal article
Language
en
Open access
bronze

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