4.5 Article

Autophagy as a crosstalk mediator of metabolic organs in regulation of energy metabolism

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出版社

SPRINGER
DOI: 10.1007/s11154-013-9272-6

关键词

Autophagy; Insulin resistance; Non-cell-autonomous effect; FGF21; Mitokine; IL-1 beta

资金

  1. Global Research Laboratory Grant of the National Research Foundation of Korea [K21004000003-10A0500-00310]
  2. Samsung Biomedical Research Institute [SP1-B2-051-2, GE1B30911]
  3. National Research Foundation of Korea [2010-00347] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Autophagy plays an important role in the regulation of cellular homeostasis through elimination of aggregated proteins, damaged organelles, and intracellular pathogens. Autophagy also contributes to the maintenance of energy balance through degradation of energy reserves such as lipids, glycogen, and proteins in the setting of increased energy demand. Recent studies have suggested that autophagy, or its deficiency, is implicated in the pathogenesis of insulin resistance, obesity, and diabetes. These effects of autophagy or its deficiency in regulation of energy metabolism are mediated not only by cell-autonomous effects, such as direct autophagic degradation of energy stores or intracellular organelles (endoplasmic reticulum and mitochondria) but also by non-cell-autonomous effects, such as induction/suppression of secreted factors or changes of sympathetic tone. In the present review, we highlight a recent surge in the research on the autophagy in the regulation of energy homeostasis, with a focus on its role as a mediator for crosstalk between metabolic organs.

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