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. 2019 Jul 11;31(6):487–501. doi: 10.1089/ars.2018.7626

FIG. 2.

FIG. 2.

The main regulators of autophagy in adipose tissue. Autophagy is regulated both transcriptionally and post-translationally. Nutrient stress such as overfeeding or starvation modulates autophagy through two main arms: mTORC1 activation (overfeeding) and AMPK (starvation). Phosphorylation of ULK1-FIP200-ATG13 complex by mTORC1 leads to its dissociation and inactivation. In contrast, during starvation, AMPK is activated, leading to ULK1/FIP200-ATG13 activation and autophagy initiation. AMPK also phosphorylates the mTORC1 inhibitor TSC2, thus activating autophagy. PKA activates autophagy in beige adipose tissue in response to β-adrenergic stimulation. The effect of PKA on autophagy may involve the transcription factors CREB, Mitf, and FoxO3. Similarly, mTORC1 activation inhibits the nuclear translocation of Tfeb, a transcription factor important for autophagy/lysosomal function. AMPK, adenosine monophosphate-activated protein kinase; CREB, cAMP response element binding; mTOR, mammalian target of rapamycin; mTORC1, mTOR complex 1; PKA, protein kinase A; Tfeb, transcription factor EB; TSC2, tuberous sclerosis 2. Color images are available online.