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. Author manuscript; available in PMC: 2022 Oct 21.
Published in final edited form as: Mol Aspects Med. 2021 Jun 11;82:100973. doi: 10.1016/j.mam.2021.100973

Fig. 2. Physiological regulation of hepatic autophagy.

Fig. 2.

Hepatic autophagy fluctuates with hormonal cues that respond to feeding and fasting cycles. During fasting, neuronal and hormonal cues (eg. Glucagon, ghrelin and GLP-1), as well as decreased levels of circulating metabolites, such as glucose, and amino acids trigger autophagy. In contrast, feeding leads to elevated levels of circulating insulin, adipokines, glucose, amino acids and bile acid, all of which inhibit hepatic autophagy. Basal hepatic autophagy also exhibits a rhythmic behavior and is coordinated with fluctuations in nutrient status. Nutrient flux also initiates transcriptional regulation of hepatic autophagy. Farnesoid X Receptor (FXR); Forkhead box O (FOXO); Glucagon-Like Protein-1 (GLP1); G protein-coupled receptor (GPCR); Peroxisome proliferator-activated receptor (PPAR); transcription factor EB (TFEB); Zinc Finger With KRAB And SCAN Domains 3 (ZKSCAN3).