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Publication

A feed-forward regulatory loop in adipose tissue promotes signaling by the hepatokine FGF21.

Genes & development | 2021

The cJun NH2-terminal kinase (JNK) signaling pathway is activated by metabolic stress and promotes the development of metabolic syndrome, including hyperglycemia, hyperlipidemia, and insulin resistance. This integrated physiological response involves cross-talk between different organs. Here we demonstrate that JNK signaling in adipocytes causes an increased circulating concentration of the hepatokine fibroblast growth factor 21 (FGF21) that regulates systemic metabolism. The mechanism of organ crosstalk is mediated by a feed-forward regulatory loop caused by JNK-regulated FGF21 autocrine signaling in adipocytes that promotes increased expression of the adipokine adiponectin and subsequent hepatic expression of the hormone FGF21. The mechanism of organ cross-talk places circulating adiponectin downstream of autocrine FGF21 expressed by adipocytes and upstream of endocrine FGF21 expressed by hepatocytes. This regulatory loop represents a novel signaling paradigm that connects autocrine and endocrine signaling modes of the same hormone in different tissues.

Pubmed ID: 33334822 RIS Download

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Associated grants

Agency: NIDDK NIH HHS, United States
Id: R01 DK116774
Agency: NIA NIH HHS, United States
Id: P01 AG051459
Agency: NIDDK NIH HHS, United States
Id: P30 DK045735
Agency: NIDDK NIH HHS, United States
Id: R01 DK121545
Agency: NIDDK NIH HHS, United States
Id: P30 DK034989
Agency: NIDDK NIH HHS, United States
Id: R01 DK107220
Agency: NIDDK NIH HHS, United States
Id: R01 DK055758
Agency: NCI NIH HHS, United States
Id: R00 CA215315
Agency: NCATS NIH HHS, United States
Id: UL1 TR001863
Agency: NIDDK NIH HHS, United States
Id: R01 DK112698
Agency: NIDDK NIH HHS, United States
Id: R01 DK114793

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