Authors:

Jinying Yang

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Beiging of adipocytes is characteristic of a higher number of mitochondria, the central hub of metabolism in the cell. However, studies show that beiging can improve metabolic healt h or cause metabolic disorders. Here we discuss a liver-fat crosstalk for iron flux associat ed with healthy beiging of adipocytes. Deletion of the transcription factor, a protein t hat control gene activity, FoxO1 in adipocytes (adO1KO mice) induces a higher iron flux from the liver to white adipose tissue, concurrent with higher activity of mitochondrial bioge nesis that increases iron demands. In addition, adO1KO mice adopt an alternate mechan ism to sustain mitophagy, which enhances mitochondrial quality control, thereby im proving mitochondrial respiratory capacity and metabolic health. However, the liver-fat cros stalk is not detectable in adipose Atg7 knockout (ad7KO) mice, which undergo b eiging of adipocytes but have metabolic dysregulation. Autophagic clearance of mitoc hondria is blocked in ad7KO mice, which accumulates dysfunctional mitochondria a nd elevates mitochondrial content but lowers mitochondrial respiratory capacity. M itochondrial biogenesis is comparable in the control and ad7KO mice, and the iron influx in to adipocytes and iron efflux from the liver remain unchanged. Therefore, activation of the liver-fat crosstalk is critical for mitochondrial quality control that underlies healthy beiging of adipocytes.

Source:

University of Florida / Jinying Yang, Limin Shi, Anna L. Cubito, James F. Collins, / 2024

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Co-authors:

Jinying Yang