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Abstract
Accumulating evidence from rodent and human studies indicates that the activity of thermogenic adipocytes positively correlates with optimal metabolic function. In this issue of the JCI, Yesian et al. uncover a paracrine signaling pathway from type 2 innate lymphoid cells to preadipocytes via IL-13 that increases beige adipogenesis through a PPARγ-dependent pathway. Mice with deletion of Il13ra1 demonstrated glucose dysregulation, and variants near the human IL13RA1 locus were associated with body weight and diabetic status. It is tempting to speculate that targeting IL-13 holds therapeutic potential for improving metabolic fitness in humans.
Authors
Margo P. Emont, Jun Wu
Figure 1
IL-13 signaling primes preadipocytes to differentiate into beige adipocytes.
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ILC2s secrete IL-13, which signals through IL-13Rα1 on preadipocytes. Subsequent activation of STAT6 and p38 MAPK recruits PGC-1α to PPARγ to drive a thermogenic transcriptional program. The expression of thermogenic genes promotes differentiation of the cells into beige adipocytes with elevated mitochondrial respiration capacity.
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ISSN: 0021-9738 (print), 1558-8238 (online)