The recent identification of GFRAL as a receptor for GDF15, mediating its anorexic effects has led to a flurry of recent work into the function of this hormone. The sources (at least in the absence of cancer) of this hormone are still not entirely clear, but in this recent paper, Zhang et al explored how fasting regulates hepatic GDF15 and some of the consequences of its production. They found that prolonged fasting, carbohydrate restriction, or beta cell destruction led to elevations in GDF15 production in the liver. They suggest hepatic ER stress as a mediator of this process, and show that knockdown of GDF15 by adenoviral siRNA impairs hepatic lipid oxidation. These data also suggest a novel hepatokine action of GDF15 in regulating adipocyte lipolysis. These data suggest that GDF15 may have roles in addition to appetite regulation, and may be a larger co-ordinator of nutrient homeostasis.
These comments are crossposted on F1000 prime.
The recent identification of GFRAL as a receptor for GDF15, mediating its anorexic effects has led to a flurry of recent work into the function of this hormone. The sources (at least in the absence of cancer) of this hormone are still not entirely clear, but in this recent paper, Zhang et al explored how fasting regulates hepatic GDF15 and some of the consequences of its production. They found that prolonged fasting, carbohydrate restriction, or beta cell destruction led to elevations in GDF15 production in the liver. They suggest hepatic ER stress as a mediator of this process, and show that knockdown of GDF15 by adenoviral siRNA impairs hepatic lipid oxidation. These data also suggest a novel hepatokine action of GDF15 in regulating adipocyte lipolysis. These data suggest that GDF15 may have roles in addition to appetite regulation, and may be a larger co-ordinator of nutrient homeostasis. These comments are crossposted on F1000 prime.
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