A protein involved in fasting’s epigenetic effects

This 2018 Illinois rodent study conducted a series of experiments on a protein that’s activated by fasting:

“Jumonji D3 (JMJD3) histone demethylase epigenetically regulates development and differentiation, immunity, and tumorigenesis by demethylating a gene repression histone mark, H3K27-me3. JMJD3 has what we believe to be a novel metabolic role and epigenetically regulates mitochondrial β-oxidation.

Epigenetic modifications play a critical role in linking environmental signals, such as changes in nutrient and hormonal levels and the circadian rhythm, to regulate genes to maintain homeostasis. Epigenetics is particularly relevant to metabolic regulation.

In response to fasting, the interaction of JMJD3 with both SIRT1 and PPARα is induced, which leads to epigenetic activation of their own genes and of β-oxidation network genes. Downregulation of hepatic JMJD3 leads to intrinsic defects in β-oxidation, which results in liver steatosis as well as glucose and insulin intolerance.

JMJD3 was required for the beneficial effects mediated by expression of SIRT1 in obese mice and vice versa. Restoration of JMJD3 to normal levels in HFD [high-fat diet]-fed obese mice leads to improved fatty acid β-oxidation and ameliorates metabolic symptoms of obesity and these beneficial effects are largely dependent on SIRT1.”


Have to hand it to the researchers who named this protein to coincidentally rhyme with a children’s book and movie. It certainly provokes more interest than other ways of naming discoveries, such as after what it resembles and/or the discoverer’s name.

https://www.jci.org/articles/view/97736 “Fasting-induced JMJD3 histone demethylase epigenetically activates mitochondrial fatty acid β-oxidation”

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