AI Article Synopsis

  • Eating too much food can lead to health problems like insulin resistance, which affects how our body uses sugar.
  • In experiments with mice, activating a special protein called Nrf2 helped these mice stay healthy even when they ate a lot of fat by keeping their sugar levels balanced and helping them process fats better.
  • The mice with a special gene also showed fewer bad fat cells and better overall health because of improved metabolism and how their bodies used energy.

Article Abstract

Chronic nutrient excess leads to metabolic disorders and insulin resistance. Activation of stress-responsive pathways via Nrf2 activation contributes to energy metabolism regulation. Here, inducible activation of Nrf2 in mice and transgenesis of the Nrf2 target, NQO1, conferred protection from diet-induced metabolic defects through preservation of glucose homeostasis, insulin sensitivity, and lipid handling with improved physiological outcomes. NQO1-RNA interaction mediated the association with and inhibition of the translational machinery in skeletal muscle of NQO1 transgenic mice. NQO1-Tg mice on high-fat diet had lower adipose tissue macrophages and enhanced expression of lipogenic enzymes coincident with reduction in circulating and hepatic lipids. Metabolomics data revealed a systemic metabolic signature of improved glucose handling, cellular redox, and NAD metabolism while label-free quantitative mass spectrometry in skeletal muscle uncovered a distinct diet- and genotype-dependent acetylation pattern of SIRT3 targets across the core of intermediary metabolism. Thus, under nutritional excess, NQO1 transgenesis preserves healthful benefits.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7678866PMC
http://dx.doi.org/10.1038/s41514-020-00051-6DOI Listing

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