Muscle fitness and mass deteriorate under the conditions of obesity and aging for reasons yet to be fully elucidated. Herein, we describe a novel pathway linking peripheral nutrient sensing and skeletal muscle function through the sweet taste receptor TAS1R2 and the involvement of ERK2-PARP1-NAD signaling axis. Muscle-specific deletion of TAS1R2 (mKO) in mice produced elevated NAD levels due to suppressed PARP1 activity, improved mitochondrial function, increased muscle mass and strength, and prolonged running endurance. Deletion of TAS1R2 in obese or aged mice also ameliorated the decline in muscle mass and fitness arising from these conditions. Remarkably, partial loss-of-function of TAS1R2 (rs35874116) in older, obese humans recapitulated the healthier muscle phenotype displayed by mKO mice in response to exercise training. Our findings show that inhibition of the TAS1R2 signaling in skeletal muscle is a promising therapeutic approach to preserve muscle mass and function.
This article examines the effect of two recent and connected developments on fisheries management in New Zealand. The first development is a change to s 13 of the Fisheries Act 1996, that Act’s central operative sustainability provision. The second development is the Supreme Court’s decision in the Kahawai case. This article argues that these two developments mean that the operation and interpretation of the Fisheries Act favour commercial interests over recreational ones. It argues that the minority’s interpretation in the Kahawai case was correct and that, therefore, the change to s 13 was unnecessary. This article concludes that the structural bias in the Fisheries Act is undesirable, as catch allowance decisions are (and should be) essentially political.
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