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Contrasting with these actions of GIPR activation to reduce food intake, Gipr knockout (KO) mice, and humans with impaired function GIPR variants, are protected against obesity, also probably through a central effect, as similar observations were made in global KO mice or mice lacking Gipr in nestin, synapsin or VGAT-expressing cells 4,5,9,10,11,12

Elevated levels could reflect a protective response to injury rather than a causal factor

Its protein levels are maintained at low levels through the ubiquitin-proteasome pathway, mediated by Kelch-like ECH-associated protein 1 (Keap1) (47)

Thus, the crucial equilibrium between ROS production and antioxidant reserve is vital to ensure cellular redox homeostasis and general well-being [29]

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