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111 Therefore, abnormal Hippo/YAP pathways may be the potential pathogenesis of IR and other metabolic disease (Fig
Also, glutamate excitotoxicity, itself, forms fragmented mitochondria, contributing to oxidative stress through the dysfunctional mitochondria (80)
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From this result, it can be assumed that proline administration itself causes oxidative stress in the liver, and it may be probably attributable to the metabolism of proline
That is one reason many clinicians prefer to confirm stable thyroid function before or soon after initiating a GLP-1 or GLP-1/GIP medication
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