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Overall, these studies underscore the intricate relationships between DPP-4, glucose regulation, obesity, and inflammation, highlighting its complexity and interactions with bone metabolism, along with its regulatory mechanisms, suggesting potential therapeutic implications [4, 32, 36]

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Progesterone attenuates Abeta25-35-induced neuronal toxicity via JNK inactivation and progesterone receptor membrane component 1-dependent inhibition of mitochondrial apoptotic pathway