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This observation led to the development of (Pro3)GIP, an analog of GIP with a glutamic-acid-to-proline substitution at position 3, improving glucose homeostasis and preventing weight gain in animal models of diabetes and obesity (Sparre-Ulrich et al., 2016)

An mTORC1-to-CDK1 switch maintains autophagy suppression during Mitosis

Established therapies such as platelet-rich plasma (PRP) have more extensive clinical evidence and regulatory approval for certain applications

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Glucagon receptor activation appears counterintuitive in obesity and diabetes therapy because glucagon acutely increases hepatic glucose output