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PTHrP promotes chondrogenesis and suppresses hypertrophy from both bone marrow-derived and adipose tissue-derived MSCs

In conclusion, whatever medication that increases endogenous portal insulin (signaling) in T2DM patients, regardless of the glucose level (specifically sulfonylurea derivatives and peroxisome proliferatoractivated receptor [PPAR-] agonists, but not dipeptidyl peptidase-4 inhibitor [DPP4i], or glucagonlike peptide-1 [GLP-1] analogues) will lead to an increase in body weight, even when caloric intake is not increased

There may also be long-term risks due to limited human studies