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By contrast, preclinical in vivo and in vitro studies both indicate that incretin receptor agonism can attenuate fibrogenic signalling in models of kidney disorders, and thus the positive clinical trial data on kidney function outcome measures may, in part, be mediated by inhibition of fibrosis

Hence, the pathophysiological role of LPL activity in NAFLD remains elusive ( Figure 4 )

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A study in 2019 identified the HLA-DQB1*0609 serotype as increasing the risk of POTS by over 8-fold.[ref] Other genetic variants increase susceptibility to POTS in different ways