IL-6 and TNFα drive lipolysis in abnormal glucose metabolism following acute pancreatitis, suggesting lipolysis modulation as a potential therapeutic target.
May warrant caution against targeting IL-6/TNFα in post-AP AGM; hypothesis-generating and leaves open need for prospective trials.
Lipolysis appears to be an important pathogenetic mechanism in glucose derangements after diseases of the exocrine pancreas. IL-6 and TNFα are the driving forces behind lipolysis in individuals with AGM after AP. Modulation of lipolysis may be a promising therapeutic modality.
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Pendharkar et al. (2017) studied this question.
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