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The pathophysiology of MASLD/MASH encompasses complex interactions among genetic background, impaired insulin signaling, hepatic lipid accumulation, inflammatory cascades, and progressive fibrosis

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The first GIP receptor antagonist was introduced in 1986 ( Figure 3 ), and in recent years, the truncated and deactivated form of GIP, GIP(3-30)NH 2 , has proven to be a potent and specific GIP receptor antagonist in humans in high concentrations, and suitable for studies of endogenous GIP physiology and pathophysiology (14) ( Table 1 )

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Probiotic supplementation and late-onset sepsis in preterm infants: a meta-analysis