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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 )

GLP-1 stimulates insulin secretion by PKC-dependent TRPM4 and TRPM5 activation

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