The apparent contrast between the present study and earlier findings [ 43 ] [ 45 ] may thus suggest that metformin acts (1) on GLP-1 secretion independently of AMPK, as recently reported in studies of hepatic gluconeogenesis [ 47 ], or (2) that there may be significant differences between the impact of acute and chronic activation of L-cell AMPK on a “gut-brain-liver axis”, with the latter acting chiefly to alter cell mass.
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Proglucagon Promoter Cre-Mediated AMPK Deletion in Mice Increases Circulating GLP-1 Levels and Oral Glucose Tolerance.
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