Response to Hinke et al.
- Edoardo Mannucci, MD12 and
- Carlo M. Rotella, MD1
- 1Section of Endocrinology, Department of Clinical Pathophysiology, University of Florence Medical School, Florence, Italy
- 2Section of Geriatrics, Department of Critical Care, University of Florence Medical School, Florence, Italy
We agree with Hinke et al. (1) that metformin acts mainly through the inhibition of hepatic glucose output and the enhancement of peripheral insulin sensitivity, through unidentified molecular mechanisms in the liver and skeletal muscle. However, it has been observed that metformin could enhance glucose-induced insulin secretion in some experimental conditions (2), although the relevance of this effect for the antihyperglycemic action of metformin is questionable. Furthermore, glucagon-like peptide (GLP)-1 has been shown to increase insulin sensitivity and non–insulin-mediated glucose disposal (3,4), suggesting that DPP-IV inhibitors, which increase GLP-1 levels, could …
