Talk:Pavlovic 2022 Abstract Bioblast
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Comments by the Reviewer
Moreno-Sanchez Rafael 2022-05-31
- This abstract describes work that analyzes a highly important issue with clinical relevance. The elucidation of the biochemical mechanisms involved in the hypoglucemia-induced drug Metformin is certainly needed for improving clinical protocols of dosing for diabetic patients. Metformin has also been proposed as an anti-cancer drug. A few observations are listed below intended to gain strength in delivering the message.
- It is stated that metformin treatment decreased the ROUTINE respiration and the “OXPHOS state” (the authors may be referring to the OXPHOS capacity), and increased “depolarization of the mitochondrial inner membrane” in mouse skeletal muscle cells. These are interesting results, but the results on ET capacity, LEAK respiration and residual O2 consumption should be also disclosed, as they may have key mechanistic clues.
- The metformin effects on ROUTINE respiration and OXPHOS capacity “were more pronounced in the low glucose medium”. An effort should be made to elaborate a mechanistic explanation for this observation. Did gene transcription change when cells were cultured in low glucose vs. high glucose? Was the phospholipid membrane composition altered, in which a higher membrane permeability developed as a result of increased unsaturated fatty acid content and decreased cardiolipin level (this phospholipid regulates activity of several respiratory complexes and ATP/ADP translocase)?
- Erase the sentence in the 3rd paragraph “5 mM metformin…”, because it repeats information stated in the preceding text.
