scholarly journals Administration of metformin in clinical medicine; an updated mini-review on current findings

2018 ◽  
Vol 7 (2) ◽  
pp. 61-65
Author(s):  
Mahrang Hedaiaty

Metformin is in the biguanide class that has been considered as the treatment for insulin resistance diabetes and polycystic ovarian disease. Many mechanisms have been suggested for it such as inhibition of the mitochondrial respiratory chain and mitochondrial glycerophosphate dehydrogenase, activation of adenosine monophosphate-activated protein kinase, inhibition of glucagon-induced elevation of cyclic adenosine monophosphate with reduced activation of protein kinase A, an effect on gut microbiota and activation of adenosine monophosphateactivated protein kinase. Metformin is a suppressor for transforming growth factor-β1 via directly binding and interact with transforming growth factor-β1 receptor. Lactic acidosis is one of the adverse and noxious effects of metformin. Nowadays, metformin has an important role in inflammation pathways and antioxidant pathways that can prevent or decrease kidney fibrosis, cardiac remodeling in hypertensive heart disease, and cell death in cerebral ischemia, kidney crystal formation, immunological diseases and cancer. Although there has been strong evidence for the potential harm caused by metformin, several studies have shown beneficial effects for it. Hence, it is necessary to revision and modification in contraindications for prescription of this drug

1996 ◽  
Vol 318 (2) ◽  
pp. 519-525 ◽  
Author(s):  
Andrée R. OLIVIER ◽  
Gurdip HANSRA ◽  
Trevor R. PETTITT ◽  
Michael J. O. WAKELAM ◽  
Peter J. PARKER

Bombesin induces the down-regulation of protein kinase C-Δ (PKC-Δ) and PKC-ϵ in Swiss 3T3 cells. Simultaneous addition of transforming growth factor β1 (TGFβ1) selectively blocks PKC-Δ down-regulation at mid-S-phase, whereas PKC-ϵ levels continue to decline. Northern blot analysis shows that PKC-ϵ levels could be controlled in part at the level of transcription; PKC-Δ mRNA levels remained constant at these later times. Bombesin induces a sustained elevation of some species of diacylglycerol (DAG), consistent with the observed loss of PKC-Δ and PKC-ϵ. Interestingly, the combination of bombesin and TGF-β1 produces an even greater DAG response. Flow cytometric analysis demonstrates that bombesin induces only 15% of the cells to enter the cell cycle, in contrast to the combination of TGFβ1 plus bombesin which induces 75–80% of the cells to progress through the cycle. The protection of PKC-Δ from down-regulation under conditions of sustained DAG elevation correlates with the mitogenic response and implies that the down-regulation process itself is regulated. Consistent with this, it is demonstrated that bombesin plus TGFβ1 protects PKC-Δ from phorbol ester-induced down-regulation.


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