Buformin suppresses the expression of glyceraldehyde 3-phosphate dehydrogenase.

  title={Buformin suppresses the expression of glyceraldehyde 3-phosphate dehydrogenase.},
  author={A. Yano and Masafumi Kubota and K. Iguchi and S. Usui and K. Hirano},
  journal={Biological \& pharmaceutical bulletin},
  volume={29 5},
The biguanides metformin and buformin, which are clinically used for diabetes mellitus, are known to improve resistance to insulin in patients. Biguanides were reported to cause lactic acidosis as a side effect. Since the mechanism of the side effect still remains obscure, we have examined genes whose expression changes by treating HepG2 cells with buformin in order to elucidate the mechanisms of the side effect. A subtraction cDNA library was constructed by the method of suppressive… Expand
Regulation of glyceraldehyde 3-phosphate dehydrogenase expression by metformin in HepG2 cells.
Signal transducers, adenylate cyclase (AC), protein kinase A (PKA), and AMPK, are involved in the signaling pathway triggered by metformin and CRE-binding protein is one of the transcription factors for the GAPD gene down-regulated by met formin. Expand
Buformin suppresses osteosarcoma via targeting AMPK signaling pathway
Buformin could suppress tumor growth and invasion of osteosarcoma through directly targeting the AMPK signaling pathway and therefore represents a new potential treatment option for osteosARcoma. Expand
Buformin exhibits anti-proliferative and anti-invasive effects in endometrial cancer cells.
Buformin has significant anti-proliferative and anti-metastatic effects in endometrial cancer cells through modulation of the AMPK/mTOR pathway, and IC50 values were lower for buformin than metformin, suggesting that bu formin may be more potent for endometricrial cancer treatment and worthy of further investigation. Expand
Buformin suppresses proliferation and invasion via AMPK/S6 pathway in cervical cancer and synergizes with paclitaxel
It is demonstrated for the first time that buformin suppresses cellular proliferation and invasion through the AMPK/S6 signaling pathway, which arrests cell cycle and inhibits cellular invasion in cervical cancer cells. Expand
Systematic analysis of diabetes- and glucose metabolism-related proteins and its application to Alzheimer's disease
Alzheimer disease has been defined as Type 3 Diabetes due to their shared metabolic profiles. Like our previously research, results of Alzheimer’s disease and other neurodegenerative diseases,Expand
Can acute overdose of metformin lead to lactic acidosis?
Apparent metformin mono-overdose is associated with MALA, a multicenter poison control database review of Illinois and Washington Poison Centers between the 2001-2006 and 1999-2006 periods. Expand


The mechanisms by which mild respiratory chain inhibitors inhibit hepatic gluconeogenesis.
The effects of phenylethylbiguanide (phenformin) on the rate of gluconeogenesis and metabolite profiles in the perfused liver are similar to those caused by DCMU, supporting a mitochondrial locus of action for this hypoglycaemic agent. Expand
The mechanism of action of phenformin in starved rats.
The ability of phenformin to lower the blood glucose concentration after an intraperitoneal glucose load, with a concomitant increase in blood lactate concentration, indicated that the drug wasExpand
Effects of benfluorex on fatty acid and glucose metabolism in isolated rat hepatocytes: from metabolic fluxes to gene expression.
It is suggested that benfluorex mainly via S 422-1 reduces gluconeogenesis by affecting gene expression and metabolic status of hepatocytes. Expand
The effect of alkylguanidines on mitochondrial metabolism.
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Findings indicate that the alkylguanidines combine with an energy-rich intermediate involved in the phosphorylation process, and oligomycin inhibited oxidation equally well in both the active and resting phases of respiration. Expand
Effects of guanidine derivatives on mitochondrial function. 3. The mechanism of phenethylbiguanide accumulation and its relationship to in vitro respiratory inhibition.
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The data appear to be more consistent with a nonionic diffusion mechanism of biguanide uptake, with final distribution determined by the transmembrane pH gradient, than with distribution according to a trans Membrane electrical potential. Expand
Obligatory role of membrane events in the regulatory effect of metformin on the respiratory chain function.
The data strongly support the view that MET may recognise some specific membranous sites, likely belonging to effector systems, before penetrating the cell in a bound state via an obscure endocytotic event which still has to be identified. Expand
Evidence that the flux control coefficient of the respiratory chain is high during gluconeogenesis from lactate in hepatocytes from starved rats. Implications for the hormonal control of gluconeogenesis and action of hypoglycaemic agents.
It is concluded that the hormonal increase in mitochondrial matrix volume stimulates fatty acid oxidation and respiratory-chain activity, allowing stimulation of pyruvate carboxylation and thus gluconeogenesis to occur without major changes in [ATP]/[ADP] or [NADH]/,[NAD+] ratios. Expand
Mode of action of hypoglycemic agents. V. Studies with phenethylbiguanide in isolated perfused rat liver.
The results presented and discussed are interpreted to indicate that phenethylbiguanide influences hepatic gluconeogenesis by an indirect mechanism. Expand
Interaction of biguanides with mitochondrial and synthetic membranes.
It is concluded that a similar mechanism of action applies to synthetic and natural membranes as well, suggesting that screening of functional negative sites interferes with the translocation of cations linked to electron transport and the primary reactions in conservation of respiratory energy. Expand
Effect of metformin on fatty acid and glucose metabolism in freshly isolated hepatocytes and on specific gene expression in cultured hepatocytes.
It was shown that the main effect of metformin on hepatic gluconeogenesis was located upstream of the formation of dihydroxyacetone phosphate, and this work suggests that met formin could reduce hepatic glucose production through short-term (metabolic) and long- term (genic) effects. Expand