Evidence that pioglitazone, metformin and pentoxifylline are inhibitors of glycation

Rahbar, Samuel; Natarajan, Rama; Yerneni, KiranKumar; Scott, Stephen; Gonzales, Noe; Nadler, Jerry L.

doi:10.1016/s0009-8981(00)00327-2

Cited by 136 publications

(76 citation statements)

References 46 publications

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“…Even though the mechanisms whereby metformin prevents the non-enzymatic glycation of ApoA-I are not known, its structural similarity to aminoguanidine suggests that it probably attenuates the non-enzymatic glycation of ApoA-I by similar pathways [36,37]. However, the current results show that aminoguanidine and metformin are not equally effective in reducing methylglyoxal-mediated modifications to ApoA-I.…”

Section: Discussioncontrasting

confidence: 62%

Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I

et al. 2008

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Aims/hypothesis Hyperglycaemia, a key feature of diabetes, is associated with non-enzymatic glycation of plasma proteins. We have shown previously that the reactive α-oxoaldehyde, methylglyoxal, non-enzymatically glycates apolipoprotein (Apo)A-I, the main apolipoprotein of HDL, and prevents it from activating lecithin:cholesterol acyltransferase (LCAT), the enzyme that generates almost all of the cholesteryl esters in plasma. This study investigates whether the glycation inhibitors aminoguanidine and pyridoxamine, the insulin sensitiser metformin and the cross-link breaker alagebrium can inhibit and/or reverse the methylglyoxal-mediated glycation of ApoA-I and whether these changes can preserve or restore the ability of ApoA-I to activate LCAT.

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Section: Discussioncontrasting

confidence: 62%

Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I

et al. 2008

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“…We believe that PTX decreases TNFα levels, probably in part by inhibiting AGE and RAGE expression in the liver and arteries. In addition, a report indicated that PTX has strong inhibitory effects on AGE formation and AGE crosslinking [42] . .…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline alleviates high-fat diet-induced non-alcoholic steatohepatitis and early atherosclerosis in rats by inhibiting AGE and RAGE expression

Zhao

Zheng

et al. 2010

Acta Pharmacol Sin

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Aim:To investigate the expression of advanced glycation end products (AGEs) and their receptor RAGE in the livers and blood vessels of rats with non-alcoholic steatohepatitis (NASH) and the effect of pentoxifylline (PTX) on liver and artery function in rats with NASH. Methods: Sprague-Dawley rats were fed a high-fat diet for 12 weeks and given PTX by gavage for 4 weeks. The effects of PTX on hepatic liver and vessel function as well as the expression of AGE and RAGE in rats with NASH were assessed. The intima-media thickness (IMT) of the aorta and carotid artery was evaluated using ultrasonography. Results: Serum aspartic aminotransferase (AST) and blood levels of glucose (GLU) were reduced in the PTX group relative to the NASH group. The IMT of the aorta and carotid artery was increased in the NASH group compared with the control group. The IMT was reduced in NASH rats after treatment with PTX. Rats with NASH demonstrated higher AGE and RAGE protein levels in the liver and arteries compared with those of control rats. PTX treatment in NASH rats resulted in a decrease in AGE and RAGE protein levels in the liver and arteries compared with those in the NASH group. Conclusion: Early atherosclerosis was observed in rats with NASH induced by a 16-week high-fat diet. High expression of AGE and RAGE in the livers and arteries of rats with NASH may contribute to the pathogenesis of NASH and early atherosclerosis. PTX showed protective effects on hepatic and arterial function, partially through inhibition of AGE and RAGE expression.

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“…Out of the drugs currently used to treat diabetes, metformin and pioglitazone have been shown to reduce AGE formation in vitro [21]. Interestingly, acetylsalicylic acid -a drug widely use in patients suffering from atherosclerotic disease -and pentoxifyllin -a drug used in patients with peripheral artery disease -also inhibit non-enzymatic glycation [23]. Finally, the β-HMG CoA reductase inhibitor cerivastatin has been shown to inhibit AGE formation [24].…”

Section: Advanced Glycation End Products (Age)mentioning

confidence: 99%

Mechanisms by which diabetes increases cardiovascular disease

Gleissner

Galkina

Nadler

et al. 2007

Drug Discovery Today: Disease Mechanisms

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Diabetes mellitus is one of the major risk factors for cardiovascular disease which is the leading cause of death in the U.S. Increasing prevalence of diabetes and diabetic atherosclerosis makes identification of molecular mechanisms by which diabetes promotes atherogenesis an important task. Targeting common pathways may ameliorate both diseases. This review focuses on well known as well as newly discovered mechanisms which may represent promising therapeutic targets.

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Evidence that pioglitazone, metformin and pentoxifylline are inhibitors of glycation

Cited by 136 publications

References 46 publications

Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I

Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I

Pentoxifylline alleviates high-fat diet-induced non-alcoholic steatohepatitis and early atherosclerosis in rats by inhibiting AGE and RAGE expression

Mechanisms by which diabetes increases cardiovascular disease

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