Captopril Inhibits Glucose Accumulation in Retinal Cells in Diabetes

Zhang, Jin Z.; Gao, Ling; Widness, M.; Xia, Xi; Kern, Timothy S.

doi:10.1167/iovs.02-1193

Cited by 50 publications

(28 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the influence of other AGE inhibitors on glycaemic control as well as cellular uptake of glucose has not yet been defined. Similar results in retinal cells using captopril [101] also showed a reduction in glucose-mediated damage via GLUT-1 (membrane glucose transport protein) and the results of both these studies appear to be insulin-mediated occurrences.…”

Section: Metabolic Disturbancessupporting

confidence: 68%

A New Perspective on Therapeutic Inhibition of Advanced Glycation in Diabetic Microvascular Complications: Common Downstream Endpoints Achieved Through Disparate Therapeutic Approaches?

Sourris¹,

Harcourt²,

Forbes³

2009

Am J Nephrol

View full text Add to dashboard Cite

A commonality among the chemically disparate compounds that inhibit the formation and accumulation of advanced glycation end products (AGEs) or their signalling pathways is their end organ protection in experimental models of diabetes complications. Although this group of therapeutics are structurally and functionally distinct with numerous mechanisms of action, the most important factor governing their therapeutic capability is clearly their ability to alleviate the tissue burden of advanced glycation, rather than the biochemical mechanism by which this is achieved. However, it remains to be determined if it is the reduction in tissue AGE levels per se or inhibition of downstream signal pathways which is ultimately required for end organ protection. For example, a number of these agents stimulate antioxidant defences, modify lipid profiles and inhibit low-grade inflammation. These novel actions emphasise the importance of further examination of the advanced glycation pathway and in particular the diverse action of these agents in ameliorating the development of diabetic complications such as nephropathy.

show abstract

Section: Metabolic Disturbancessupporting

confidence: 68%

A New Perspective on Therapeutic Inhibition of Advanced Glycation in Diabetic Microvascular Complications: Common Downstream Endpoints Achieved Through Disparate Therapeutic Approaches?

Sourris¹,

Harcourt²,

Forbes³

2009

Am J Nephrol

View full text Add to dashboard Cite

show abstract

“…16 In addition, treatment with captopril but not atenolol prevents uptake of glucose into cultured retinal endothelial cells. 43 With this in mind, it is possible that the improvement in neuronal function observed in this study is related to improvements in the retinal vasculature.…”

Section: Effect Of Valsartan and Atenolol On Diabetic Neuronal Lossesmentioning

confidence: 84%

Retinal Dysfunction in Diabetic Ren-2 Rats Is Ameliorated by Treatment with Valsartan but Not Atenolol

Phipps

Wilkinson-Berka

Fletcher

2007

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

show abstract

“…Hepatocytes isolated and cultured as described above were washed three times with PBS, followed by incubation as indicated previously (81) for 1 h at 37°C, 5% CO 2 in glucose-free DMEM [instead of the Williams medium E] to which was added 6, 20, or 30 mM glucose. Medium was then removed and hepatocytes were washed with ice-cold 100 mM MgCl 2 containing 0.1 mM phloretin as an inhibitor of glucose transport (131). Hepatocytes were then scraped from the dishes with PBS and protease inhibitor at 4°C followed by disruption with a probe sonicator (Sonic Dismembrator 550, Fisher Scientific, Waltham, MA) at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…After centrifugation at 10,000 g, 4°C, for 20 min, the supernatant and a standard curve of glucose were used for quantitating glucose analysis with an Amplite Glucose Quantitation Kit (AAT Bioquest Sunnyvale, CA) as in Ref. 131 [1-3 H]glucose at the same specific activity, was prepared for culturing mouse primary hepatocytes for 0 or 6 h incubation. Hepatocytes were then washed with PBS followed by determination of 3 H incorporation into triacylglycerols (TG) and unesterified LCFAs as well as quantitation of TG and unesterified LCFA mass as described previously (5).…”

Section: Methodsmentioning

confidence: 99%

Impact of L-FABP and glucose on polyunsaturated fatty acid induction of PPARα-regulated β-oxidative enzymes

Petrescu

Huang

Martin

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

. Impact of L-FABP and glucose on polyunsaturated fatty acid induction of PPAR␣-regulated ␤-oxidative enzymes. Am J Physiol Gastrointest Liver Physiol 304: G241-G256, 2013. First published December 13, 2012; doi:10.1152/ajpgi.00334.2012.-Liver fatty acid binding protein (L-FABP) is the major soluble protein that binds very-long-chain n-3 polyunsaturated fatty acids (n-3 PUFAs) in hepatocytes. However, nothing is known about L-FABP's role in n-3 PUFA-mediated peroxisome proliferator activated receptor-␣ (PPAR␣) transcription of proteins involved in long-chain fatty acid (LCFA) ␤-oxidation. This issue was addressed in cultured primary hepatocytes from wild-type, L-FABP-null, and PPAR␣-null mice with these major findings: 1) PUFA-mediated increase in the expression of PPAR␣-regulated LCFA ␤-oxidative enzymes, LCFA/LCFA-CoA binding proteins (L-FABP, ACBP), and PPAR␣ itself was L-FABP dependent; 2) PPAR␣ transcription, robustly potentiated by high glucose but not maltose, a sugar not taken up, correlated with higher protein levels of these LCFA ␤-oxidative enzymes and with increased LCFA ␤-oxidation; and 3) high glucose altered the potency of n-3 relative to n-6 PUFA. This was not due to a direct effect of glucose on PPAR␣ transcriptional activity nor indirectly through de novo fatty acid synthesis from glucose. Synergism was also not due to glucose impacting other signaling pathways, since it was observed only in hepatocytes expressing both L-FABP and PPAR␣. Ablation of L-FABP or PPAR␣ as well as treatment with MK886 (PPAR␣ inhibitor) abolished/ reduced PUFA-mediated PPAR␣ transcription of these genes, especially at high glucose. Finally, the PUFA-enhanced L-FABP distribution into nuclei with high glucose augmentation of the L-FABP/ PPAR␣ interaction reveals not only the importance of L-FABP for PUFA induction of PPAR␣ target genes in fatty acid ␤-oxidation but also the significance of a high glucose enhancement effect in diabetes. polyunsaturated; fatty acid; oxidation; glucose; liver fatty acid binding protein; peroxisome proliferator activated receptor-␣; hepatocyte THE SEVERAL FORMS OF DIABETES mellitus and associated complications are the sixth leading cause of death in the US, and incidence is rising (22,101,123,132). Nearly 80% of people with diabetes die of cardiovascular disease (CVD), particularly coronary heart disease (20, 102). Thus benefits of any lipid intervention may be greatest in these individuals (97,102,114). Although dietary improvements, exercise, and statins have significantly decreased the incidence and severity of CVD, residual CVD risk remains especially high (62-82%) among individuals with diabetes mellitus, even with optimum statin therapy (102,113). This difference is thought to be due primarily to a residual dyslipidemia in this population, particularly hypertriglyceridemia (113).The liver is key in maintaining homeostasis of long-chain fatty acid (LCFA) and glucose metabolism (14, 105). Hepatic peroxisome proliferator activated receptor-␣ (PPAR␣) is the major transcription factor con...

show abstract

Captopril Inhibits Glucose Accumulation in Retinal Cells in Diabetes

Abstract: Inhibition of glucose accumulation within retinal cells probably contributes at least in part to the observed inhibition of diabetic retinopathy by ACE inhibitors.

Cited by 50 publications

References 17 publications

A New Perspective on Therapeutic Inhibition of Advanced Glycation in Diabetic Microvascular Complications: Common Downstream Endpoints Achieved Through Disparate Therapeutic Approaches?

A New Perspective on Therapeutic Inhibition of Advanced Glycation in Diabetic Microvascular Complications: Common Downstream Endpoints Achieved Through Disparate Therapeutic Approaches?

Retinal Dysfunction in Diabetic Ren-2 Rats Is Ameliorated by Treatment with Valsartan but Not Atenolol

Impact of L-FABP and glucose on polyunsaturated fatty acid induction of PPARα-regulated β-oxidative enzymes

Contact Info

Product

Resources

About