Effect of pioglitazone on the early stage of type 2 diabetic nephropathy in KK/Ta mice

Tanimoto, Masuhisa; Fan, Qiuling; Gohda, Tomohito; Shike, Toshihide; Makita, Yuichiro; Tomino, Yasuhiko

doi:10.1016/j.metabol.2004.06.016

Cited by 60 publications

(58 citation statements)

References 37 publications

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“…Yoshimoto et al (1997) demonstrated that therapy with pioglitazone not only improved lipid and glucose metabolism, but also lowered blood pressure, decreased proteinuria, and prevented glomerular injury, renal arteriolosclerosis and aortic medial wall thickening in genetically obese diabetic rats (35). Pioglitazone also improved the urinary albumin/creatinine ratio (ACR) and the glomerular and Bowman's capsule volume ratios, and reduced endothelial constitutive nitric oxide synthetase (ecNOS) in the endothelium of glomerular vessels in early stage of type 2 diabetic nephropathy in mice (75). An increase in renal tubular cell albumin uptake induced by pioglitazone has also been reported (76).…”

Section: Diabetic Nephropathymentioning

confidence: 99%

Peroxisome proliferator-activated receptor gamma agonists in renal disease

Iglesias

Díez

2006

eur j endocrinol

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Type 2 diabetes is a well recognised cause of chronic renal failure (CRF). Only few oral antidiabetic drugs can be used for treating type 2 diabetes in patients with CRF. Among them are repaglinide, a rapid-acting prandial insulin releaser, and peroxisome proliferator-activated receptor gamma (PPARg) agonists, such as rosiglitazone and pioglitazone. These compounds are metabolised in the liver, therefore accumulation of the drug and the risk of severe and prolonged hypoglycaemia are minimised. PPARg receptors are expressed in many tissues including the kidney. Recently, numerous healthful effects of PPARg agonists on several aspects related to renal function have been increasingly reported. These drugs have shown to possess many advantageous anti-inflammatory, haemodynamic, vascular and metabolic effects. In the present paper we have reviewed the more recent experimental studies that evaluated these potential beneficial effects of PPARg agonists on renal function and revised the results of their utilisation in patients with different degrees of renal impairment, in dialysis patients, and in patients with diabetes mellitus after kidney transplantation. Finally, tolerability and safety profile of PPARg agonists in patients with reduced glomerular filtration rate are also analysed. European Journal of Endocrinology 154 613-621

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Section: Diabetic Nephropathymentioning

confidence: 99%

Peroxisome proliferator-activated receptor gamma agonists in renal disease

Iglesias

Díez

2006

eur j endocrinol

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“…Studies on humans, particularly in diabetic patients, have suggested that PPARg agonists significantly, although to a small extent, decrease blood pressure and proteinuria (Sarafidis et al 2010). Furthermore, studies on rodent models of diabetic and non-diabetic kidney disease have shown that the renoprotective effects of TZDs may lie beyond their effects on blood pressure and glucose homeostasis (Yoshimoto et al 1997, Buckingham et al 1998, Ma et al 2001, Tanimoto et al 2004, and it has, therefore, been suggested that PPARg agonists may show promise as therapeutic agents for diabetic renal injury.…”

Section: Introductionmentioning

confidence: 99%

Diabetic nephropathy and long-term treatment effects of rosiglitazone and enalapril in obese ZSF1 rats

Bilan¹,

Salah²,

Bastacky³

et al. 2011

Journal of Endocrinology

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Diabetic nephropathy (DN) is a major cause of end-stage renal disease. Yet the pathogenic mechanisms underlying the development of DN are not fully defined, partially due to lack of suitable models that mimic the complex pathogenesis of renal disease in diabetic patients. In this study, we describe early and late renal manifestations of DN and renal responses to long-term treatments with rosiglitazone or high-dose enalapril in ZSF1 rats, a model of metabolic syndrome, diabetes, and chronic renal disease. At 8 weeks of age, obese ZSF1 rats developed metabolic syndrome and diabetes (hyperglycemia, glucosuria, hyperlipidemia, and hypertension) and early signs of renal disease (proteinuria, glomerular collagen IV deposition, tubulointerstitial inflammation, and renal hypertrophy). By 32 weeks of age, animals developed renal histopathology consistent with DN, including mesangial expansion, glomerulosclerosis, tubulointerstitial inflammation and fibrosis, tubular dilation and atrophy, and arteriolar thickening. Rosiglitazone markedly increased body weight but reduced food intake, improved glucose control, and attenuated hyperlipidemia and liver and kidney injury. In contrast, rosiglitazone markedly increased cardiac hypertrophy via a blood pressure-independent mechanism. High-dose enalapril did not improve glucose homeostasis, but normalized blood pressure, and nearly prevented diabetic renal injury. The ZSF1 model thus detects the clinical observations seen with rosiglitazone and enalapril in terms of primary and secondary endpoints of cardiac and renal effects. This and previous reports indicate that the obese ZSF1 rat meets currently accepted criteria for progressive experimental diabetic renal disease in rodents, suggesting that this may be the best available rat model for simulation of human DN.

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“…17 Pioglitazone reduces glomerular and Bowman's capsule volume ratios in early stages of diabetic nephropathy in mice. 18 It remains possible that pioglitazone could also cause a true deterioration in renal function even if offset by declining cardiovascular risk through other mechanisms.…”

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confidence: 99%