Effects of troglitazone and temocapril in spontaneously hypertensive rats with chronic renal failure

Yoshida, Kazunori; Kohzuki, Masahiro; Xu, Hong; Wu, Xuemei; Kamimoto, Masahiro; Sato, Tokutaro

doi:10.1097/00004872-200103000-00019

Cited by 25 publications

(24 citation statements)

References 38 publications

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“…Hyperinsulinemia may have also played a role in progression of kidney disease in this model. In the present study, insulin levels were elevated, and it is known that treatment with troglitazone to correct hyperinsulinemia slows progression of kidney disease (35). Lipotoxicity is an attractive mechanism, inasmuch as the cholesterol derangements in fructose feeding are striking, and treatment with statins has been shown to slow the progression of kidney disease in the RK model (20).…”

Section: Discussionsupporting

confidence: 45%

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Gersch

Mu²,

Cirillo³

et al. 2007

American Journal of Physiology-Renal Physiology

188

145

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The metabolic syndrome has recently been recognized as a risk factor for kidney disease, but the mechanisms mediating this risk remain unclear. High fructose consumption by animals produces a model of the metabolic syndrome with hypertension, hyperlipidemia, and insulin resistance. The present study was conducted to test the hypothesis that consumption of a high-fructose diet could accelerate the progression of chronic kidney disease. Three groups of 14 male Sprague-Dawley rats were pair fed a specialized diet containing 60% fructose (FRU) or 60% dextrose (DEX) or standard rat chow (CON). After the animals were fed their assigned diet for 6 wk, five-sixths nephrectomy was performed, and the assigned diet was continued for 11 wk. Proteinuria was significantly increased and creatinine clearance was decreased in the FRU group compared with the CON and DEX groups, and blood urea nitrogen was higher in the FRU group than in the CON and DEX groups. Kidneys from the FRU group were markedly larger than kidneys from the CON and DEX groups. Glomerular sclerosis, tubular atrophy, tubular dilatation, and cellular infiltration appeared markedly worse in kidneys from the FRU group than in kidneys from the DEX and CON groups. Monocyte chemoattractant protein-1 (MCP-1) was measured in renal tissue homogenate and found to be increased in the FRU group. In vitro studies were conducted to determine the mechanism for increased renal MCP-1, and fructose stimulation of proximal tubular cells resulted in production of MCP-1. In conclusion, consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model. metabolic syndrome; high-fructose corn syrup; monocyte chemoattractant protein-1

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Section: Discussionsupporting

confidence: 45%

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Gersch

Mu²,

Cirillo³

et al. 2007

American Journal of Physiology-Renal Physiology

188

145

View full text Add to dashboard Cite

show abstract

“…This may help explain the beneficial effects of TZD in animal models of glomerulosclerosis that are not associated with insulin resistance (16,17) and extend the potential relevance of these compounds to glomerulopathies that are mediated by inflammatory mechanisms. Accordingly, a recent study showed that TZD renoprotective activity in crescentic glomerulonephritis is paralleled by inhibition of glomerular monocyte infiltration (51).…”

Section: Discussionmentioning

confidence: 94%

“…This seems, at least in part, independent of their metabolic action as beneficial effects are also seen in nondiabetic models of glomerulosclerosis such as the spontaneous hypertensive rat and the remnant kidney model (16,17). Of interest, TZD are also potent monocyte inhibitors (18) and prevent MCP-1 overexpression in a rat model of myocardial infarction (19), raising the possibility that their renoprotective properties are mediated by their anti-inflammatory action.…”

mentioning

confidence: 99%

Mechanical Stretch Induces Monocyte Chemoattractant Activity via an NF-κB-Dependent Monocyte Chemoattractant Protein-1-Mediated Pathway in Human Mesangial Cells

Gruden¹,

Setti²,

Hayward³

et al. 2005

Journal of the American Society of Nephrology

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Hemodynamic abnormalities are important in the pathogenesis of the glomerular damage in diabetes. Glomerular macrophage infiltration driven by the chemokine monocyte chemoattractant protein-1 (MCP-1) is an early event in diabetic nephropathy. The thiazolidinedione rosiglitazone ameliorates albumin excretion rate in diabetic patients with microalbuminuria and has anti-inflammatory properties, raising the possibility of a relationship between its renoprotective and anti-inflammatory activity. Investigated was whether mesangial cell stretching, mimicking in vitro glomerular capillary hypertension, enhances MCP-1 expression and monocyte chemoattractant activity. The effect of the combination of stretch with high glucose on MCP-1 production was studied and, finally, the effect of rosiglitazone on these processes was assessed. Stretching of human mesangial cells significantly enhanced their monocyte chemoattractant activity. This effect was mediated by MCP-1 as it was paralleled by a significant rise in both MCP-1 mRNA and protein levels and was completely abolished by MCP-1 blockade. Combined exposure to both stretch and high glucose further increased MCP-1 production. Stretch activated the IB-NF-B pathway, and NF-B inhibition, with the use of the specific inhibitor SN50, completely abolished stretch-induced MCP-1, indicating that stretch-induced MCP-1 was NF-B dependent. The addition of rosiglitazone significantly diminished stretch-induced NF-B activation, MCP-1 production, and monocyte chemotaxis. In conclusion, stretching of mesangial cells stimulates their monocyte chemoattractant activity via an NF-B-mediated, MCP-1-dependent pathway, and this effect is prevented by rosiglitazone.

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“…This speed (20 m/min) corresponds to 70% VO2 max in SHR (21). The systolic blood pressure (SBP) was measured by the indirect tailcuff method as described previously (22). After 5 h of fasting and 24 h without exercise and/or drug administration, rats were decapitated and blood was collected for biochemical analysis.…”

Section: Experimental Animalsmentioning

confidence: 99%

Regulation of Skeletal Muscle Peroxisome Proliferator-Activated Receptor .GAMMA. Expression by Exercise and Angiotensin-Converting Enzyme Inhibition in Fructose-Fed Hypertensive Rats

et al. 2004

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Effects of troglitazone and temocapril in spontaneously hypertensive rats with chronic renal failure

Abstract: The results suggest that troglitazone has renoprotective effects in this rat model. These effects might be due to the inhibition of growth factors rather than to the minute hypotensive effect, although the mechanism remains to be elucidated.

Cited by 25 publications

References 38 publications

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Mechanical Stretch Induces Monocyte Chemoattractant Activity via an NF-κB-Dependent Monocyte Chemoattractant Protein-1-Mediated Pathway in Human Mesangial Cells

Regulation of Skeletal Muscle Peroxisome Proliferator-Activated Receptor .GAMMA. Expression by Exercise and Angiotensin-Converting Enzyme Inhibition in Fructose-Fed Hypertensive Rats

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