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Deletion, but Not Heterozygosity, of eNOS Raises Blood Pressure and Aggravates Nephropathy in BTBR ob/ob Mice. | LitMetric

AI Article Synopsis

  • ob/ob mice, a model for type 2 diabetes, were genetically modified to lack eNOS in order to study how this affects diabetic nephropathy, a kidney complication associated with diabetes.
  • In experiments with various groups of mice, measurements of blood pressure, kidney function, and injury markers were taken as the mice aged.
  • Results showed that complete loss of eNOS worsened kidney injury and increased blood pressure significantly, indicating that eNOS plays a crucial protective role in diabetic kidney disease.

Article Abstract

Introduction: ob/ob mice are a leptin-deficient type 2 diabetes mellitus model, which, on a BTBR background, mimics the glomerular pathophysiology of diabetic nephropathy (DN). Since leptin deficiency reduces blood pressure (BP) and endothelial nitric oxide synthase (eNOS) lowers BP and is kidney protective, we attempted to develop a more robust DN model by introducing eNOS deficiency in BTBR ob/ob mice.

Methods: Six experimental groups included littermate male and female BTBR ob/ob or wild-type for ob (control) as well as wild-type (WT), heterozygote (HET), or knockout (KO) for eNOS. Systolic BP (by automated tail-cuff) and GFR (by FITC-sinistrin plasma kinetics) were determined in awake mice at 27-30 weeks of age, followed by molecular and histological kidney analyses.

Results: Male and female ob/ob WT presented hyperglycemia and larger body and kidney weight, GFR, glomerular injury, and urine albumin to creatinine ratio (UACR) despite modestly lower BP versus control WT. These effects were associated with a higher tubular injury score and renal mRNA expression of NGAL only in males, whereas female ob/ob WT unexpectedly had lower KIM-1 and COL1A1 expression versus control WT, indicating sex differences. HET for eNOS did not consistently alter BP or renal outcome in control or ob/ob. In comparison, eNOS KO increased BP (15-25 mm Hg) and worsened renal markers of injury, inflammation and fibrosis, GFR, UACR, and survival rates, as observed in control and, more pronouncedly, in ob/ob mice and independent of sex.

Conclusions: Deletion, but not heterozygosity, of eNOS raises blood pressure and aggravates nephropathy in BTBR ob/ob mice.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11291698PMC
http://dx.doi.org/10.1159/000536522DOI Listing

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