Type 2 diabetes mellitus represents an international health concern with its growing number of patients worldwide. At the same time, excessive
salt consumption is also seen as a major cause of diseases such as
hypertension and may expedite renal complications in diabetic patients. In this study, we investigated the effects of excessive
sodium chloride supplementation on the kidney of the Spontaneously Diabetic Torii-Leprfa (SDT fatty) rat, an obese
type 2 diabetes model. Male and female SDT fatty rats and normal Sprague-Dawley (SD) rats at 5 weeks of age were loaded with 0.3%
sodium chloride (NaCl) in
drinking water for 13 weeks. Blood serum and urinary parameters were observed throughout the experiment and kidney samples were examined in histopathological and genetical analyses. Significant changes on the
body weight, blood pressure, urine volume,
creatinine clearance, blood
urea nitrogen (BUN), relative gene expressions of
tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β),
monocyte chemotactic protein-1 (MCP-1) and
transforming growth factor-β (TGF-β) were observed in the
salt-loaded male SDT fatty rats. Urinary L-type
fatty acid-binding protein (L-FABP) and
albumin levels were higher observed in the
salt-loaded male SDT fatty rats throughout the period, but urinary
albumin levels in the female SDT fatty rats remain unchanged. In the kidney, slight Armani-Ebstein changes, tubular degeneration, hyaline cast, and inflammatory cell infiltration were observed in female SDT fatty rats while the levels of some changes were higher in the
salt-loaded group. The kidney of the
salt-loaded male SDT fatty rats demonstrated a higher degree of lesions compared to the female group and the male unloaded group. Histopathological changes in
salt-loaded SDT fatty rats show that excessive
salt consumption may act as a diabetic pathology exacerbation factor, but the pathology may be influenced by gender difference. Urinary L-FABP levels may act as a useful
biomarker to detect slight tubular damages in the kidney. Excessive
salt loading was shown to exacerbate the renal injury in SDT fatty rats.