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Query: UMLS:C0011881 (
diabetic nephropathy
)
10,836
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We investigated whether 1,25-dihydroxy-vitamin D
3
(1,25(OH)
2
D
3
) could improve early
diabetic nephropathy
through the DNA-damage-inducible transcript 4/
tuberous sclerosis 2
/mammalian target of rapamycin pathway. Rat mesangial cells were cultured in media containing normal glucose or high glucose and were treated with or without 1,25(OH)
2
D
3
. Mesangial cells proliferation was measured. Streptozotocin-induced diabetic rats were injected intravenously with a recombinant lentivirus against the rat vitamin D receptor gene. Urinary and serum albumin, fasting plasma glucose, serum triglyceride, total cholesterol, calcium, parathyroid hormone and serum 25-dihydroxy-vitamin D (25(OH)D) levels, mean glomerular volume, glomerular basement membrane thickness and total kidney volume were determined. The expressions of vitamin D receptor, DNA-damage-inducible transcript 4, and mammalian target of rapamycin were measured. 1,25(OH)
2
D
3
inhibited the proliferation of mesangial cells induced by hyperglycemia. 1,25(OH)
2
D
3
also significantly reduced albumin excretion, mean glomerular volume, glomerular basement membrane, and total kidney volume in rats with
diabetic nephropathy
. The expression of DNA-damage-inducible transcript 4 was elevated by 1,25(OH)
2
D
3
treatment. The phosphorylation of mammalian target of rapamycin was reduced by 1,25(OH)
2
D
3
treatment. Vitamin D receptor gene silencing blocked all of the above results. The current study demonstrates that 1,25(OH)
2
D
3
can effectively inhibit mesangial cells proliferation induced by hyperglycemia, thus suppressing the development of
diabetic nephropathy
. This study also shows that the nephron-protective effect of 1,25(OH)
2
D
3
occurs partly through the DDIT4/TSC2/mTOR pathway.
...
PMID:In vitro and in vivo inhibition of mTOR by 1,25-dihydroxyvitamin D
3
to improve early diabetic nephropathy via the DDIT4/TSC2/mTOR pathway. 2739 20