Advanced glycation end products and diabetic nephropathy: a comparative study using diabetic and normal rats with methylglyoxal-induced glycation

被引：34

作者：

Rodrigues, Lisa ^{[1
]}

Matafome, Paulo ^{[1
,2
,3
]}

Crisostomo, Joana ^{[1
]}

Santos-Silva, Daniela ^{[1
]}

Sena, Cristina ^{[1
]}

Pereira, Paulo ^{[2
]}

Seica, Raquel ^{[1
]}

机构：

[1] Univ Coimbra, Lab Physiol, IBILI, Fac Med, Coimbra, Portugal

[2] Univ Coimbra, Fac Med, Ctr Ophthalmol & Visual Sci, IBILI, Coimbra, Portugal

[3] Univ Coimbra, Fac Med, P-3000354 Coimbra, Portugal

来源：

JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY | 2014年 / 70卷 / 01期

关键词：

Advanced glycation end products; Methylglyoxal; Diabetic nephropathy; Type; 2; diabetes; ENDOTHELIAL GROWTH-FACTOR; RENAL-FUNCTION; COMPLICATIONS; OBESITY; KIDNEY; CELLS; OVEREXPRESSION; GLYCOXIDATION; DYSFUNCTION; EXPRESSION;

D O I：

10.1007/s13105-013-0291-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Hyperglycemia-related advanced glycation end product (AGE) formation is a key mechanism in diabetic nephropathy. Since methylglyoxal (MG) is a potent AGE precursor, we aimed to assess the role of MG-related AGE formation in the progression of renal damages. A comparative study between Wistar (W, normal) and Goto-Kakizaki (GK, nonobese type 2 diabetic) rats was performed at 6 and 14 months old and after 14 weeks of MG administration to 6-month-old rats. Diabetic rats showed progressive structural, biochemical, and functional alterations, including AGE, albuminuria, and tissue hypoxia, which were partially mimicked by MG administration to young GK rats. Aged Wistar rats had an impairment of some parameters, whereas MG administration caused a phenotype similar to young GK rats, including oxidative stress, impaired apoptotic and angiogenic markers, and structural lesions. MG accumulation specifically impaired several of the renal disease markers progressively observed in diabetic rats, and thus, it contributes to the progression of diabetic nephropathy.

引用

页码：173 / 184

页数：12

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