title: Dietary n-3 polyunsaturated fatty acids revert renal responses induced by a combination of 2 protocols that increase the amounts of advanced glycation end product in rats.
abstract: Renal dysfunction is a severe complication that is caused by diabetes mellitus. Many factors associate the progression of this complication with high levels of proinflammatory and pro-oxidant substances, such as advanced glycation end products (AGEs), which form a heterogeneous group of compounds that can accumulate in tissues such as retinas, joints, and kidneys. The hypothesis of this study is that n-3 polyunsaturated fatty acids (n-3 PUFAs) have a nephroprotective effect on rats after exposing them to a combination of 2 protocols that increase the AGE amounts: a high-fat diet enriched with AGEs and a diabetes rat model. Adult Wistar rats were divided into 6 groups that received the following diets for 4 weeks: (1) control group; 2) HAGE: high AGE fat-containing diet group; (3) HAGE + n-3: high AGE fat-containing diet plus n-3 PUFAs group; (4) diabetic group; (5) Db + HAGE: high AGE fat-containing diet diabetic group; and (6) Db + HAGE + n-3: high AGE fat-containing diet plus n-3 PUFAs diabetic group. Diabetes mellitus was induced by an intraperitoneal injection of alloxan (150 mg kg(-1)). In diabetic and nondiabetic rats, the high HAGE fat-containing diet increased the serum creatinine, tumor necrosis factor-α, thiobarbituric acid reactive substances, and reactive oxygen species levels, as well as the superoxide dismutase/catalase + glutathione peroxidase ratio and the superoxide dismutase 2 and receptor for advanced glycation end products immunocontent of the kidneys. n-3 Polyunsaturated fatty acids attenuated these alterations and influenced the receptor for advanced glycation end products/oxidative stress/tumor necrosis factor-α axis. In summary, this study showed that the extrinsic AGE pathway (HAGE diet) had a greater effect on renal metabolism than the intrinsic AGE pathway (diabetes induction) and that n-3 PUFAs appear to prevent renal dysfunction via antioxidant and anti-inflammatory pathways.
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil; Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil. Electronic address: amassis@terra.com.br.
authors.forename: Adriano M
authors.initials: AM
authors.lastname: de Assis
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Anderson
authors.initials: A
authors.lastname: Rech
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Aline
authors.initials: A
authors.lastname: Longoni
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Maurílio
authors.initials: M
authors.lastname: da Silva Morrone
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Matheus A
authors.initials: MA
authors.lastname: de Bittencourt Pasquali
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil; Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Marcos L S
authors.initials: ML
authors.lastname: Perry
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil; Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: Diogo O
authors.initials: DO
authors.lastname: Souza
authors.affiliation: Postgraduate Program in Biochemistry, ICBS, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil; Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil.
authors.forename: José C F
authors.initials: JC
authors.lastname: Moreira
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000150:complications; D003928:Diabetic Nephropathies / Q000097:blood / Q000517:prevention & control*; D004032:Diet; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology / Q000627:therapeutic use*; D017127:Glycation End Products, Advanced / Q000097:blood*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism*; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015525:Fatty Acids, Omega-3; D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D003404:Creatinine
keywords: Dietary n-3 polyunsaturated fatty acids; High AGE fat–containing diet; Oxidative stress; Proinflammatory status; Renal parameters