Protein restriction in lactation confers nephroprotective effects in the male rat and is associated with increased antioxidant expression.
Telomere shortening has been implicated in the aging process and various age-associated disorders, including renal disease. Moreover, oxidative stress has been identified as an initiator of accelerated telomere shortening. We have shown previously that maternal protein restriction during lactation leads to reduced renal telomere shortening, reduced albuminuria, and increased longevity in rats. Here we address the hypothesis that maternal protein restriction during lactation is nephroprotective and associated with increased expression of antioxidative enzymes and decreased age-dependent renal telomere shortening. Newborn rats were suckled by a dam fed either a control (20% protein) or low-protein (8% protein) diet. All animals were weaned onto standard chow. Offspring that had been suckled by protein-restricted mothers had reduced albuminuria, N-acetyl-glucosaminidase, and urinary aldosterone excretion. These animals also did not show significant age-dependent renal telomere shortening and hence had significantly longer telomeres at 12 mo of age. This lack of renal telomere shortening was associated with increased levels of the antioxidant enzymes manganese superoxide dismutase, glutathione peroxidase, and glutathione reductase. These findings suggest that beneficial effects of slow growth during lactation are associated with increased antioxidant capacity and prevention of age-dependent telomere shortening in the kidney.
Tarry-Adkins
Jane L
JL
Department of Clinical Biochemistry, University of Cambridge, Addenbrookes Hospital, Hills Road, Cambridge, UK. jane.adkins@ntlworld.com
Joles
Jaap A
JA
Chen
Jian-Hua
JH
Martin-Gronert
Malgorzata S
MS
van der Giezen
Dionne M
DM
Goldschmeding
Roel
R
Hales
C Nicholas
CN
Ozanne
Susan E
SE
D000118:Acetylglucosaminidase / Q000652:urine; D000419:Albuminuria / Q000378:metabolism / Q000652:urine; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D015415:Biomarkers; D001724:Birth Weight / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004032:Diet; D018753:Diet, Protein-Restricted; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007668:Kidney / Q000254:growth & development / Q000473:pathology / Q000648:ultrastructure; D007672:Kidney Cortex / Q000473:pathology / Q000648:ultrastructure; D007674:Kidney Diseases / Q000473:pathology / Q000517:prevention & control*; D007677:Kidney Function Tests; D007774:Lactation / Q000502:physiology*; D008297:Male; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D016615:Telomere / Q000502:physiology / Q000648:ultrastructure; D000094765:Glutathione Peroxidase GPX1
D000975:Antioxidants; D015415:Biomarkers; D000450:Aldosterone; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D000118:Acetylglucosaminidase; D000094765:Glutathione Peroxidase GPX1; C000722069:Gpx1 protein, rat