Dietary modulation of the progression of nephropathy in aging rats: an evaluation of the importance of protein

Masoro, Edward J.; Iwasaki, Keisuke; Gleiser, Chester A.; McMahan, C. Alex; Seo, Eunhui; Yu, Bo

doi:10.1093/ajcn/49.6.1217

Cited by 151 publications

(102 citation statements)

References 28 publications

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“…Transglomerular capillary pressures are not markedly elevated in proteinuric OZRs (35,36), pair-feeding has not been shown to reduce blood pressure (37), and reduction of blood pressure in OZRs with pharmacological agents does not uniformly lead to reduction in renal disease (38). Protein restriction reduces the progression of renal disease pathology in rats, but caloric restriction without protein restriction accomplishes the same effect (39,40). In addition, studies evaluating this effect generally restrict protein by 60% to 65% compared with controls vs. the more modest 25% restriction of both calories and protein used in our study (41).…”

Section: Discussionmentioning

confidence: 81%

Hyperphagia as a Mediator of Renal Disease Initiation in Obese Zucker Rats

et al. 2001

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Objective: We sought to determine whether prevention of overeating would block the very earliest manifestations of renal injury in young obese Zucker rats (OZRs). Research Methods and Procedures: Three groups of rats were studied, obese (fa/fa) Zucker rats and lean (Fa/Fa). Zucker controls were allowed to feed ad libitum, whereas a group of obese (fa/fa) Zucker rats was pair-fed to the lean group. Urine albumin and serum lipids were studied weekly from 6 to 10 weeks of age. Renal pathology and renal glomerular gene expression were examined when the rats were killed at 10 weeks of age. Results: Obese rats fed ad libitum developed significant albuminuria by 6 weeks of age, increasing at each subsequent time-point. This increase was completely blocked by pair-feeding. Serum triglycerides were significantly increased in obese rats fed ad libitum vs. the other groups. Urine albumin correlated significantly with both body weight and serum triglyceride level. Renal histopathology was normal in all groups. Analysis of gene expression of glomerular proteins by reverse transcriptase-polymerase chain reaction revealed that pair-feeding attenuated the increased expression of glomerular desmin, fibronectin, and the 92-kDa collagenase that was seen in obese animals fed ad libitum. Discussion: Prevention of overeating in young OZR normalizes albuminuria and attenuates the pathogenic alterations in glomerular gene expression seen at the initiation of renal disease in obese animals allowed to feed ad libitum. This model may be relevant for studying the early endorgan effects of obesity.

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Section: Discussionmentioning

confidence: 81%

Hyperphagia as a Mediator of Renal Disease Initiation in Obese Zucker Rats

et al. 2001

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“…Furthermore, restriction of yeast is reported to extend life span in flies more robustly than restriction of glucose [110]. On the other hand, dietary restriction without reduction in protein extends life span as well as dietary restriction with reduction of protein [111]. Furthermore, reduction of lipids only without reduction of caloric intake failed to increase life span [112].…”

Section: Problemsmentioning

confidence: 99%

Secrets of the lac Operon

Mobbs¹,

Mastaitis²,

Zhang³

et al. 2006

Interdisciplinary Topics in Gerontology

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Elevated blood glucose associated with diabetes produces progressive and apparently irreversible damage to many cell types. Conversely, reduction of glucose extends life span in yeast, and dietary restriction reduces blood glucose. Therefore it has been hypothesized that cumulative toxic effects of glucose drive at least some aspects of the aging process and, conversely, that protective effects of dietary restriction are mediated by a reduction in exposure to glucose. The mechanisms mediating cumulative toxic effects of glucose are suggested by two general principles of metabolic processes, illustrated by the lac operon but also observed with glucose-induced gene expression. First, metabolites induce the machinery of their own metabolism. Second, induction of gene expression by metabolites can entail a form of molecular memory called hysteresis. When applied to glucose-regulated gene expression, these two principles suggest a mechanism whereby repetitive exposure to postprandial excursions of glucose leads to an age-related increase in glycolytic capacity (and reduction in ␤-oxidation of free fatty acids), which in turn leads to an increased generation of oxidative damage and a decreased capacity to respond to oxidative damage, independent of metabolic rate. According to this mechanism, dietary restriction increases life span and reduces pathology by reducing exposure to glucose and therefore delaying the development of glucose-induced glycolytic capacity.

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“…These findings have led to speculation that a reduction in dietary protein intake rather than caloric intake is the dietary factor responsible for life extension. This speculation ignores the finding that a reduction in food intake by 40% without reducing protein intake is as effective in extending life as reducing the intake of food including protein by 40% (Masoro et al 1989). Clearly, there is no need to reduce the intake of protein for food restriction to extend the life of rats.…”

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confidence: 99%

Role of Hormesis in Life Extension by Caloric Restriction

Masoro¹

2007

Dose-Response

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ᮀ Caloric restriction (CR) markedly extends the life of rats, mice and several other species, and it also modulates age-associated physiological deterioration and delays the occurrence and/or slows progression of age-associated diseases. The level of CR that retards the aging processes is a low-intensity stressor, which enhances the ability of rats and mice of all ages to cope with intense stressors. CR thus exhibits a hormetic action in these species, and therefore it is hypothesized that hormesis plays a role in the life-extending and anti-aging actions of CR. Both the findings in support of this hypothesis and those opposing it are critically considered. However, it is likely that hormesis is not the only process contributing to CR-induced life extension. It is proposed that two general processes are involved in CR-induced life extension. One is the reduced endogenous generation of damaging agents, such as reactive oxygen species. The second is hormesis, which enhances processes that protect against the action of damaging agents and also promotes processes that repair the damage once it occurs.

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Dietary modulation of the progression of nephropathy in aging rats: an evaluation of the importance of protein

Cited by 151 publications

References 28 publications

Hyperphagia as a Mediator of Renal Disease Initiation in Obese Zucker Rats

Hyperphagia as a Mediator of Renal Disease Initiation in Obese Zucker Rats

Secrets of the lac Operon

Role of Hormesis in Life Extension by Caloric Restriction

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