Dietary lipoic acid supplementation can mimic or block the effect of dietary restriction on life span

Merry, B.J.; Kirk, Austin J.; Goyns, M.H.

doi:10.1016/j.mad.2008.04.004

Cited by 31 publications

(44 citation statements)

References 44 publications

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“…In contrast, switching rats not fed lipoic acid between ad libitum feeding and CR also switched the survival trajectory. These results suggest that supplementation with lipoic acid induced a "memory effect" on the animals, locking them into the survival trajectory of the feeding regimen before the switch (Merry et al, 2008). It is noteworthy that animals fed lipoic acid and switched from CR to ad libitum feeding gained weight, just like animals not fed lipoic acid, and thus it seems that although the longevity effects of CR were preserved, other effects of CR were not.…”

Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 88%

“…In fact, histone deacetylases, like sirtuins, modify epigenetic patterns (Fraga and Esteller, 2007). Merry et al (2008) showed in rats that dietary supplementation with ␣-lipoic acid, although by itself unable to extend lifespan, allowed animals switched from CR to ad libitum feeding at 12 months of age to maintain the survival trajectory and extended longevity characteristic of CR; conversely, animals switching from ad libitum to CR did not exhibit extended longevity. In contrast, switching rats not fed lipoic acid between ad libitum feeding and CR also switched the survival trajectory.…”

Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 99%

“…It is noteworthy that animals fed lipoic acid and switched from CR to ad libitum feeding gained weight, just like animals not fed lipoic acid, and thus it seems that although the longevity effects of CR were preserved, other effects of CR were not. Because lipoic acid can induce hyperacetylation of histones and potentially acts as a histone deacetylase inhibitor, the hypothesis that epigenetic mechanisms are involved in this memory effect that specifically influences the life-extending effects of CR is attractive (Merry et al, 2008), although it is also possible that changes in energy uptake or utilization could be involved, and further work is needed to elucidate the underlying mechanisms.…”

Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 99%

See 2 more Smart Citations

Genome-Environment Interactions That Modulate Aging: Powerful Targets for Drug Discovery

Magalhães

Wuttke

Wood

et al. 2012

Pharmacological Reviews

121

125

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Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 88%

Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 99%

Section: Future Prospects In Epigenetics and Agingmentioning

confidence: 99%

See 1 more Smart Citation

Genome-Environment Interactions That Modulate Aging: Powerful Targets for Drug Discovery

Magalhães

Wuttke

Wood

et al. 2012

Pharmacological Reviews

121

125

View full text Add to dashboard Cite

“…Alpha lipoic acid ( α LA) is a disulfide derivative of octanoic acid that forms an intra-molecular disulfide bond that is readily reduced to dihydrolipoic acid intra-cellularly [23]. Anorectic effects in rodents have been reported for α LA as well as improved hypertriglyceridemia in Zucker diabetic fatty rats [24].…”

Section: Introductionmentioning

confidence: 99%

Lipoic Acid Attenuates Innate Immune Infiltration and Activation in the Visceral Adipose Tissue of Obese Insulin Resistant Mice

Deiuliis

Kampfrath

Zhao

et al. 2011

Lipids

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Visceral adipose inflammation mediated by innate and adaptive immune alterations plays a critical role in diet-induced obesity and insulin resistance (IR). The dietary supplement α-lipoic acid (αLA) has been shown to ameliorate inflammatory processes in macrophages, however the relative significance of these effects in the context of visceral adipose inflammation and IR remain unknown. In this study we investigated its effects via both intraperitoneal and oral administration in lean and obese transgenic mice expressing yellow fluorescent protein (YFP) under control of a monocyte specific promoter (c-fmsYFP+). αLA significantly improved indices of insulin-resistance concomitant with a decrease in total (YFP+CD11b+) and activated (YFP+CD11b+CD11c+) visceral adipose tissue macrophages. Histologically, the visceral adipose tissue of obese mice receiving αLA had fewer “crown-like structures,” a hallmark of adipose inflammation in murine obesity. Monocyte adhesion assessed by intravital microscopy of cremasteric venules was attenuated by αLA. In cultured WT and toll-like receptor 4 (TLR4) null primary mouse macrophages, αLA significantly decreased basal CCR-2, MCP-1 and TNF-α expression levels. LPS treatment resulted in increased TNFα, MCP-1, and IL-6 expression while αLA partially abrogated the LPS effect on MCP-1 and TNFα; Interestingly, CCR-2 was not coordinately regulated. AαLA prevented LPS-induced nuclear factor kappa B (NFκB) activation in the same cultured macrophages. These data suggest that αLA may modulate visceral adipose inflammation, a critical determinant of IR via TLR4 and NF-κB pathways.

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“…Rat tissues used in this study were supplied from a previous experiment (Merry et al 2008). All animal husbandry procedures undertaken in this study were carried out in accordance with the provisions of the United Kingdom Animals (Scientific Procedures) Act 1986.…”

Section: Methodsmentioning

confidence: 99%

A-to-I RNA editing does not change with age in the healthy male rat brain

et al. 2013

Self Cite

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RNA editing is a post-transcriptional process, which results in base substitution modifications to RNA. It is an important process in generating protein diversity through amino acid substitution and the modulation of splicing events. Previous studies have suggested a link between gene-specific reductions in adenosine to inosine RNA editing and aging in the human brain. Here we demonstrate that changes in RNA editing observed in humans with age are not observed during aging in healthy rats. Furthermore, we identify a conserved editing site in rats, in Cog3. We propose that either age-related changes in RNA editing are specific to primates or humans, or that they are the manifestation of disease pathology. Since rodents are often used as model organisms for studying aging, these findings demonstrate the importance of understanding species-specific differences in RNA biology during aging.Electronic supplementary materialThe online version of this article (doi:10.1007/s10522-013-9433-8) contains supplementary material, which is available to authorized users.

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Dietary lipoic acid supplementation can mimic or block the effect of dietary restriction on life span

Cited by 31 publications

References 44 publications

Genome-Environment Interactions That Modulate Aging: Powerful Targets for Drug Discovery

Genome-Environment Interactions That Modulate Aging: Powerful Targets for Drug Discovery

Lipoic Acid Attenuates Innate Immune Infiltration and Activation in the Visceral Adipose Tissue of Obese Insulin Resistant Mice

A-to-I RNA editing does not change with age in the healthy male rat brain

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