The “rejuvenatory” impact of lipoic acid on mitochondrial function in aging rats may reflect induction and activation of PPAR-γ coactivator-1α

McCarty, Mark F.; Barroso-Aranda, Jorge; Contreras, Francisco

doi:10.1016/j.mehy.2008.07.043

Cited by 32 publications

(25 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Indeed, Acadl is a specific target of Pparα [36], a key transcriptional factor involved in fatty acid metabolism that is able to decrease fat accumulation by increasing fatty acid degradation [37]. Supporting this theory, our results and those from other groups [13,38] demonstrate that LA treatment is able to increase the expression of Pparα. In addition, it is important to note the emerging and pivotal role of Pgc-1β in the prevention of hepatic steatosis [39], as well as its ability to regulate transcriptional activity of Pparα [40].…”

Section: Discussionsupporting

confidence: 86%

“…Regarding the first gene, some studies described that LA is able to stimulate the expression of Pgc-1α in different tissues, such as skeletal muscle [58] or hepatocytes [13]. A stimulatory effect of LA on Pgc-1α in the liver of rats fed with an HFD was observed, although this effect seems to be secondary to caloric restriction since no significant differences were found between the OLIP and PFO groups.…”

Section: Discussionmentioning

confidence: 98%

“…Also, LA acts as a cofactor of several mitochondrial bioenergetic enzymes [11] and in several processes of aerobic metabolism. Apart from its role in the mitochondria, when supplemented in diets, LA exerts beneficial physiological effects such as attenuation of oxidative stress [12], overcoming of aging decay [13], modulation of glucose metabolism [14], prevention of body weight gain induced by HFD [15], as well as a reduction of energy efficiency [16]. In addition, the ability of LA to reduce serum and tissue lipid levels has been reported by other investigators [17,18].…”

Section: Introductionmentioning

confidence: 85%

See 2 more Smart Citations

Lipoic acid administration prevents nonalcoholic steatosis linked to long-term high-fat feeding by modulating mitochondrial function

Valdecantos

Pérez-Matute

González‐Muniesa

et al. 2012

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 85%

See 1 more Smart Citation

Lipoic acid administration prevents nonalcoholic steatosis linked to long-term high-fat feeding by modulating mitochondrial function

Valdecantos

Pérez-Matute

González‐Muniesa

et al. 2012

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

“…Recent evidence suggests the induction of PPARg coactivator 1a (PGC-1a) may be a key mechanism of this action. 48 There is evidence that peroxisome proliferator-activated gamma coactivator-1a (PGC-1a) enhances the expression of a wide range of compounds that contribute importantly to the antioxidant protection of mitochondria: superoxide dismutase, thioredoxin, and catalase. There are numerous reasons to believe that ALA might increase the expression and/or activity of PGC-1a.…”

Section: Oxidative Stress Aging and Ala/dhlamentioning

confidence: 99%

Antioxidant Properties of an Endogenous Thiol: Alpha-lipoic Acid, Useful in the Prevention of Cardiovascular Diseases

Ghibu¹,

Richard²,

Vergely³

et al. 2009

Journal of Cardiovascular Pharmacology

138

View full text Add to dashboard Cite

In the past few years, a growing interest has been given to the possible antioxidant functions of a natural acid, synthesized in human tissues: alpha-lipoic acid (ALA). Both the oxidized (disulfide) and reduced (dithiol: dihydrolipoic acid, DHLA) forms of ALA show antioxidant properties. ALA administered in the diet accumulates in tissues, and a substantial part is converted to DHLA via a lipoamide dehydrogenase. Commercial ALA is usually a racemic mixture of the R and S forms. Chemical studies have indicated that ALA scavenges hydroxyl radicals, hypochlorous acid, and singlet oxygen. ALA exerts antioxidant effects in biological systems not only through direct ROS quenching but also via transition metal chelation. ALA has been shown to possess a number of beneficial effects both in the prevention and treatment of diabetes in experimental conditions. ALA presents beneficial effects in the management of symptomatic diabetic neuropathy and has been used in this context in Germany for more than 30 years. In cardiovascular disease, dietary supplementation with ALA has been successfully employed in a variety of in vivo models: ischemia-reperfusion, heart failure, and hypertension. More mechanistic and human in vivo studies are needed to determine whether optimizing the dietary intake of ALA can help to decrease cardiovascular diseases. A more complete understanding of cellular biochemical events that influence oxidative damage is required to guide future therapeutic advances.

show abstract

“…Lipoic acid also has been shown to possess the ability to scavenge ROS in vitro; however, there is no clear evidence that this actually occurs in vivo. Recent findings suggest that lipoic acid can boost mitochondrial membrane potential and oxygen consumption, while decreasing mitochondrial production of oxidants (280). This occurs by lipoic acid amplifying key antioxidant protective mechanisms via PPARg coactivator-1a (PGC-1a) mediation (280).…”

mentioning

confidence: 99%

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Massaad

Klann

2011

Antioxidants & Redox Signaling

454

326

View full text Add to dashboard Cite

The brain is a metabolically active organ exhibiting high oxygen consumption and robust production of reactive oxygen species (ROS). The large amounts of ROS are kept in check by an elaborate network of antioxidants, which sometimes fail and lead to neuronal oxidative stress. Thus, ROS are typically categorized as neurotoxic molecules and typically exert their detrimental effects via oxidation of essential macromolecules such as enzymes and cytoskeletal proteins. Most importantly, excessive ROS are associated with decreased performance in cognitive function. However, at physiological concentrations, ROS are involved in functional changes necessary for synaptic plasticity and hence, for normal cognitive function. The fine line of role reversal of ROS from good molecules to bad molecules is far from being fully understood. This review focuses on identifying the multiple sources of ROS in the mammalian nervous system and on presenting evidence for the critical and essential role of ROS in synaptic plasticity and memory. The review also shows that the inability to restrain either age-or pathology-related increases in ROS levels leads to opposite, detrimental effects that are involved in impairments in synaptic plasticity and memory function.

show abstract

The “rejuvenatory” impact of lipoic acid on mitochondrial function in aging rats may reflect induction and activation of PPAR-γ coactivator-1α

Cited by 32 publications

References 74 publications

Lipoic acid administration prevents nonalcoholic steatosis linked to long-term high-fat feeding by modulating mitochondrial function

Lipoic acid administration prevents nonalcoholic steatosis linked to long-term high-fat feeding by modulating mitochondrial function

Antioxidant Properties of an Endogenous Thiol: Alpha-lipoic Acid, Useful in the Prevention of Cardiovascular Diseases

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Contact Info

Product

Resources

About