Aging-US: Green tea catechins enhance fitness

Image: Figure 6. Scheme. Green tea catechins improve the fitness and longevity of Caenorhabditis elegance by inhibiting complex I.
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Credit: Correspondence to: Corina T. Madreiter-Sokolowski E-Mail: corina.madreiter@medunigraz.at and Michael Ristow E-Mail: michael-ristow@ethz.ch

Aging-US published “Green Tea Catechins EGCG and EKG Increase the Fitness and Lifespan of Caenorhabditis elegans by Complex I Inhibition,” which reported that green tea catechins are associated with a delay in aging. The authors designed the current study to examine the effects and uncover the goal of the most abundant green tea catechins, epigallocatechin gallate and epicatechin gallate.

Catechins hindered mitochondrial respiration in C. Long-term effects included a significantly reduced fat content and increased SOD and CAT activity, which are necessary for the positive effects of catechins on longevity. Through adaptive reactions, catechins reduced the fat content, improved the ROS defense and improved long-term health margins.

Dr. Corina T. Madreiter-Sokolowski and Dr. Michael Ristow said, “Clinical studies and epidemiological studies have shown health benefits associated with green tea consumption, including significant reductions in systolic blood pressure [1] and fasting glucose [2] and weight loss in type 2 diabetics [3] and in women with central obesity “

The most common polyphenols found in green tea leaves are epigallocatechin gallate, epicatechin gallate, epigallocatechin, and epicatechin, which make up 30-42% of the solid green tea extract. EGCG makes up about 50% and EKG 20% of the total amount of catechins in green tea leaves. A randomized, placebo-controlled clinical trial testing daily supplementation with 400 mg EGCG confirmed the safety of a one-year administration of EGCG.

In addition, green tea water containing polyphenols extended the lifespan of male C57BL / 6 mice.

In addition, treatment of Caenorhabditis elegans with EGCG at concentrations of 50-300 μM enhanced lifespan during early to middle adulthood, and 200 μM EGCG was the most potent dose to increase lifespan by inducing a mitohormetic response via AMPK / SIRT1 and FOXO extend.

However, the low bioavailability of green tea catechins in mammals makes it unlikely that this concentration would be reached in humans after oral administration. Experiments in isolated liver mitochondria from mice showed that EGCG and EKG inhibit complex I activity. The inhibition of complex I was accompanied by a transient ROS formation and a fall in ATP after 6 h EGCG and 12 h ECG treatment in C. elegans.

The extension of the lifespan of C. elegans by EGCG and EKG proved to be dependent on the presence of the energy sensors AMP-activated kinase AAK-2 and NAD-dependent protein deacetylase SIR-2.1, the homologues of mammalian AMPK and SIRT1 as well as the ROS- sensing mitogen-activated protein kinase PMK-1, the orthologue of the mammalian mitogen-activated protein kinase p38 MAPK, and below its downstream targets protein Skinhead-1, the orthologue of the nuclear factor erythroid 2-related factor 2, and DAF-16, the ortholog of a mammalian clevis transcription factor.

The Madreiter-Sokolowski / Ristow research team concluded in their aging US research output: “The application of the green tea catechins EGCG and EKG in low doses extends the life of C. elegans by inducing a mitohormetic response. As a result, the inhibition of complex I causes a transient increase in ROS, which stimulates the antioxidant defense enzymes SOD and CAT and activates the PMK-1 / SKN-1 / DAF-16 signaling pathway (Figure 6, scheme). It also causes the inhibition of Complex I a transient drop in cellular ATP levels and, consequently, the activation of AAK-2 / SIR-2.1 signaling. In the long term, rewiring these energy- and ROS-dependent tracks reduces the fat content and extends health and lifespan. “

Full text – https://www.aging-us.com/article/203597/text

Correspondence: Corina T. Madreiter-Sokolowski E-mail: corina.madreiter@medunigraz.at and Michael Ristow E-mail: michael-ristow@ethz.ch

Keywords: Aging, reactive oxygen species, mitochondria, polyphenols, C. elegans

About the Aging US

Aging-US was founded in 2009 and publishes publications of general interest and biological importance in all areas of aging research as well as on topics beyond traditional gerontology, including but not limited to cell and molecular biology, age-related diseases in humans, pathology in model organisms, cancer , Signal transduction pathways (e.g. p53, sirtuins and PI-3K / AKT / mTOR among others) and approaches for modulating these signal pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or contact @AgingJrnl

Aging-US is published by Impact Journals, LLC. Please visit http://www.ImpactJournals.com or contact @ImpactJrnls

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SELECTED NOBEL ARTICLES

• Elizabeth Blackburn, a member of Aging’s editorial committee, won the 2009 Nobel Prize in Physiology or Medicine while serving on the board. Elizabeth Blackburn is the co-author of an article published in the first (opening) issue of Aging.

• Andrew V. Schally, Nobel Laureate, published his work in Aging.

• Shinya Yamanaka was awarded the Nobel Prize in Physiology and Medicine in 2012. Shinya Yamanaka is the co-author of a paper published in Aging.

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“Green tea catechins EGCG and EKG increase the fitness and lifespan of Caenorhabditis elegans through complex I inhibition”

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