Butyrates

Publication Title: 
Experimental Gerontology

We tested the effects of a Class I histone deacetylase inhibitor (HDAcI), sodium butyrate (NaBu), on the longevity of normal- and long-lived strains of Drosophila melanogaster. This HDAcI has mixed effects in the normal-lived Ra strain as it decreases mortality rates and increases longevity when administered in the transition or senescent spans, but decreases longevity when administered over the health span only or over the entire adult lifespan. Mostly deleterious effects are noted when administered by either method to the long-lived La strain.

Author(s): 
McDonald, Philip
Maizi, Brian M.
Arking, Robert
Publication Title: 
The Journal of Clinical Investigation

Children conceived by assisted reproductive technologies (ART) display a level of vascular dysfunction similar to that seen in children of mothers with preeclamspia. The long-term consequences of ART-associated vascular disorders are unknown and difficult to investigate in healthy children. Here, we found that vasculature from mice generated by ART display endothelial dysfunction and increased stiffness, which translated into arterial hypertension in vivo. Progeny of male ART mice also exhibited vascular dysfunction, suggesting underlying epigenetic modifications.

Author(s): 
Rexhaj, Emrush
Paoloni-Giacobino, Ariane
Rimoldi, Stefano F.
Fuster, Daniel G.
Anderegg, Manuel
Somm, Emmanuel
Bouillet, Elisa
Allemann, Yves
Sartori, Claudio
Scherrer, Urs
Publication Title: 
Anticancer Research

BACKGROUND: Butyric acid is a short chain fatty acid produced by large bowel bacterial flora. It serves as an antiinflammatory agent and nutrient for normal colon cells. Butyric acid has also been shown to induce apoptosis in colon and many other cancer cells. Artemisinin is a compound extracted from the wormwood Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and to be effective in treating animal and human cancer. We and others have found that the artemisinin analog, dihydroartemisinin (DHA), kills cancer cells by apoptosis.

Author(s): 
Singh, Narendra P.
Lai, Henry C.
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

The precise cause of neuronal death in Huntington's disease (HD) is unknown. Although no single specific protein-protein interaction of mutant huntingtin has emerged as the pathologic trigger, transcriptional dysfunction may contribute to the neurodegeneration observed in HD. Pharmacological treatment using the histone deacetylase inhibitor sodium butyrate to modulate transcription significantly extended survival in a dose-dependent manner, improved body weight and motor performance, and delayed the neuropathological sequelae in the R6/2 transgenic mouse model of HD.

Author(s): 
Ferrante, Robert J.
Kubilus, James K.
Lee, Junghee
Ryu, Hoon
Beesen, Ayshe
Zucker, Birgit
Smith, Karen
Kowall, Neil W.
Ratan, Rajiv R.
Luthi-Carter, Ruth
Hersch, Steven M.
Publication Title: 
Diabetes

OBJECTIVE: We examined the role of butyric acid, a short-chain fatty acid formed by fermentation in the large intestine, in the regulation of insulin sensitivity in mice fed a high-fat diet. RESEARCH DESIGN AND METHODS: In dietary-obese C57BL/6J mice, sodium butyrate was administrated through diet supplementation at 5% wt/wt in the high-fat diet. Insulin sensitivity was examined with insulin tolerance testing and homeostasis model assessment for insulin resistance. Energy metabolism was monitored in a metabolic chamber.

Author(s): 
Gao, Zhanguo
Yin, Jun
Zhang, Jin
Ward, Robert E.
Martin, Roy J.
Lefevre, Michael
Cefalu, William T.
Ye, Jianping
Publication Title: 
PloS One

Diet is one of the major lifestyle factors affecting incidence of colorectal cancer (CC), and despite accumulating evidence that numerous diet-derived compounds modulate CC incidence, definitive dietary recommendations are not available. We propose a strategy that could facilitate the design of dietary supplements with CC-preventive properties. Thus, nutrient combinations that are a source of apoptosis-inducers and inhibitors of compensatory cell proliferation pathways (e.g., AKT signaling) may produce high levels of programmed death in CC cells.

Author(s): 
Drago, Eric
Bordonaro, Michael
Lee, Seon
Atamna, Wafa
Lazarova, Darina L.
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