1978
DOI: 10.1016/s0021-9258(17)34804-4
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Suppression of histone deacetylation in vivo and in vitro by sodium butyrate.

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Cited by 420 publications
(43 citation statements)
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“…HDACs are subdivided into two protein subfamilies, which differ in protein structure and mechanism of action: the classical HDAC family and the sirtuins family [103]. The pharmacological compounds SRT1720 and EX-527 were designed to inhibit sirtuins [84,90], whereas sodium butyrate [104], Trichostatin A [85], valproic acid [105], and D-βhydroxybutyrate [101] inhibit the classic HDACs. Given that the same intergenerational effects were obtained with compounds that interfere with different subfamilies of HDACs, which may also have different target proteins, these results would suggest that the effects are not direct.…”
Section: Discussionmentioning
confidence: 99%
“…HDACs are subdivided into two protein subfamilies, which differ in protein structure and mechanism of action: the classical HDAC family and the sirtuins family [103]. The pharmacological compounds SRT1720 and EX-527 were designed to inhibit sirtuins [84,90], whereas sodium butyrate [104], Trichostatin A [85], valproic acid [105], and D-βhydroxybutyrate [101] inhibit the classic HDACs. Given that the same intergenerational effects were obtained with compounds that interfere with different subfamilies of HDACs, which may also have different target proteins, these results would suggest that the effects are not direct.…”
Section: Discussionmentioning
confidence: 99%
“…Among them, the classical ones are a new promising class of targets of drugs against cancers. Sodium butyrate is a fatty acid and acts as an HDAC inhibitor in some studies [21][22][23]. Diabetes seems to significantly influence the function of the kidney according to the evidence that diabetes was associated with enhanced plasma urea and creatinine levels, while significant changes of total protein, plasma albumin and relative kidney weight were not found.…”
Section: Discussionmentioning
confidence: 99%
“…Although our results indicate that SCFAs regulate ClC-2 activity directly, an SCFA-dependent mechanism involving G-coupled receptors cannot be ruled out. Indeed, SCFAs not only act as energy sources [37] and histone deacetylase inhibitors [38] in enterocytes but also bind and stimulate G-coupled receptors [39]. GPR41, GPR43, and GPR109A are G-coupled receptors expressed in several cell types, including intestinal epithelial cells that are activated by SCFAs in the concentration range found in the intestinal lumen [40][41][42].…”
Section: Discussionmentioning
confidence: 99%