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Naturally Occurring Histone Deacetylase (HDAC) Inhibitors in the Treatment of Cancers
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Sujatha Puttalingaiah, Murthy V. Greeshma, Mahadevaswamy G. Kuruburu, Venugopal R. Bovilla, SubbaRao V. Madhunapantula
HDACis are broadly classified into six main classes according to their structure (Gottesfeld and Pandolfo, 2009). They are: (a) hydroxamic acids (trichostatin-A [TSA], suberoylanilide hydroxamic acid [SAHA], PXD101); (b) benzamides; (c) cyclic peptides and depsipeptides; (d) short-chain fatty acids (propionic acid, butyric acid, valeric acid, caproic acid and valproic acid); (e) sulfur-containing compounds (diallyl disulfide [DADS], diallyl trisulfide [DATS], sulforaphane [SFN]); (f) phenolic compounds (benzoic acid and cinnamic acid derivatives); and (g) hybrid molecules (Figure 8.3 and Table 8.1).
Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Short chain saturated fatty acids, including acetic, propionic, and butyric acids, are formed during fiber fermentation in the proximal colon. They are quickly absorbed by portal circulation and transported to the liver where they are transformed into glucose. Importantly, butyric and partially also propionic acids are used in metabolism, proliferation and restoration of colon cells (70). Other functions of short chain saturated fatty acids in the colon also include stimulation of water, sodium, chloride and bicarbonate absorption and blood flow through mucous membrane of the colon. Other roles are proliferation of colon cells, mucus production, limited reproduction of saprophytic bacteria and putrefaction due to decreased acidity (70). As previously cited, long chain saturated fatty acids such as lauric, myristic, palmitic and stearic acids have significant atherogenic and thrombogenic potentials and increase levels of cholesterol, especially low-density lipoprotein (LDL) cholesterol or ‘bad’ cholesterol (70). These saturated fatty acids are mainly abundant in butter, lard, beef tallow, poultry skin, coconut oil, cocoa butter, palm kernel oil, chocolate, and so on.
An Overview of Drug-Induced Nephropathies *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Jean Paul Fillastre, Michel Godin
A distinct clinical syndrome associated with NSAID exposure and completely different from the renal failure described previously due to enhanced renal vasoconstriction has become apparent in the last several years. This disorder is characterized by an interstitial nephritis on renal biopsy, but often presents clinically as the nephrotic syndrome. The first 2 cases of acute renal failure with nephrotic syndrome were reported in 1979 (Brezin et al., 1979) and more than 100 cases have been described since. The incidence of this unusual disorder is unknown, but is believed to be rare. It seems to be more frequent when propionic acid derivatives are prescribed. Fenoprofen was implicated in a large number of cases.
Probiotics for the Treatment of Gastric Diseases
Published in Nutrition and Cancer, 2022
Yingying Xing, Xinyue Gu, Guojing Ruan, Simiao Chen
SCFAs are important metabolites produced by microorganisms during the fermentation process. They primarily include formic acid, acetic acid, propionic acid, butyric acid, and lactic acid. It is commonly known that SCFAs can curb the growth and reproduction of pathogenic bacteria and maintain the balance of intestinal flora. In recent years, various studies have reported that SCFAs may also be used to treat gastric diseases. The ethanol-induced gastric ulcer (GU) mouse model confirmed that butyric acid produced by Clostridium butyricum can reverse the destruction of gastric mucus by ethanol, which may have a therapeutic effect on GU by enhancing mucosal defense activity (19). H. pylori can produce highly active urease, which can hydrolyze urea to generate ammonia and bicarbonate. This can ultimately form a neutral environment around pathogenic bacteria to reduce the viscosity of the mucus layer and promote the passage of these microbes through the mucus layer (12). In addition, a variety of experimental studies have confirmed that acetic acid and lactic acid produced by probiotics can reduce pH levels and have a dose-dependent inhibitory effect on the growth of H. pylori. This is not only reflected in the direct effect on H. pylori but also indirectly on urease (20). Additionally, Bengoa et al. also found that organic acids such as lactic acid and acetic acid produced by L. paracasei can inhibit nuclear factor (NF)-κB signaling and consequently reduce the level of pro-inflammatory cytokines to exert an anti-inflammatory effect (17).
Mucin degrader Akkermansia muciniphila accelerates intestinal stem cell-mediated epithelial development
Published in Gut Microbes, 2021
Seungil Kim, Yun-Chan Shin, Tae-Young Kim, Yeji Kim, Yong-Soo Lee, Su-Hyun Lee, Mi-Na Kim, Eunju O, Kwang Soon Kim, Mi-Na Kweon
Treatment with A. muciniphila had a greater effect on the production of propionic acid than on acetic acid. Previously, it was suggested that A. muciniphila and propionic acid regulate the expression of genes associated with the host lipid metabolism and activate the epigenome.50 Accumulating evidence suggests that propionic acid may modulate host physiology in several ways. For example, propionic acid stimulates the release of peptide YY and glucagon-like peptide-1 in human colonic cells, and thereby reduces energy intake and weight gain.51 Intriguingly, propionic acid stimulates Muc2 production by IECs by regulating the expression of the prostaglandins.52 A recent study proposed that supplementation of propionic acid improves the Treg/Th17 imbalance in multiple sclerosis patients.53 Taken together with our results, we conclude that propionic acid may play an important role in IEC homeostasis and the overall gut, and therefore may modulate host physiology.
Desulfovibrio vulgaris, a potent acetic acid-producing bacterium, attenuates nonalcoholic fatty liver disease in mice
Published in Gut Microbes, 2021
Ying Hong, Lili Sheng, Jing Zhong, Xin Tao, Weize Zhu, Junli Ma, Juan Yan, Aihua Zhao, Xiaojiao Zheng, Gaosong Wu, Bingbing Li, Bangxing Han, Kan Ding, Ningning Zheng, Wei Jia, Houkai Li
To further determine whether the increased acetic acid levels were derived from APS or gut microbiota itself, we detected SCFAs production by fecal bacteria from mice with or without oral antibiotic pre-treatment (500 mg/L vancomycin in drinking water for 5 days) under anaerobic culture condition. As expected, the SCFAs were accumulated in the medium containing fecal bacteria over time, in which acetic acid and propionic acid were found in higher concentrations than butyric acid (Figure 3c). The addition of APS to the bacterial medium further increased the contents of acetic acid time-dependently (p < .001) but not that of propionic acid or butyric acid. The capability for acetic acid and butyric acid production was abolished in bacteria that were pre-treated by antibiotics even in the presence of APS (p < .001, Figure 3c, Supplementary Figure 5). On the contrary, the levels of propionic acid were increased in bacteria from antibiotic-treated mice (p < .01, Figure 3c). These results indicated that APS was mainly fermented into acetic acid by gut microbiota, instead of propionic acid and butyric acid.