Adaptative metabolic response of human colonic epithelial cells to the adverse effects of the luminal compound sulfide

Leschelle, Xavier; Goubern, Marc; Andriamihaja, Mireille; Blottière, Hervé M.; Couplan, Elodie; Barroso, Gérard; Petit, Caroline; Pagniez, Anthony; Chaumontet, Catherine; Mignotte, Bernard; Bouillaud, Frédéric; Blachier, François

doi:10.1016/j.bbagen.2005.06.002

Cited by 167 publications

(121 citation statements)

References 45 publications

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“…To optimize administration of the H 2 S donor for in vitro experiments we first performed a dose-response in isolated cardiac mitochondria to determine its effect on respiration. As has been previously reported in a placental cell line (23) we found a dose-dependent reduction in mitochondrial oxygen consumption followed by complete recovery to baseline. Based on these findings, we selected 10 M, which reduced mitochondrial respiration rate by 65%, in a clear and reproducible manner.…”

Section: Discussionsupporting

confidence: 69%

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Elrod¹,

Calvert²,

Morrison

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

1,040

892

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The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemiareperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H2S by cardiac-specific overexpression of cystathionine ␥-lyase (␣-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.

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Section: Discussionsupporting

confidence: 69%

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Elrod¹,

Calvert²,

Morrison

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

1,040

892

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“…In the case of succinate, this metabolite has been shown to be transported within the colonic mucosa (74) and to increase oxygen consumption in colonocytes (31). Because the large intestine epithelial layer is renewed within a few days (with important corresponding anabolic ATP-consuming pathways) (54), together with consumption of ATP by colonocytes through the membrane-bound ATPase involved in colonic electrolyte transport (7), ATP has to be synthesized at a rate matching its cellular utilization to maintain a constant ATP cell content, a necessary condition to maintain the viability of epithelial cells (41). The other monocarboxylic acids (valerate, isobutyrate, isovalerate, formate, and D-lactate), which have not yet been tested for their capacity to be oxidized in colonocyte, are present in much lower amounts than SCFA and succinate.…”

Section: Discussionmentioning

confidence: 99%

High-protein diet modifies colonic microbiota and luminal environment but not colonocyte metabolism in the rat model: the increased luminal bulk connection

Liu

Blouin

Santacruz

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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AM. Highprotein diet modifies colonic microbiota and luminal environment but not colonocyte metabolism in the rat model: the increased luminal bulk connection. Am J Physiol Gastrointest Liver Physiol 307: G459-G470, 2014. First published June 26, 2014; doi:10.1152/ajpgi.00400.2013.-High-protein diets are used for body weight reduction, but consequences on the large intestine ecosystem are poorly known. Here, rats were fed for 15 days with either a normoproteic diet (NP, 14% protein) or a hyperproteichypoglucidic isocaloric diet (HP, 53% protein). Cecum and colon were recovered for analysis. Short-and branched-chain fatty acids, as well as lactate, succinate, formate, and ethanol contents, were markedly increased in the colonic luminal contents of HP rats (P Ͻ 0.05 or less) but to a lower extent in the cecal luminal content. This was associated with reduced concentrations of the Clostridium coccoides and C. leptum groups and Faecalibacterium prausnitzii in both the cecum and colon (P Ͻ 0.05 or less). In addition, the microbiota diversity was found to be higher in the cecum of HP rats but was lower in the colon compared with NP rats. In HP rats, the colonic and cecal luminal content weights were markedly higher than in NP rats (P Ͻ 0.001), resulting in similar butyrate, acetate, and propionate concentrations. Accordingly, the expression of monocarboxylate transporter 1 and sodium monocarboxylate transporter 1 (which is increased by higher butyrate concentration) as well as the colonocyte capacity for butyrate oxidation were not modified by the HP diet, whereas the amount of butyrate in feces was increased (P Ͻ 0.01). It is concluded that an increased bulk in the large intestine content following HP diet consumption allows maintenance in the luminal butyrate concentration and thus its metabolism in colonocytes despite modified microbiota composition and increased substrate availability.protein; microbiota; SCFA; transport; metabolism HIGH-PROTEIN (HP) diets are commonly used for body weight loss (36,38). In fact, such diets have been shown to increase satiety, to modify lipid metabolism, and to facilitate short-and middle-term weight reduction (24,61,72). However, the consequences on gut microbiota composition, on microbial-derived metabolites in the large intestine luminal content, and on colonocyte epithelial cell metabolic capacities have been little studied.Increasing protein intake induces an increase in the proportion of nitrogenous compounds, mainly protein, peptides, and to a lesser extent amino acids, entering the large intestine (13,23,25,51,64). They are subjected to luminal proteolysis and subsequent metabolism by the large number of microorganisms of the large intestine microbiota (about 10 11 to 10 12 viable bacteria/g content) (29) leading to the production of numerous amino acid-derived metabolites (53), including phenols, indoles, amines, sulfide, ammonia, and monocarboxylic acids. Monocarboxylic acids include short-chain fatty acids (SCFA), branched-chain fatty acids (BCFA) and several other organ...

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“…H 2 S reduces overall metabolic activity of the intestinal epithelial cells leading to a reduction in the oxidation of glutamine, butyrate, and acetate (Leschelle et al, 2005). This reduction in overall metabolic activity and slow down of all cell cycle phases leads to a reduction in mitotic activity.…”

Section: Toxic Metabolitesmentioning

confidence: 99%

The Gut Microbiota: Ecology and Function

Willing

Jansson

2014

The Fecal Bacteria

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Adaptative metabolic response of human colonic epithelial cells to the adverse effects of the luminal compound sulfide

Cited by 167 publications

References 45 publications

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

High-protein diet modifies colonic microbiota and luminal environment but not colonocyte metabolism in the rat model: the increased luminal bulk connection

The Gut Microbiota: Ecology and Function

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