Oleic acid stimulates glucagon-like peptide-1 release from enteroendocrine cells by modulating cell respiration and glycolysis

Clara, R; Langhans, Wolfgang; Mansouri, Ali

doi:10.1016/j.metabol.2015.10.003

Cited by 23 publications

(10 citation statements)

References 52 publications

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“…The S R % values of DMY combined with malonic acid, iodoacetic acid, and sodium phosphate were 24.18%, 8.26%, and 17.26% against E. coli respectively, and 28.26%, 7.47%, and 19.18% against S. aureus , respectively. The lowest superposition rate represents the highest probability of an inhibiting pathway forming [48]. Therefore, these results imply that the respiratory metabolism of S. aureus and E. coli was inhibited by DMY through the TCA pathway.…”

Section: Resultsmentioning

confidence: 99%

Antibacterial Activity and Mode of Action of Dihydromyricetin from Ampelopsis grossedentata Leaves against Food-Borne Bacteria

et al. 2019

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Dihydromyricetin (DMY) has recently attracted increased interest due to its considerable health-promoting activities but there are few reports on its antibacterial activity and mechanism. In this paper, the activity and mechanisms of DMY from Ampelopsis grossedentata leaves against food-borne bacteria are investigated. Moreover, the effects of pH, thermal-processing, and metal ions on the antibacterial activity of DMY are also evaluated. The results show that DMY exhibits ideal antibacterial activity on five types of food-borne bacteria (Staphylococcus aureus, Bacillus subtilis, Escherichia coli, Salmonella paratyphi, and Pseudomonas aeruginosa). The activities of DMY against bacteria are extremely sensitive to pH, thermal-processing, and metal ions. The morphology of the tested bacteria is changed and damaged more seriously with the exposure time of DMY. Furthermore, the results of the oxidative respiratory metabolism assay and the integrity of the cell membrane and wall tests revealed that the death of bacteria caused by DMY might be due to lysis of the cell wall, leakage of intracellular ingredients, and inhibition of the tricarboxylic acid cycle (TCA) pathway.

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Section: Resultsmentioning

confidence: 99%

Antibacterial Activity and Mode of Action of Dihydromyricetin from Ampelopsis grossedentata Leaves against Food-Borne Bacteria

et al. 2019

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“…For glucose‐induced mitochondrial respiration measurement, the base XF assay medium was supplemented with 17.5 mM glucose, 2 mM Glutamax, 1 mM sodium pyruvate, and 100 U/ml Penicillin–Streptomycin (Fan et al, ). Mitochondrial respiration was determined by measuring OCR in response to modulators of mitochondrial respiration (i.e., ATP synthase inhibitor oligomycin [4 µg/ml, Sigma–Aldrich], mitochondrial uncoupler carbonyl cyanide‐4‐(trifluoromethoxy)phenylhydrazone [FCCP; 500 nM], complex I inhibitor rotenone [5 µM, Sigma–Aldrich], complex III inhibitor antimycin A [5 µg/ml, Sigma–Aldrich]) (Clara et al, , ).…”

Section: Methodsmentioning

confidence: 99%

“…For the measurement of glycolysis and glucose oxidation, the base XF assay medium (Seahorse Bioscience) was supplemented with 2 mM Glutamax, 1 mM sodium pyruvate (Gibco), and 100 U/ml Penicillin–Streptomycin (Fan et al, ). Glycolysis was determined by measuring ECAR in response to glucose (0, 5.5, and 17.5 mM) and the glycolytic pathway inhibitor 2‐DG (100 mM) (Clara, Langhans, & Mansouri, ). Glucose oxidation was determined by measuring OCR in response to glucose (0, 5.5, and 17.5 mM) and the glucose oxidation pathway inhibitor UK5099 (15 µM, Sigma–Aldrich) (Clara et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…Glycolysis was determined by measuring ECAR in response to glucose (0, 5.5, and 17.5 mM) and the glycolytic pathway inhibitor 2‐DG (100 mM) (Clara, Langhans, & Mansouri, ). Glucose oxidation was determined by measuring OCR in response to glucose (0, 5.5, and 17.5 mM) and the glucose oxidation pathway inhibitor UK5099 (15 µM, Sigma–Aldrich) (Clara et al, ). For glucose‐induced mitochondrial respiration measurement, the base XF assay medium was supplemented with 17.5 mM glucose, 2 mM Glutamax, 1 mM sodium pyruvate, and 100 U/ml Penicillin–Streptomycin (Fan et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…Mitochondrial respiration was determined by measuring OCR in response to modulators of mitochondrial respiration (i.e., ATP synthase inhibitor oligomycin [4 µg/ml, Sigma-Aldrich], mitochondrial uncoupler carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone [FCCP; 500 nM], complex I inhibitor rotenone [5 µM, Sigma-Aldrich], complex III inhibitor antimycin A [5 µg/ml, Sigma-Aldrich])(Clara et al, 2016(Clara et al, , 2017.…”

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confidence: 99%

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Glucose stimulates intestinal epithelial crypt proliferation by modulating cellular energy metabolism

Zhou

Ramachandran

Mansouri

et al. 2017

Journal Cellular Physiology

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The intestinal epithelium plays an essential role in nutrient absorption, hormone release, and barrier function. Maintenance of the epithelium is driven by continuous cell renewal by stem cells located in the intestinal crypts. The amount and type of diet influence this process and result in changes in the size and cellular make-up of the tissue. The mechanism underlying the nutrient-driven changes in proliferation is not known, but may involve a shift in intracellular metabolism that allows for more nutrients to be used to manufacture new cells. We hypothesized that nutrient availability drives changes in cellular energy metabolism of small intestinal epithelial crypts that could contribute to increases in crypt proliferation. We utilized primary small intestinal epithelial crypts from C57BL/6J mice to study (1) the effect of glucose on crypt proliferation and (2) the effect of glucose on crypt metabolism using an extracellular flux analyzer for real-time metabolic measurements. We found that glucose increased both crypt proliferation and glycolysis, and the glycolytic pathway inhibitor 2-deoxy-d-glucose (2-DG) attenuated glucose-induced crypt proliferation. Glucose did not enhance glucose oxidation, but did increase the maximum mitochondrial respiratory capacity, which may contribute to glucose-induced increases in proliferation. Glucose activated Akt/HIF-1α signaling pathway, which might be at least in part responsible for glucose-induced glycolysis and cell proliferation. These results suggest that high glucose availability induces an increase in crypt proliferation by inducing an increase in glycolysis with no change in glucose oxidation.

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Neuroendocrine Peptides of the Gut and Their Role in the Regulation of Food Intake

Schalla

Taché

Stengel

2021

Comprehensive Physiology

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Oleic acid stimulates glucagon-like peptide-1 release from enteroendocrine cells by modulating cell respiration and glycolysis

Cited by 23 publications

References 52 publications

Antibacterial Activity and Mode of Action of Dihydromyricetin from Ampelopsis grossedentata Leaves against Food-Borne Bacteria

Antibacterial Activity and Mode of Action of Dihydromyricetin from Ampelopsis grossedentata Leaves against Food-Borne Bacteria

Glucose stimulates intestinal epithelial crypt proliferation by modulating cellular energy metabolism

Neuroendocrine Peptides of the Gut and Their Role in the Regulation of Food Intake

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