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Journal: Journal of Lipid Research
Article Title: Phosphatidylcholine with C26:0 moiety, a precursor of a diagnostic marker for X-ALD, is synthesized by LPLAT10/LPEAT2
doi: 10.1016/j.jlr.2025.100973
Figure Lengend Snippet: Chemical synthesis of C26:0 FFA- d 4 . A: C26:0 FFA was converted to the corresponding 8-aminoquinoline amide. Deuterium incorporation was first achieved selectively at the β-position under palladium catalysis, followed by the introduction of two deuterium atoms at the α-position using potassium carbonate. Finally, the resulting tetradeuterated amide was converted in two steps to furnish C26:0 FFA- d 4 . B: The ion spectra of the C26:0 FFA- d 4 obtained by a high-resolution mass spectrometer. ca ., circa; eq, equivalent; y., yield.
Article Snippet: C30:0-CoA, C28:0-CoA, C26:0-CoA, C24:0-CoA, and C16:0-
Techniques: Mass Spectrometry
Journal: Journal of Lipid Research
Article Title: Phosphatidylcholine with C26:0 moiety, a precursor of a diagnostic marker for X-ALD, is synthesized by LPLAT10/LPEAT2
doi: 10.1016/j.jlr.2025.100973
Figure Lengend Snippet: Metabolic analysis of C26:0 FFA- d 4 in ABCD1 and LPLAT10-DKO HeLa cells. A: Schematic illustration of the possible metabolic pathway of exogenously administered C26:0 FFA- d 4 . Note that the C26:0- d 4 moiety is subjected to hydrolysis by lipases, resulting in C26:0 FFA- d 4 . B–K: The amounts of C26:0 FFA- d 4 (B) and lipid species with C26:0- d 4 moiety (C–K) present within HeLa cells. Data represent the mean ± SD; statistical analysis was performed using one-way ANOVA, followed by the Dunnett’s test (vs. ABCD1 KO). ∗P < 0.01, ∗∗P < 0.001. ACAT, acyl-CoA:cholesterol acyltransferase; CerS, ceramide synthase; DG, diacylglycerol; DGAT, diacylglycerol O-acyltransferase; DH-Sph, dihydrosphingosine; FC, free cholesterol; GSL, glycosphingolipid; MG, monoacylglycerol; MOGAT, monoacylglycerol O-acyltransferase; PAP, phosphatidic acid phosphatase; PLA 2 , phospholipase A 2 ; PLC, phospholipase C.
Article Snippet: C30:0-CoA, C28:0-CoA, C26:0-CoA, C24:0-CoA, and C16:0-
Techniques:
Journal: Journal of Advanced Research
Article Title: Metformin attenuates colitis via blocking STAT3 acetylation by reducing acetyl-CoA production
doi: 10.1016/j.jare.2025.03.058
Figure Lengend Snippet: Elevated acetyl-CoA levels exacerbate UC by promoting STAT3 acetylation. (A) Schematic representation of the experimental model. WT mice (n = 6) were gavaged with acetate (500 mg/kg) or PBS for 3 weeks, followed by treatment with metformin (200 mg/kg) and 3 % DSS for 7 days. (B) Relative acetyl-CoA levels in mice. (C-D) Representative IF images of ac-STAT3 K685 and IHC images of p-STAT3 Y705 in mice. (E) Alterations in body weight and DAI. (F-G) Gross morphology and colon length measurements in mice. (H) Representative images of H&E staining for morphological analysis and IHC analysis of AB-PAS and MUC-2 expression. (I) Histological evaluation of colonic tissue based on morphological examination of colon sections. (J-K) Representative immunofluorescence images of ZO-1 and TUNEL staining, along with quantitative analysis. (L) Representative electron microscopy images of colonic tissue segments. (M) WB analysis of colonic protein expression in mice. (N) ELISA analysis of relative intracellular acetyl-CoA levels (n = 3). NCM460 cells were exposed to acetate (5 mM) or PBS for 24 h, followed by treatment with metformin and LPS. (O) WB analysis of relevant protein expression in cells treated with acetate or PBS. (P-R) Representative immunofluorescence images of ZO-1, p-STAT3Y 705 , and ac-STAT3 K685 in cells.
Article Snippet: In a separate experiment, to reduce
Techniques: Staining, Expressing, Immunofluorescence, TUNEL Assay, Electron Microscopy, Enzyme-linked Immunosorbent Assay