Journal: Foods

Article Title: Chemical Composition Analysis of Highland Barley ( Hordeum vulgare L.) with Different Modification Methods and Lipid Metabolism Mechanism Analysis of Highland Barley with Microwave Fluidization Modification

doi: 10.3390/foods15081396

Figure Lengend Snippet: Protein expression levels ( A , H ) including ( B ) PPARγ, ( C ) Fabp4, ( D ) CD36, ( E ) SREBP-1c, ( F ) ADIPOQ, ( G ) SCD-1, ( I ) TLR4, ( J ) IKKβ, and ( K ) p-P65 in liver tissues among NCD, HFCD, and HFCD + HB-1. Data were expressed as mean ± SD ( n = 3) based on Dunnett’s test. ** indicated p < 0.01, *** indicated p < 0.001, **** indicated p < 0.0001.

Article Snippet: The specific antibody concentrations used in this study were as follows: anti-rabbit antibodies against Peroxisome proliferator-activated receptor γ (PPARγ) (1:1000, 58 kDa, Affinity, 16643-1-AP), FABP4 (1:1000, 15 kDa, Affinity, DF6035), CD36 (1:1000, 88 kDa, Affinity, DF13262), SREBP-1c (1:1000, 122 kDa, Affinity, AF6283), ADIPOQ (1:1000, 26 kDa, Affinity, DF7000), SCD-1 (1:1000, 41 kDa, Bioss, bs-3787R), p-P65 (1:1000, 65 kDa, Affinity, AF2006, Serine Ser536), TLR4 (1:1000, 100 kDa, Affinity, AF7017), IKKβ (1:1000, 87 kDa, Affinity, AF6010), and GAPDH (1:1000, 37 kDa, Xianzhi Biotech, AB-P-R 001).

Techniques: Expressing

Journal: Cell Death and Differentiation

Article Title: SIRT3 promotes lipophagy and chaperon-mediated autophagy to protect hepatocytes against lipotoxicity

doi: 10.1038/s41418-019-0356-z

Figure Lengend Snippet: SIRT3 suppresses lipogenesis in lipotoxic hepatocytes. a SCD1 protein level in vector and SIRT3OE hepatocytes treated with or without P/O mixture for 24 h. b SIRT3 and SCD1 protein levels in SIRT3 and SCD1 double overexpressed hepatocytes. The lipid content c and the cellular TG content d in SIRT3 and SCD1 double overexpressed hepatocytes. White: blank, vector; gray: blank, SIRT3OE; light gray: P/O, vector; black: P/O, SIRT3OE. Data are shown as mean ± S.D., n = 6, * p < 0.05, and *** p < 0.001, vector vs. SIRT3OE, ### p < 0.001 blank vs. P/O treatment. && p < 0.01, &&& p < 0.001, SCD1OE vs. vector. One-way ANOVA was used to calculate the p -values

Article Snippet: The plasmid of pCMV3-SCD1-N-Myc was purchased from Sino Biological (MG51311-NM, Wayne, PA, USA).

Techniques: Plasmid Preparation

Journal: Cell Death and Differentiation

Article Title: SIRT3 promotes lipophagy and chaperon-mediated autophagy to protect hepatocytes against lipotoxicity

doi: 10.1038/s41418-019-0356-z

Figure Lengend Snippet: Schematic of the role of SIRT3 in protecting hepatocytes against lipotoxicity. SIRT3 activates AMPK to enhance macroautophagy and CMA on LDs and promote LDs dispersion on detyrosinated MTs, inhibits SCD1 expression to suppress lipogenesis, and deacetylates LCAD to increase fatty acid oxidation in mitochondria, resulting in attenuation of lipotoxicity in hepatocytes

Article Snippet: The plasmid of pCMV3-SCD1-N-Myc was purchased from Sino Biological (MG51311-NM, Wayne, PA, USA).

Techniques: Expressing

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Glavonoid-rich oil supplementation reduces stearoyl-coenzyme A desaturase 1 expression and improves systemic metabolism in diabetic, obese KK-A y mice.

doi: 10.1016/j.biopha.2021.111714

Figure Lengend Snippet: Fig. 9. GRO supplementation reduced the protein levels of SCD1 and PPARα and increased the level of phosphorylated AMPK in the liver. (A) Western blot analysis of SCD1 in the liver of 20-week-old mice. (B) Western blot analysis of PPARα in the liver of 20-week-old mice. (C) The ratio of phosphorylated AMPK to total AMPK levels in the liver of 20-week-old mice, as determined by Western blot analysis. Cont: control mice; GRO8: 0.8% GRO mice. The data were analyzed with Student’s t- test. *p < 0.05, *p < 0.01. Values are means ± SD (n = 5).

Article Snippet: After electrophoresis, the separated proteins were transferred to a polyvinylidene difluoride membrane (Immobilon, 0.2 μm pore, (Merck Millipore Burlington, MA, USA)) and incubated overnight at 4 ◦C with the following primary antibodies: polyclonal rabbit anti-mouse PPARα (1:3000, GeneTex, Los Angeles, CA, USA), β-actin (1:3000, GeneTex), total AMPKα1 (1:3000, GeneTex), phosphorylated AMPKα1 (Thr172) (1:1000, Cell Signaling Technology, Danvers, MA, USA), and SCD1 (1:1000, R&D Systems Minneapolis, MN, USA).

Techniques: Western Blot, Control

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Ethanol and its Nonoxidative Metabolites Promote Acute Liver Injury by Inducing ER Stress, Adipocyte Death, and Lipolysis

doi: 10.1016/j.jcmgh.2022.10.002

Figure Lengend Snippet: Binge ethanol increases hepatic FFAs and increases adipose tissue lipolysis. Mice were subjected to a single ethanol binge (5 or 7 g/kg) or isocaloric maltose and were killed 9 hours after alcohol gavage. ( A ) Liver tissues were subjected to microarray analyses. The heatmap and ingenuity pathway analysis (IPA) analyses for liver mRNA expression are shown. ( B ) Sera were collected for FFA measurement. Liver FFA and TG levels were measured. ( C ) Gas chromatography–mass spectrometry was used to perform specific FFA studies on liver tissues. Hepatic FASN and SCD1 proteins were analyzed using Western blot. ( D ) Collected white adipose tissues was analyzed using Western blot. Data are expressed as the means ± SEM. ∗ P < .05, ∗∗ P < .01 vs the corresponding controls. ctrl, control.

Article Snippet: For Western blot analysis, antibodies against ADH1 (5295s; CST), ALDH2 (ab194587; Abcam), CYP2E1 (AB1252; Sigma), phosphorylated stress-activated protein kinase/Jun-amino-terminal kinase (p-SAPK/JNK) (Thr183/Tyr185) (#4668s; CST), SAPK/JNK (#9258; CST), phosphylated PERK (Thr982) (#3179s; CST), PERK (C33E10) (#3192; CST), p-eIF2α (Ser51) (#3398; CST), eIF2α (#5324; CST), p-IRE1α (phospho-S724) (ab48187; Abcam), IRE1α (14C10) (#3294; CST), X-box binding protein 1 (E9V3E) (#40435; CST), CHOP (#5554s; CST), BAD (D24A9) (#9239; CST), BIM (C34C5) (#2933; CST), BiP (#3177s; CST), p-histone H2A histone family member X (Ser139) (#9718; CST), hypoxia-inducible factor 1 alpha (D2U3T) (#14179; CST), Activating transcription factor 6 (D4Z8V) (#65880; CST), FASN (#3189; CST), SCD1 (C12H5) (#2794; CST), adipose triglyceride lipase (#2138; CST), ER oxidoreductin 1-L alpha (#3264; CST), phosphorylated protein kinase A c (Thr197) (#4781; CST), PKA c (#4782; CST), p-HSL (Ser660) (#4126; CST), HSL (#4107; CST), phosphorylated signal transducer and activator of transcription 3 (Tyr705) (#9145; CST), and STAT3 (#30835; CST) were used.

Techniques: Microarray, Expressing, Gas Chromatography, Mass Spectrometry, Western Blot, Control