Figure S2 B. (E) Body weight ( n = 15), (F) lean mass and fat mass, ( n = 15) and (G) fasted glycemia ( n = 5) in chow diet fed 11-week-old Cre and AT-A8-KO mice. Data are means ± SEM. Groups were compared using unpaired t-test. For Cre vs. KO: ∗ p ≤ 0.033, ∗∗ p ≤ 0.002, ∗∗∗ p < 0.001. VAT, visceral adipose tissue; SAT, subcutaneous adipose tissue, BAT, brown adipose tissue. " width="100%" height="100%">
Journal: iScience
Article Title: Adipocyte Angptl8 deletion improves glucose and energy metabolism and obesity associated inflammation in mice
doi: 10.1016/j.isci.2024.111292
Figure Lengend Snippet: Construction and validation of adipose-specific conditional Angptl8 KO mice (A) Diagram of the Angptl8 gene with targeted ΔNeo allele, and the disrupted A8 allele. LoxP sites were placed upstream of exon 1 and downstream of exon 4. A vNEO cassette was inserted after exon 4. Mice with the targeted ΔNeo allele (Fl/Fl) were crossed with mice expressing Cre under the control of the adiponectin promoter to inactivate A8 in adipocytes (As-A8−/− mice). NDEL1 and NDEL2 primers used for genotyping are indicated. (B) The presence of the WT, Adipo-Cre transgene or the floxed A8 alleles was evaluated in DNA obtained from ear tissue biopsies using the primers as described in Methods. Specific amplification of a 686 bp DNA fragment corresponds to the floxed- A8 allele while a 569 bp DNA fragment corresponds to the WT A8 allele, the presence of a 600 bp DNA fragment denotes the Adipo-Cre transgene, as verified by genomic PCR. (C) Angptl8 mRNA expression in VAT, SAT, BAT and Liver tissue ( n = 4) were measured in 11-week-old male Cre and AT-A8-KO mice, 3 weeks after TMX treatment. Values are means ± SEM. Multiple unpaired t-test for multiple comparison were performed with Holm-Šídák correction using Graphpad Prism 10. (D) Angptl8 protein expression in collagenase treated mature adipocytes from VAT and SAT tissue in chow diet fed Cre and KO mice (n = 3–4); MM, Pre-stained Molecular weight markers. Quantification are shown in Figure S2 B. (E) Body weight ( n = 15), (F) lean mass and fat mass, ( n = 15) and (G) fasted glycemia ( n = 5) in chow diet fed 11-week-old Cre and AT-A8-KO mice. Data are means ± SEM. Groups were compared using unpaired t-test. For Cre vs. KO: ∗ p ≤ 0.033, ∗∗ p ≤ 0.002, ∗∗∗ p < 0.001. VAT, visceral adipose tissue; SAT, subcutaneous adipose tissue, BAT, brown adipose tissue.
Article Snippet: Additionally, plasma insulin (AL204, PerkinElmer, Vaughan, ON, Canada), leptin (AL225, PerkinElmer), FFA (Fujifilm, Lexington, MA), adiponectin (22-ADPMS-E01, Alpco, Salem, NH), and inflammation markers (IL-6, TNFα, MCP-1) were quantified at the Metabolomic Core Facility of CRCHUM using EnVision (PerkinElmer).
Techniques: Biomarker Discovery, Expressing, Control, Amplification, Comparison, Staining, Molecular Weight
Figure S2 B. (E) Body weight ( n = 15), (F) lean mass and fat mass, ( n = 15) and (G) fasted glycemia ( n = 5) in chow diet fed 11-week-old Cre and AT-A8-KO mice. Data are means ± SEM. Groups were compared using unpaired t-test. For Cre vs. KO: ∗ p ≤ 0.033, ∗∗ p ≤ 0.002, ∗∗∗ p < 0.001. VAT, visceral adipose tissue; SAT, subcutaneous adipose tissue, BAT, brown adipose tissue. " width="250" height="auto" />
