pparg flox flox  (Jackson Laboratory)

Journal: bioRxiv

Article Title: BAT protects against hepatic oxidative stress by remodeling the circulating metabolome

doi: 10.64898/2026.05.12.722834

Figure Lengend Snippet: A. Schematic overview of the strategy we used to study how BAT affects systemic metabolite and lipid profiles in vivo. Step 1, generating the BAT ablation mouse model ( Ucp1 -Cre; Pparg flox/flox , herein BAT-mice) and littermate control ( Pparg flox/flox , herein BAT+ mice); Step 2, collecting the serum samples from these mice under acute cold (6 °C for 1 and 3 h), chronic cold (6 °C for 3 days), and thermoneutrality (28 °C for 3 days), with ad libitum feeding; Step 3, quantifying the dynamic profiles of metabolites and lipids across different temperature conditions by LC-MS; Step 4, selecting the metabolites and lipids altered by BAT ablation and clustering them based on their profile similarity. The altered molecules included those accumulated in BAT-ablated mice, which might be cleared by BAT, and those elevated in mice with intact BAT, which might be derived from BAT. N = 8 for BAT-ablated mice and N = 10 for littermate controls. B-C. Correlation clustering of circulating metabolites ( B ) and lipids ( C ) altered by BAT ablation. An unpaired t-test was used to determine the significance of each circulating metabolite or lipid between BAT+ and BAT- mice under each temperature condition. A total of 206 metabolites and 249 lipids with p < 0.05 in at least one condition were included for correlation clustering. Clustering analysis was performed using Mfuzz package in R software, and pairwise Pearson correlation coefficients between molecules were used to generate heatmaps. Table S1 lists the p values and fold changes between the BAT+ and BAT- groups for these metabolites and lipids. N = 8 for BAT-ablated mice and N = 10 for littermate controls. BAT- > BAT+, molecules were accumulated in BAT-ablated mice. BAT+ > BAT-, molecules were elevated in littermate controls with intact BAT. BAT-, BAT-ablated mice; BAT+, littermate controls. C-1h, 6 °C for 1 hour; C-3h, 6 °C for 3 hours; C-3d, 6 °C for 3 days; TN-3d, 28 °C for 3 days. Mice were provided with ad libitum access to food and water throughout the experiment. AMP, adenosine monophosphate; γ-Glu-Glu, glutamyl-glutamic acid; Pyro-Glu, pyroglutamic acid, SAM, S-adenosylmethionine; GSSG, oxidized glutathione; GSH, reduced glutathione; GABA, γ-aminobutyric acid; TG, triglyceride; DG, diglyceride; PE, phosphatidylethanolamine; PC, phosphatidylcholine; SM, sphingomyelin; Cer, ceramide; EtherPE, ether-linked phosphatidylethanolamine; EtherPC, ether-linked phosphatidylcholine; CE, cholesterol ester; LPE, lysophosphatidylethanolamine; LPC, lysophosphatidylcholine; LNAPE, N-acyl-lysophosphatidylethanolamine; HexCer, hexosylceramide; CAR, acylcarnitine; OHFA, hydroxy fatty acid; DiOHFA, dihydroxy fatty acid; DHA, docosahexaenoic acid. D-E. Representative quantitative profiles of known BAT-regulated metabolites ( D ) and lipids ( E ). Relative units: quantitative peak areas from LC-MS normalized to the average. N = 8 for BAT-ablated mice and N = 10 for littermate controls. Statistic: unpaired t-test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Ad libitum conditions. C-1h, 6 °C for 1 hour; C-3h, 6 °C for 3 hours; C-3d, 6 °C for 3 days; TN-3d, 28 °C for 3 days. F. Representative quantitative profiles of metabolites and lipids newly identified as BAT-regulated in this study. Relative units: quantitative peak areas from LC-MS normalized to the average. N = 8 for BAT-ablated mice and N = 10 for littermate controls. Statistic: unpaired t-test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Ad libitum conditions. C-1h, 6 °C for 1 hour; C-3h, 6 °C for 3 hours; C-3d, 6 °C for 3 days; TN-3d, 28 °C for 3 days. G. Relative quantitative profiles of indicated fatty acids and 12, 13-diHOME in serum from BAT-ablated mice and littermate controls. Relative units: quantitative peak areas from LC-MS normalized to the average. N = 8 for BAT-ablated mice and N = 10 for littermate controls. Statistic: unpaired t-test. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Ad libitum conditions. C-1h, 6 °C for 1 hour; C-3h, 6 °C for 3 hours; C-3d, 6 °C for 3 days; TN-3d, 28 °C for 3 days.

Article Snippet: PPARg flox/flox (Stock No. 004584), and Ucp1 -Cre (Stock No. 024670) mice were obtained from the Jackson Laboratory.

Techniques: In Vivo, Control, Liquid Chromatography with Mass Spectroscopy, Derivative Assay, Software

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Body weight progression between 18 weeks and 26 weeks of special diets in cohort #1 (A), and changes in body weight (B), fat mass (C), lean mass (D), and free fluid mass (E) during the 8 weeks of HFCF diet from mice of cohort #1. Body weight progression between 18 weeks and 25 weeks of special diets in Cohort #2 (F), and changes in body weight (G), fat mass (H), lean mass (I), and free fluid mass (J) during the 8 weeks of HFC+Fr diet from mice of cohort #2. Weight of urogenital (K, UG), mesenteric (L, MES), subcutaneous (M, SC), and brown (N, BAT) adipose tissue from mice in cohorts #1 and #2. Plasma levels of TG (O), cholesterol (P), NEFA (Q), and insulin (R), and blood glucose levels (S) from mice in cohort #1 and #2. Data are shown as mean ± standard error of the mean (SEM). Letters (a-d) indicates significant differences between LF-fed and HF-fed control mice. Greek symbols indicate significant differences (p<0.05) between 0-4 and 4-8 or 0-8 weeks between HF-control mice (ε), HF- Pparg ΔHep mice (η), HFCF-control mice (κ), HFCF- Pparg ΔHep mice (λ), HFC+Fr-control mice (κ), HFC+Fr- Pparg ΔHep mice (λ). Exclamation marks (!) indicate significant differences between HF-fed and HFCF-control mice in Cohort #1 or HF-fed and HFC+Fr-control mice in Cohort #2. Plus signs (+) indicate significant differences between HF-fed and HFCF- Pparg ΔHep mice in Cohort #1 or HF-fed and HFC+Fr- Pparg ΔHep mice in Cohort #2. Asterisks indicate significant differences between control and Pparg ΔHep mice. a, !, * p<0.05; b, !!, ++, p<0.01; c, +++, p<0.001; d, !!!!, ++++, ****, p<0.0001. n= 5-11 mice/group in cohort #1 and 7-8 mice/group in cohort #2.

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques: Clinical Proteomics, Control

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Liver weight (A), liver TG content (B), liver cholesterol content (C), plasma ALT level (D), MASLD activity score (E), and picrosirius red-stained fibrotic area (F) of mice in cohorts #1 [LF, HF, and HFCF-fed mice] and #2 [LF, HF, and HFC+Fr-fed mice]. Representative pictures of hematoxylin & eosin (H&E)- and picrosirius red/fast green (SR/FG)-stained liver section of mice in cohort #1 (G, LF, HF, and HFCF-fed mice) and cohort #2 (H, LF, HF, and HFC+Fr-fed mice). Hepatic gene expression of Pparg (I), Cidec (J), Col1a1 (K), Timp1 (L), Tnfa (M), Ccl2 (N), Trem2 (O), Gnmt (P), Pemt (Q), and Bhmt (R) of mice in cohort #1 (HF, and HFCF-fed mice) and cohort #2 (HF, and HFC+Fr-fed mice). I-R, expression level is represented as relative values of HF-fed control mice in cohort #1 or coho rt #2. Data are shown as mean ± standard error of the mean (SEM). Letters (a-d) indicate significant differences between LF-fed and HF-fed control mice. Exclamation marks (!) indicate significant differences between HF-fed and HFCF-control mice in Cohort #1 or HF-fed and HFC+Fr-control mice in Cohort #2. Plus signs (+) indicate significant differences between HF-fed and HFCF- Pparg ΔHep mice in Cohort #1 or HF-fed and HFC+Fr- Pparg ΔHep mice in Cohort #2. Asterisks indicate significant differences between control and Pparg ΔHep mice. a, !, * p<0.05; b, !!, ++, ** p<0.01; !!!,+++, *** p<0.001; d, !!!!, ++++, ****, p<0.0001. n= 5-11 mice/group in cohort #1 and 7-8 mice/group in cohort #2.

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques: Clinical Proteomics, Activity Assay, Staining, Gene Expression, Expressing, Control

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Body weight progression (A), and changes in body weight (B, BW), fat mass (C), lean mass (D), and free fluid mass (E) during the 24 weeks of HFC+Fr diet in male mice. Body weight progression (F), and changes in body weight (G, BW), fat mass (H), lean mass (I), and free fluid mass (J) during the 24 weeks of HFC+Fr diet in female mice. Weight of urogenital fat (K, UG-fat), mesenteric fat (L, MES-fat), retroperitoneal fat (M, RP-fat). subcutaneous fat (N, SC-fat), brown adipose tissue (O, BAT) from male and female mice. Plasma levels of TG (P), cholesterol (Q), NEFA (R), insulin (S), and blood glucose levels (T) from male and female mice. Area under the curve (U, AUC), and glucose tolerance test of male (V) and female (W) mice. Data are shown as mean ± standard error of the mean (SEM). Letters (a-d) indicate significant differences between LF-fed and HFC+Fr-fed control mice. Asterisks indicate significant differences between HFC+Fr-fed control and HFC+Fr-fed Pparg ΔHep mice. # indicate significant differences between LF-fed control and HFC+Fr-fed control in t=0 of the glucose tolerance test. a, * p<0.05; b, **, ## p<0.01; c, p<0.001; d, ****, p<0.0001. n= 4-9 male mice/group and 8-11 female mice/group.

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques: Clinical Proteomics, Control

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Body weight (A), respiratory exchange ratio (B, RER), energy expenditure (C), food consumption (D), volume of oxygen consumption (E), and volume of carbon dioxide production (F). Data are shown as mean ± standard error of the mean (SEM). Letters (b-d) indicate significant differences between LF-fed and HFC+Fr-fed control mice. Asterisks indicate significant differences between HFC+Fr-fed control and HFC+Fr-fed Pparg ΔHep mice. * p<0.05; b, p<0.01; d, p<0.0001. n= 11-13 mice/group

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques: Control

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Liver weight (A), liver TG content (B), liver cholesterol content (C), plasma ALT level (D), MASLD activity score (E), picrosirius red-stained fibrotic area of liver sections (F, SR), western blot for hepatic COL1A1 (G, top) with its Ponceau S staining (G, bottom) and quantification from male and female mice (G). Representative pictures of hematoxylin & eosin (H&E)- and picrosirius red (SR)-stained liver section of male (H) and female (I) mice. Hepatic gene expression of Pparg mRNA (J) and western blot for hepatic PPARγ (K, top) with its Ponceau S blot (K, bottom) and quantification of PPARγ1 and PPARγ2 from male and female mice (K). Hepatic gene expression of Cidea (L), Cidec (M), Ccl2 (N), Trem2 (O), Col1a1 (P), Timp1 (Q), Mat1a (R), Gnmt (S), Pemt (T), Ahcy (U), Bhmt (V), Cbs (W) of male and female. L-W, the expression level is represented as relative values of LF-fed control mice. Western blots for hepatic CIDEC (X, top) and BHMT (Y, top) with their Ponceau S staining (X, Y, bottom) and quantification from male and female mice. Data are shown as mean ± standard error of the mean (SEM). Letters (a-d) indicate significant differences between LF-fed and HFC+Fr-fed control mice. Asterisks indicate significant differences between HFC+Fr-fed control and HFC+Fr-fed Pparg ΔHep mice. a, * p<0.05; b, **, p<0.01; c,*** p<0.001; d, ****, p<0.0001. n= 4-9 male mice/group and 8-11 female mice/group.

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques: Clinical Proteomics, Activity Assay, Staining, Western Blot, Gene Expression, Expressing, Control

Journal: bioRxiv

Article Title: Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

doi: 10.64898/2026.02.25.707976

Figure Lengend Snippet: Volcano plots showing the differentially expressed genes (DEG, padj<0.05) by HFC+Fr diet (A) and Pparg ΔHep (B) in male and female mice. Heatmaps showing the regulation of PPARγ-target genes: Cidea , Cidec , monoacylglycerol O-acyltransferase 1 ( Mogat1 ), fatty acid translocase ( Cd36 ), perilipin 4 ( Plin4 ), the inflammation-related genes: Tnfa , Ccl2 , Trem2 , the fibrosis-related genes: Col1a1 , metalloproteinase 12 ( Mmp12 ), Timp1 , and the methionine metabolism-related genes: Pemt , Gnmt , Bhmt , by HFC+Fr diet (C) and Pparg ΔHep (D) in male and female mice. Asterisk (p<0.05) indicate significant regulation. Selected groups of genes identified by the enrichment analysis of DEG by HFC+Fr diet (E) and Pparg ΔHep (F) in male and female mice. The number of upregulated (green) or downregulated (red) DEG in the volcano plots or enrichment analysis are indicated in brackets. n= 4-6 male mice/group and 5 female mice/group.

Article Snippet: Pparg floxed mice ( ) in a C57BL/6J background were purchased from Jackson Laboratories (Strain 004584, B3.129-Ppargtm2Rev/J, Bar Harbor, ME), and bred as homozygotes under controlled temperature (22-24°C) and humidity in a specific-pathogen-free facility with 14 h light/10 h dark cycle (lights on at 6:00 am).

Techniques:

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet:

Article Snippet: Pparg flox mice; B6.129-Ppargtm2Rev/J , Jackson Lab , IMSR_JAX:004584; RRID:IMSR_JAX:004584.

Techniques: Virus, Plasmid Preparation, Recombinant, cDNA Synthesis, SYBR Green Assay, Quantitation Assay, Enzyme-linked Immunosorbent Assay, Software

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet: ΔPparg mice develop an increase in bone volume (A) qPCR analysis of Pparg mRNA levels in the femur of male control and ΔPparg mice (n = 6–8 mice per genotype). (B) Allele-specific PCR analysis of Pparg gene recombination in tissues isolated from a ΔPparg mouse. (C) Body weight of male control and ΔPparg mice (n = 6–11 mice per genotype). (D) Representative microCT images of the distal femur in male control and ΔPparg mice at the indicated ages. (E–G) MicroCT quantification of trabecular bone volume per tissue volume (BV/TV, E), trabecular number (Tb.N, F) and trabecular thickness (Tb.Th, G) in the distal femur of male control and ΔPparg mice (n = 8–10 mice per genotype). (H) Representative microCT images of the femoral mid-diaphysis from male 24-week-old control and ΔPparg mice. (I–K) MicroCT quantification of cortical tissue area (Tt.Ar, I), cortical bone area per tissue area (Ct.Ar/Tt.Ar, J) and cortical thickness (Ct.Th, K) at the femoral mid-diaphysis of control and ΔPparg mice (8–10 mice per genotype). (L–O) Dynamic histomorphometric quantification of osteoblastic activity in 16-week-old male control and ΔPparg mice including assessment of mineralizing surface per bone surface (MS/BS, L), representative calcein and alizarin red labeled sections (M), mineral apposition rate (MAR, N), and bone formation rate per bone surface (BFR/BS, O) (n = 6–7 mice per genotype). (P) Representative histological images stained for tartrare-resistant acid phosphate activity (10× original magnification). (Q) Quantification of osteoclast number per bone surfaces (Oc.N/BS) in the distal femur (7 mice per genotype). (R) Representative hematoxylin and eosin-stained histological sections to identify marrow adipocytes (10× original magnification). Data presented as mean and standard deviation. ∗, p < 0.05 comparison between control and knockout, #, p < 0.05 comparison between an 8-week timepoint and the labeled timepoint in control mice. Data were analyzed by unpaired Student’s t test.

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques: Control, Isolation, Activity Assay, Labeling, Staining, Standard Deviation, Comparison, Knock-Out

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet: ΔPparg mice have reduced fat mass and increase insulin sensitivity (A–C) Mass of the gonadal (gWAT, A), inguinal (iWAT, B), and intrascapular brown (BAT, C) adipose were assessed in male control and ΔPparg mice and normalized to body weight (n = 9–11 mice per genotype). (D) Representative histological sections of iWAT and BAT stained with hematoxylin and eosin or immunostained for UCP1 expression (10× original magnification) from 16-week-old male mice. (E) Food intake during 12 h light and dark periods (n = 7 mice per genotype). (F) Energy expenditure assessed by indirect calorimetry (n = 7 mice per genotype). (G and I) qPCR analysis of gene expression in iWAT isolated from 16-week-old male mice (n = 6 mice per genotype). (H and J) Representative western blot analysis of protein expression in iWAT. (K) qPCR analysis of gene expression in intrascapular brown adipose tissue (n = 6 mice per genotype). (L–N) Random fed serum lipid analysis in 16-week-old male control and ΔPparg mice (n = 8–9 mice per genotype). (O and P) Random fed glucose and serum insulin levels (n = 9 mice per genotype). (Q and R). Representative hematoxylin and eosin stained histological sections of pancreatic b-cell islets (20× original magnification) and quantification of islet area (n = 6 mice per genotype). (S and T) Glucose tolerance (S) and insulin tolerance (T) test at age 16 weeks(n = 8–9 mice per genotype). (U) Western blot analysis of AKT phosphorylation in iWAT, quadriceps and liver before and after insulin injection. Fold change in phosphorylation levels relative to untreated samples are show for each tissue (n = 8 mice per genotype). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test.

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques: Control, Staining, Expressing, Gene Expression, Isolation, Western Blot, Phospho-proteomics, Injection, Standard Deviation

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet: ΔPparg mice are resistant to high fat diet feeding Male control and ΔPparg mice were fed a high fat diet (60% kcal from fat) from ages 4 to 16 weeks. (A and B) MicroCT quantification of trabecular bone volume per tissue volume (BV/TV) in the distal femur (A) and cortical tissue area (Tt.Ar, B, (n = 8 mice per genotype)). (C) Weekly assessment of body weights in control and ΔPparg mice fed a high fat diet (n = 9–10 mice per genotype). (D–F) Mass of white adipose tissue depots (D), BAT (E), and liver (F) normalized to body weight (n = 8–10 mice per genotype). (G) Representative hematoxylin and eosin histological sections of iWAT, BAT, and liver (10× original magnification). (H) Size distribution of adipocytes in histological sections of iWAT (n = 5 mice per genotype). (I–K) qPCR and western blot analysis of genes (I) and proteins (J) involved in fatty acid synthesis and genes involved in fatty acid catabolism or beiging (K) (n = 6 mice per genotype). (L) Quantification of triglycerides liver tissue (n = 8–10 mice per genotype). (M and N) qPCR and western blot analysis of genes and proteins involved in fatty acid synthesis and steatosis in the liver of high fat diet fed control and ΔPparg mice (n = 6 mice per genotype). (O and P) Random fed glucose and insulin levels (n = 8–10 mice per genotype). (Q and R) Glucose tolerance (Q) and insulin tolerance test (R) after 12 weeks of high-fat diet feeding (n = 8–10 mice per genotype). (S–U) Random fed serum lipid analysis in high fat diet fed control and ΔPparg mice (n = 8–10 mice per genotype). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test.

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques: Control, Western Blot, Standard Deviation

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet: PPARγ in osteoblasts regulated sclerostin production to influence metabolism (A) qPCR analysis of Sost mRNA levels in the femur of male control and ΔPparg mice (n = 6–8 mice per genotype). (B) Quantification of serum sclerostin levels in male control and ΔPparg mice (n = 6–8 mice per genotype). (C and D) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 8–10 mice per genotype, D) were quantified in male control and ΔPparg mice fed a high fat diet (60% kcal from fat) from ages 4 to 16 weeks. (E and F) Sost mRNA levels (n = 6 mice per genotype, C) and serum sclerostin levels (n = 6–8 mice per genotype, D) were quantified in female control and ΔPparg mice. (G) qPCR analysis of Sost mRNA levels in cultures of control and ΔPparg primary osteoblasts after 14 days of differentiation (n = 11 samples per group). (H and I) qPCR analysis of Sost (H) and Axin2 (I) mRNA levels in Ocy454 cells 24 h after treatment with vehicle or rosiglitazone (n = 6 samples per group). (J) Western blot analysis of active, non-phosphorylated b-catenin and total b-catenin in the iWAT of 16-week-old male control and ΔPparg mice. (K and L) qPCR analysis of Axin2 and Ctnnb1 mRNA levels in the iWAT of control and ΔPparg mice fed a chow diet (K) or a high fat diet from ages 4 to 16 weeks (n = 5–6 mice per genotype). (M–Y) 8-week-old control and ΔPparg mice were injected with AAV-8 constructs directing the expression of Sost or GFP and then aged for an additional 8 weeks. (M) Serum sclerostin levels (n = 8–10 mice per group). (N) Western blot analysis of active, non-phosphorylated β-catenin and total β-catenin in the iWAT. (O) Weight gained during the 8-week experiment (n = 8–10 mice per group). (P and Q) Representative microCT images of the distal femur and quantification of trabecular bone volume (n = 8–10 mice per group). (R) iWAT mass (n = 8–10 mice per group). (S) Representative hematoxylin and eosin histological sections of iWAT (10× original magnification). (T and U) qPCR analysis of Fasn and Ucp1 mRNA levels in iWAT (n = 8–9 mice per group). (V) Random fed blood glucose (n = 8–10 mice per group). (W) Serum insulin levels (n = 8–10 mice per group). (X and Y) Insulin tolerance testing and area under the curve analysis (n = 8–10 mice per group). Data presented as mean and standard deviation. ∗, p < 0.05. Data were analyzed by unpaired Student’s t test or Anova followed by Tukey’s multiple comparison post hoc test.

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques: Control, Western Blot, Injection, Construct, Expressing, Standard Deviation, Comparison

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet:

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques: Virus, Plasmid Preparation, Recombinant, cDNA Synthesis, SYBR Green Assay, Quantitation Assay, Enzyme-linked Immunosorbent Assay, Software

Journal: iScience

Article Title: Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression

doi: 10.1016/j.isci.2023.106999

Figure Lengend Snippet: qPCR Primers

Article Snippet: Pparg flox/flox mice were obtained from The Jackson Laboratory (Strain #004584, Pparg tm2Rev /J).

Techniques:

Journal: bioRxiv

Article Title: Distinct mechanisms for sebaceous gland self-renewal and regeneration provide durability in response to injury

doi: 10.1101/2023.05.05.539454

Figure Lengend Snippet:

Article Snippet: Mouse: B6.129-Pparg tm2Rev/J (Pparg-flox) , The Jackson Laboratory (by way of Dr. Y. Eugene Chen) , Cat # 004584.

Techniques: Recombinant, Irradiation, RNAscope, In Situ, Software