leptin deficient ob ob mice  (Charles River Laboratories)

Journal: The Journal of Clinical Investigation

Article Title: Characterization of intestinal immune responses in generalized human and murine lipodystrophy

doi: 10.1172/JCI192322

Figure Lengend Snippet: ( A ) Experimental design: After 1 DSS cycle (1.5%), lipodystrophic or WT mice were transplanted with 500–600 mg adipose tissue from WT or leptin-deficient ob/ob donors by mini-laparotomy before undergoing another 2 cycles of DSS. Image on right shows vascularized transplanted fat 1 month after surgery. ( B ) Weight change of transplanted fat tissue relative to baseline. ( C ) Plasma leptin levels ( n = 4–9). ( D ) Representative images of H&E- stained colon sections from transplanted versus nontransplanted DSS-treated animals. Scale bars: 100 μm. ( E ) Box-and-whisker plots summarizing the histologic inflammation score of fat-transplanted and nontransplanted animals. Data shown were pooled from 2 independent transplantation experiments (bold symbols) and additional control data points derived from nontransplantation DSS experiments (light gray) shown in ( n = 4–18). ( F ) Liver weights of transplanted WT and Pparg fl/fl Adipoq-Cre mice ( n = 4–18; data were pooled from 5 experiments). ( G ) Representative FACS plots showing IFN-γ and IL-17A production in colonic CD4 + T cells. UNSTIM., unstimulated. ( H ) Box-and-whisker plots summarizing absolute numbers of IFN-γ– and IL-17A–producing CD4 + T cells normalized to WT mice ( n = 4–18; data were pooled from 5 experiments). Statistical differences were calculated by 1-way ANOVA with Šídák’s correction. Each point represents 1 mouse; boxes range from the 25th-75th percentiles. Whisker plots show the minimum (smallest) and maximum (largest) values while the line in the box indicates the median. ( I ) Experimental setup and representative FACS plots showing IFN-γ– and IL-17A–producing CD4 + T cells in peripheral blood of a patient with AGLCD before and 4 days after daily recombinant leptin substitution. transpl., transplantation. Data indicate the mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001, by 1-way ANOVA with Tukey’s multiple comparisons test for B , C , E , F , and H .

Article Snippet: Leptin-deficient ob/ob mice were purchased from Charles River Laboratories.

Techniques: Clinical Proteomics, Staining, Whisker Assay, Transplantation Assay, Control, Derivative Assay, Recombinant

Journal: Atherosclerosis Plus

Article Title: Prelamin A accumulation overlaps increased vascular calcification in peripheral artery disease and regulates vascular smooth muscle cells mineralization in diabetes mellitus

doi: 10.1016/j.athplu.2026.01.002

Figure Lengend Snippet: Increased prelamin A accumulation and decreased ZMPSTE24 expression in OBVD mice induced by osteogenic protocol using vitamin D in aortae from mice. (A) Immunofluorescence microphotographs showing prelamin A (red, top panel) and ZMPSTE24 expression (red, bottom panel) in aortae from mice Bars = 50 μm. (B) Quantification showed increased prelamin A accumulation in OBVD mice, n = 4–5. (#P < 0.05 vs baseline [C57CT], GLzM test). (C) Quantification showed decreased ZMPSTE24 expression in C57VD, OBCT and OBVD, n = 3 (#P < 0.05 vs baseline [C57CT]; & P < 0.05 vs all groups, GEE test). C57CT indicates PBS treated C57BL/6 mice; C57VD indicates vitamin D3 treated C57BL/6 mice; OBCT indicates PBS treated ob/ob mice; OBVD indicates vitamin D3 treated ob/ob mice.

Article Snippet: We used male homozygous leptin-deficient ob/ob mice and control male C57BL/6 littermates, aged 16–20 weeks, from the Jackson Laboratory in Bar Harbor, ME.

Techniques: Expressing, Immunofluorescence

Journal: Atherosclerosis Plus

Article Title: Prelamin A accumulation overlaps increased vascular calcification in peripheral artery disease and regulates vascular smooth muscle cells mineralization in diabetes mellitus

doi: 10.1016/j.athplu.2026.01.002

Figure Lengend Snippet: Increased accumulation of prelamin A in ob/ob mice compared to C57BL/6. (A) Alizarin red staining (red) photographs showing calcium deposition staining in C57BL/6 and ob/ob aortae VSMCs (B) Osteogenic stimulation in vitro induced increased calcium accumulation, especially in VSMCs from ob/ob mice, n = 3 (#P < 0.05 vs. NonCA [C57BL/6]; $ P < 0.05 vs. FTI [C57BL/6], NonCA [ob/ob], FTI [ob/ob]; & P < 0.05 vs. FTI [C57BL/6], CA [C57BL/6], FTICA [C57BL/6], NonCA [ob/ob], FTI [ob/ob], GEE test). (C) Representative western blotting lanes showing prelamin A (∼75 kDa), lamin A (∼70 kDa) and lamin C (∼50 kDa) expression. (D) Western Blotting analysis demonstrated that FTI treatment induced prelamin A accumulation (green) in both C57BL/6 and ob/ob VSMCs, n = 3 (#P < 0.05 vs. NonCA [C57BL/6]; $ P < 0.05 vs. CA [C57BL/6], NonCA [ob/ob], CA [ob/ob], GEE test). (E) Western blotting revealed increased lamin A expression in VSMCs from ob/ob mice that were not treated with FTI, n = 3 (#P < 0.05 vs. NonCA [C57BL/6], GEE test). PBS indicates VSMCs incubated with phosphate buffered saline solution; FTI indicates VSMCs treated with farnesyl transferase inhibitor; NonCA indicates VSMCs incubated in the absence of osteogenic stimulus; CA indicates VSMCs incubated in the presence of osteogenic stimulus; GEE indicates Generalized Estimated Equations test.

Article Snippet: We used male homozygous leptin-deficient ob/ob mice and control male C57BL/6 littermates, aged 16–20 weeks, from the Jackson Laboratory in Bar Harbor, ME.

Techniques: Staining, In Vitro, Western Blot, Expressing, Incubation, Saline

Journal: bioRxiv

Article Title: Targeting Circulating FABP4 Ameliorates Obesity-Associated Hepatic Steatosis

doi: 10.64898/2026.01.24.701451

Figure Lengend Snippet: (A) Experimental schematic of the diet-induced obesity model. C57BL/6 mice were fed a high-fat diet (HFD; 60% fat) for 3 months to induce obesity and then treated weekly with anti-FABP4 monoclonal antibody (mAb; 5 mg/kg, i.v.) or control treated Livers were collected for steatosis analyses. (B) Representative hematoxylin and eosin (H&E) and Oil Red O (ORO) staining liver sections from control treated and anti-FABP4 mAb–treated HFD-fed mice. (C) Quantification of hepatic lipid accumulation based on ORO integrated optical density (IOD) as shown in panel B. (D) Representative immunohistochemistry (IHC) staining of FABP4 (red) with hematoxylin counterstain (blue) in liver sections from control treated and anti-FABP4 mAb–treated HFD-fed mice. (E) Quantification of hepatocytic FABP4 expression based on H-score analysis in control treated and anti-FABP4 mAb–treated HFD-fed mice. (F) Experimental schematic of the genetic obesity model. Leptin-deficient ob/ob mice were treated weekly with anti-FABP4 monoclonal antibody (5 mg/kg, i.v.) or control from 8 to 13 weeks of age, followed by liver collection. (G) Representative H&E- and ORO-stained liver sections from control treated and anti-FABP4 mAb–treated ob/ob mice. (H) Quantification of hepatic lipid accumulation based on ORO integrated optical density (IOD) as shown in panel G . (I–J) Representative IHC staining of FABP4 protein accumulation (red) in hepatocytes of from control treated and anti-FABP4 mAb–treated ob/ob mice. (J) Quantification of hepatocytic FABP4 H-score is shown in panel J . Data are presented as mean ± SEM. Statistical significance was determined by Student’s t -test (** p <0.01).

Article Snippet: Leptin-deficient ob/ob mice were purchased from The Jackson Laboratory and allowed to acclimate for 4 weeks.

Techniques: Control, Staining, Immunohistochemistry, Expressing