Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Adipokine Profile in Patients with Type 2 Diabetes Depends on Degree of Obesity

doi: 10.12659/MSM.904318

Figure Lengend Snippet: Leptin/adiponectin ratio in control group and type 2 diabetic patients divided according to BMI value. K – control group, group I – type 2 diabetic patients with normal body weight, group II – type 2 diabetic patients with overweight, group III – type 2 diabetic patients with obesity and group IV – type 2 diabetic patients with severe obesity. * p<0.05 vs. group K; ** p<0.01 vs. group K; # p<0.05 vs. group I.

Article Snippet: The plasma concentrations of the studied adipokines were determined by immunoenzymatic methods using Human Leptin Quantikine ELISA Kit (R&D Systems, USA), Human Total Adiponectin/Acrp30 Quantikine ELISA (R&D Systems, USA), and Human Resistin Quantikine ELISA Kit (R&D Systems, USA), as well as Human Nicotinamide phosphoribosyltransferase, NAmPRTase ELISA Kit (Wuhan EIAab Science, China) for leptin, adiponectin, resistin, and visfatin, respectively.

Techniques: Control

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Schematic diagram of clinical significance analysis for bone marrow (BM) plasma leptin levels and blast-cell LEPR expression in 84 newly diagnosed AML patients. B BM plasma leptin levels correlate inversely with blast clearance rates in AML patients. C Leptin concentrations in BM plasma from AML patients with differential chemotherapeutic responses. D ROC curve of leptin in BM plasma for distinguishing ORR and NR groups. E Leptin levels in the BM plasma of AML patients stratified by ELN 2022 risk classification. F ROC curve of marrow plasma leptin for distinguishing between favorable and adverse risk AML groups. G ROC curve of marrow plasma leptin for distinguishing between intermediate and adverse risk AML groups. H CCK-8 analysis of cell viability in leptin-pretreated primary AML cells following 24 h Ara-C exposure ( n = 5). I The forest plot shows the results of logistic regression analysis. J Representative FCM profiles and MFI statistical analysis of LEPR expression in BM leukemia cells from high- and low-leptin groups ( n = 10 patients per group). MFI: mean fluorescence intensity. K Kaplan-Meier analysis of overall survival in AML patients stratified by LEPR expression levels from GSE1159 , GSE37642 and GSE6891 datasets. Data are presented as mean ± SD C, E, J . Significance differences were determined by two-tailed unpaired t test with Welch’s correction C , one-way ANOVA with Holm-Šídák’s multiple comparisons test (E), two-tailed paired t test H , or two-tailed unpaired t test J . ns, not significant, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Clinical Proteomics, Expressing, CCK-8 Assay, Fluorescence, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Experimental design of evaluating the role of leptin on the therapeutic effect in MLL-AF9-driven AML mice. B Kaplan-Meier survival curve of MLL-AF9 AML mice ( n = 5 mice per group). C Representative images and weight comparisons of spleen and liver in MLL-AF9 AML mice treated with PBS, Ara-C, leptin + Ara-C, or Allo-aca+ Ara-C ( n = 5 mice per group). D Representative H&E-stained sections of BM, spleen and liver (scale bars: 20 μm). E Representative FCM profiles (left) and quantification of YFP + AML cells in BM, spleen, and liver of MLL-AF9 AML mice ( n = 5 mice per group). Data are presented as mean ± SD C, E . Significance differences were determined by log-rank test B , or one-way ANOVA with Dunnett’s multiple comparisons test C, E . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Staining

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Total antioxidant capacity analysis of blast-cell from MLL-AF9 (left) and AML1-ETO9a (right) AML mice ( n = 5 mice per group). B Effect of leptin on chemosensitivity to Ara-C and DNR in human AML cell lines (U937, HL-60, and THP-1). The inhibition rates were calculated from four treatment arms: (i) PBS control; (ii) Leptin alone; (iii) Ara-C alone (or DNR) and (iv) Leptin + Ara-C (or DNR). Data represent three independent biological experiments. C Analysis of total antioxidant capacity in leptin-treated AML cells. D GSH/GSSG ratio was examined with a GSH and GSSG assay kit. E RT-qPCR analysis of antioxidant-associated genes mRNA levels in leptin-treated AML cells. Analysis of CAT F and SOD G activity. H Representative immunofluorescence images (left) and MFI quantification (right) of LEPR expression (LEPR, green) in leptin-treated AML cells (scale bars: 25 μm). Data are presented as mean ± SD. Significance differences were determined by one-way ANOVA with Dunnett’s multiple comparisons test A , or two-tailed unpaired t test B–H . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Inhibition, Control, GSSG Assay, Quantitative RT-PCR, Activity Assay, Immunofluorescence, Expressing, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Western blot analysis of LEPR expression in AML cells under indicated treatments. β-actin served as the loading control. Band intensities were quantified using ImageJ software and normalized to the control group. B–D Effect of Allo-aca on AML cell chemosensitivity by CCK-8 assay. The inhibition rates were calculated from eight treatment arms: (i) PBS; (ii) Allo-aca alone; (iii) Leptin alone; (iv) Allo-aca + Leptin; (v) Ara-C alone (or DNR); (vi) Allo-aca + Ara-C (or DNR); (vii) Leptin + Ara-C (or DNR) and (viii) Allo-aca + Leptin + Ara-C (or DNR). Data represent three independent biological replicates. E Western blot to confirm the depletion of LEPR in AML cells. β-actin served as a loading control. F Chemosensitivity analysis of LEPR -knockout AML cells with or without leptin treatment. Comparison of total antioxidant capacity G , GSH/GSSG ratio H , antioxidant-related genes mRNA levels I , CAT J and SOD K activity in AML cells with or without LEPR knockout. Data are presented as mean ± SD B–D, F–K . Significance differences were determined by two-tailed unpaired t test. ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Western Blot, Expressing, Control, Software, CCK-8 Assay, Inhibition, Knock-Out, Comparison, Activity Assay, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Numbers of DEPs located in mitochondria of MLL-AF9 leukemia cells ( n = 3 mice per group). B Venn diagram showing the overlapping DEPs that up-regulated in the leptin + Ara-C group but down-regulated in the Allo-aca + Ara-C group (versus Ara-C alone, n = 3 mice per group). C KEGG pathway enrichment analysis of B . D Heatmap analysis of OXPHOS (Ko00190) and ROS (Ko05208) pathway protein expression in MLL-AF9 leukemia cells. E Mitochondrial respiration analysis of sorted MLL-AF9 AML cells using Seahorse XF technology ( n = 5 mice per group). F Calculation of basal respiration (Basal), maximal respiratory capacity (Max), spare respiratory capacity (Spare), and mitochondrial ATP production (ATP) in MLL-AF9 leukemia cells based on the measurements in E . G Representative FCM profiles (left) and MFI quantification (right) of mtROS levels in MLL-AF9 leukemia cells by MitoSOX staining ( n = 5 mice per group). H Measurement of OCR levels in AML1-ETO9a leukemia cells. I Calculation of Basal, Max, Spare, and ATP in AML1-ETO9a leukemia cells based on the measurements in H . J Representative FCM profiles (left) and MFI statistical analysis (right) of mtROS levels in AML1-ETO9a leukemia cells. K OCR was measured (upper) and calculation of basal, Max, Spare, and ATP (lower) in leptin-treated AML cells. L Representative FCM histogram (upper) and MFI statistical analysis (lower) of mtROS levels in leptin-treated AML cells. Data are presented as mean ± SD F, G, I–L . Significance differences were determined by one-way ANOVA with Dunnett’s multiple comparisons test F, G, I, J , or two-tailed unpaired t test K, L . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Expressing, Staining, Two Tailed Test

Journal: Cell Death & Disease

Article Title: Marrow leptin-LEPR signaling rewires mitochondrial oxidative metabolism to confer chemoresistance in acute myeloid leukemia

doi: 10.1038/s41419-026-08528-0

Figure Lengend Snippet: A Gene Ontology (GO) terms enrichment analysis of up-regulated DEPs in the leptin + Ara-C group (upper) and down-regulated DEPs in the Allo-aca + Ara-C group (lower). B Heatmap analysis of mitochondrial complex I structural subunit protein expression in MLL-AF9 leukemia cells. C Structural model of mitochondrial respiratory chain complexes. D Comparison of complex I activity in AML cells treated with leptin, Allo-aca, or a combination. E Western blot analysis of p-STAT3 (727), p-STAT3 (705), STAT3, p-JAK2 (Tyr1007/1008) and JAK2 expression in AML cells under indicated treatments. β-actin served as a loading control. Rescue experiments of complex I activity F , total antioxidant capacity G and mtROS production H in AML cells. I CCK-8 analysis of the chemosensitivity in AML cells treated with leptin, JSI-124 (JAK2/STAT3 inhibitor), or leptin + JSI-124. Data are presented as mean ± SD D, F–I . Significance differences were determined by two-tailed unpaired t test D, I , or one-way ANOVA with Dunnett’s multiple comparisons test F–H . ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Marrow plasma leptin concentrations were measured using a Human Leptin ELISA Kit (Cusabio, Wuhan, Hubei, China), with Spearman’s correlation ( r ) analyzing leptin-blast clearance relationships and comparative analyses examining leptin levels between ORR and NR groups.

Techniques: Expressing, Comparison, Activity Assay, Western Blot, Control, CCK-8 Assay, Two Tailed Test

Journal: bioRxiv

Article Title: White adipose tissue undergoes pathological dysfunction in the TDP-43A315T mouse model of amyotrophic lateral sclerosis (ALS)

doi: 10.1101/2025.07.03.662925

Figure Lengend Snippet: (A) Concentration of leptin levels at diagnosis measured by ELISA in healthy controls and ALS subgrouped by sex. (B) Concentration of leptin levels at diagnosis in ALS and controls subgrouped by sex and disease progression: slow, normal and fast progression patients. (C) Concentration of leptin levels at diagnosis in ALS and controls subgrouped by sex and rate of progression in overweight patients. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Abbreviations: ALS, sporadic amyotrophic lateral sclerosis.

Article Snippet: Leptin plasma levels were measured using a Human Leptin ELISA Kit PicoKine® (Boster Biological Technology) with samples diluted 1:20 for males and 1:10 for females.

Techniques: Concentration Assay, Biomarker Discovery, Enzyme-linked Immunosorbent Assay