Journal: Pediatric Reports

Article Title: Resistin in Urine and Breast Milk: Relation to Type of Feeding and Anthropometry at 1-Month

doi: 10.3390/pediatric14010013

Figure Lengend Snippet: Correlation between resistin concentration in the breast milk and ( a ) body weight; ( b ) age; ( c ) body mass index (BMI); and ( d ) leptin concentration in mothers’ breast milk at 1 month post-partum.

Article Snippet: We analyzed urinary and breast milk resistin levels (Human Resistin ELISA kit; Arigo biolaboratories, Hsinchu City, Taiwan) and breastmilk leptin (Human Leptin Quantikine ELISA Kit; R&D Systems, Minneapolis, MI, USA) in infants using an enzyme-linked immunosorbent assay kit.

Techniques: Concentration Assay

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: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: Primary and secondary antibodies used for immunohistochemistry experiments.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Immunohistochemistry

Journal: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: Underfeeding during suckling results in lower body weight and plasma leptin levels. ( A ) Increases in litter size from six (normally fed, open bars) to nine (underfed, blue bars) pups per dam are associated with a lower body weight in pups, by the age of seven days ( n = 32 normally fed pups and 41 underfed pups of both sexes). ( B ) Underfeeding during suckling was associated with lower plasma levels of leptin at 10 days of age, as determined by ELISA ( n = 8 per group). ( C ) Illustration (40X magnification obtained with a BX43 Olympus fluorescence microscope equipped with a DP73 CCD camera) of a growing axon from an arcuate nucleus explant cultured in vitro, showing that the GHRH+ axon in green (uppermost image) expresses the leptin receptor in red (middle image). A merged image is shown at the bottom (arrow). Scale bars represent 20 µm. Data are presented as the mean ± SEM. Comparisons were performed in Mann–Whitney tests, with ** p < 0.01 and *** p < 0.001.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Fluorescence, Microscopy, Cell Culture, In Vitro, MANN-WHITNEY

Journal: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: Leptin stimulates axon growth in GHRH neurons in arcuate nucleus explants from normally fed pups. ( A ) Illustrative IHC of AgRP neurons from arcuate nucleus explants micro-dissected from one-week-old normally fed pups, in control conditions (left panels), and after stimulation with leptin (middle panels) and with leptin/IGF-1 (right panels). ( B ) Illustrative images of dual IHC for the axons of total arcuate nucleus neurons labeled with NF (top panels in red) and GHRH neurons labeled with eGFP (bottom panels in green), in the same conditions. Scale bars represent 1000 µm for AgRP+ and NF+ IHC (4X magnification) and 200 µm for GHRH+ IHC (10X magnification), for images from a BX612 Olympus fluorescence microscope equipped with a DP71 CCD camera. ( C ) Quantification of the growth of AgRP axons after 24 h of stimulation with leptin or leptin/IGF-I relative to control conditions ( n = 4 experiments), and ( D ) of the growth of NF (plain bars) and GHRH (dashed bars) axons ( n = 5–7 experiments). Data are presented as the mean ± SEM. Results were compared in a one-way ANOVA with the Newman–Keuls post hoc test (c) or a two-way ANOVA with Bonferroni correction (d), with *: p < 0.05 and **: p < 0.01 vs. control conditions and #: p < 0.05 vs. leptin stimulation.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Control, Labeling, Fluorescence, Microscopy

Journal: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: Signaling pathways involved in the axon growth of arcuate neurons in explants from normally fed pups. ( A ) Illustrative triple IHC of arcuate nucleus explants from the hypothalamus micro-dissected from one-week-old normally fed pups under control conditions (first panel), and following stimulation with leptin (second panel), leptin/NSC (third panel), leptin/LY (fourth panel) and leptin/PD (fifth panel), with NF (top panels in green), GHRH (middle panels in red) and AgRP (bottom panels in blue). Scale bars represent 100 µm for NF+ IHC (4X magnification) and 200 µm for GHRH+ and AgRP+ IHC (10X magnification), on images obtained with an Olympus BX43 fluorescence microscope equipped with a DP73 CCD camera. Quantifications of the growth of ( B ) NF ( n = 5–9 experiments), ( C ) GHRH ( n = 4–10 experiments) and ( D ) AgRP ( n = 5–10 experiments) axons stimulated for 24 h with leptin alone, or in combination with one of the three inhibitors (NSC_33994, LY_294002 or PD_0325901). Data are presented as the mean ± SEM. Results were analyzed by two-way ANOVA with Bonferroni correction, with *: p < 0.05 and ***: p < 0.001 vs. control conditions and ###: p < 0.001 vs. leptin stimulation.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Protein-Protein interactions, Control, Fluorescence, Microscopy

Journal: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: GHRH neurons from underfed pups are resistant to leptin for the stimulation of axon growth. ( A ) Illustrative IHC of arcuate nucleus explants from the hypothalamus micro-dissected from one-week-old underfed pups in control conditions (left panel), and after stimulation with leptin alone (middle panel), or with leptin/IGF-1 (right panel), with AgRP axons labeled in orange. ( B ) Axons from total arcuate nucleus neurons and GHRH neurons labeled by dual-IHC for neurofilament (NF, in red) and eGFP (in green), respectively. Scale bars represent 1000 µm for AgRP+ and NF+ IHC (4X magnification) and 200 µm for GHRH+ IHC (10X magnification), on images from an Olympus BX612 fluorescence microscope equipped with a DP71 CCD camera. ( C ) Quantification of the growth of AgRP axons stimulated by incubation for 24 h with leptin or leptin/IGF-I, relative to control conditions ( n = 5 experiments), and ( D ) quantification of the growth of NF (plain bars) and GHRH (dashed bars) axons ( n = 6 experiments). Data are presented as the mean ± SEM. Results were compared in a one-way ANOVA with the Newman–Keuls post hoc test (c) or in a two-way ANOVA with Bonferroni correction (d), with *: p < 0.05.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Control, Labeling, Fluorescence, Microscopy, Incubation

Journal: Nutrients

Article Title: Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice

doi: 10.3390/nu15051077

Figure Lengend Snippet: Alterations to leptin-stimulated signaling pathways in arcuate nucleus explants from underfed pups. The activation of the three signaling pathways by the exposure of seven-day explants to leptin (+) for 15 min was different in explants from underfed pups (blue bars) and in explants from normally fed pups (open bars). Data are presented as the fold induction of phosphorylated protein/total protein ratios (normalized against actin) for stimulated relative to unstimulated conditions for ( A ) phosphorylated Jak2/Jak2/actin ( n = 5 per group), ( B ) phosphorylated Stat3/Stat3/actin ( n = 5–7 per group), ( C ) phosphorylated-AKT/AKT/actin ( n = 9 per group), ( D ) phosphorylated MEK1/MEK1/actin ( n = 5–6 per group), ( E ) phosphorylated ERK1/ERK1/actin (left panel) and phosphorylated-ERK2/ERK2/actin (right panel; n = 8 per group). Data are presented as the mean ± SEM, with a Mann–Whitney analysis, with *: p < 0.05, **: p < 0.01.

Article Snippet: Plasma leptin concentrations in 10-day-old male mice were determined individually with the Mouse/Rat Leptin (R&D systems) ELISA kit, according to the manufacturer’s instructions.

Techniques: Protein-Protein interactions, Activation Assay, MANN-WHITNEY

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