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serum leptin concentration  (R&D Systems)


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    Structured Review

    R&D Systems serum leptin concentration
    Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) <t>serum</t> <t>leptin;</t> ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.
    Serum Leptin Concentration, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 261 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 261 article reviews
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    1) Product Images from "Bifidobacterium animalis ssp. lactis MG741 Reduces Body Weight and Ameliorates Nonalcoholic Fatty Liver Disease via Improving the Gut Permeability and Amelioration of Inflammatory Cytokines"

    Article Title: Bifidobacterium animalis ssp. lactis MG741 Reduces Body Weight and Ameliorates Nonalcoholic Fatty Liver Disease via Improving the Gut Permeability and Amelioration of Inflammatory Cytokines

    Journal: Nutrients

    doi: 10.3390/nu14091965

    Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) serum leptin; ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.
    Figure Legend Snippet: Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) serum leptin; ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.

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    A, B, Very low protein (VLP) diet leads to reduced growth and a decrease in <t>serum</t> <t>leptin</t> concentration. Mice maintained on the adequate protein (AP) and VLP diets were assessed daily for percent change in original body weight (A) and serum leptin concentration (B) at 5 weeks after beginning the feeding regimen. A, Results are shown from 1 of 2 independent experiments and consists of 5 mice per group. B, Serum leptin concentration is shown from 6 mice in each group. Error bars represent mean ± SEM. The differences in mean body weights between the VLP and AP groups were statistically significant as follows: P < .001 for day 9 and P < .0001 for days 10–38. C, Mice on the VLP diet show increased susceptibility to influenza infection. Mice maintained on the AP or VLP diets were infected with either A/PR8 or A/Mex influenza and assessed for virus-induced mortality (percent survival). Data represent results from 3 independent experiments.
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    A, B, Very low protein (VLP) diet leads to reduced growth and a decrease in <t>serum</t> <t>leptin</t> concentration. Mice maintained on the adequate protein (AP) and VLP diets were assessed daily for percent change in original body weight (A) and serum leptin concentration (B) at 5 weeks after beginning the feeding regimen. A, Results are shown from 1 of 2 independent experiments and consists of 5 mice per group. B, Serum leptin concentration is shown from 6 mice in each group. Error bars represent mean ± SEM. The differences in mean body weights between the VLP and AP groups were statistically significant as follows: P < .001 for day 9 and P < .0001 for days 10–38. C, Mice on the VLP diet show increased susceptibility to influenza infection. Mice maintained on the AP or VLP diets were infected with either A/PR8 or A/Mex influenza and assessed for virus-induced mortality (percent survival). Data represent results from 3 independent experiments.
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    Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) <t>serum</t> <t>leptin;</t> ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.
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    Figure 2. Hypothalamic vascularity is rapidly and dynamically altered by HFHS diet feeding in association with circulating <t>leptin</t> levels (A) Bodyweight of SC and HFHS diet-fed mice. The red arrow indicates the onset of HFHS-induced hypothalamic hypervascularization in mice (see Figure 1A). n = 4–7 mice per group. (B) mRNA expression of vascular endothelial growth factor A (Vegfa) in the hypothalamus and cortex from mice fed with an SC diet and an HFHS diet at different time points. n = 8 mice per group. (C) <t>Serum</t> <t>leptin</t> levels in mice fed with an SC diet or 14-day HFHS diet. Data are presented as individual mice and mean ± SEM. n = 4–7 mice per group (unpaired t test). (D) Confocal micrographs depicting the MBH vessel profile of SC diet-fed, HFHS diet-fed, and diet-reversed (DR) mice. Data are representative of the cohort depicted in Figure S1G. (E) Linear regression analysis between the length of vessels in the MBH and the body fat mass of mice fed SC, HFHS, DR, and calorie-restricted (CR) diet. The average 24-h food intake of respective groups is shown on the right. n = 6 mice per group. (F) Quantification of the number of VEGF+ cells in the MBH between groups. Data are represented as individual hemisection and mean ± SEM. n = 6 mice per group; 6–8 hemisections/mouse. (G) Quantification of serum leptin levels between groups. n = 6 mice per group. Scale bars, 100 mm (D). *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. n.s., not significant. Statistical tests included two-way ANOVA (A), one-way ANOVA (B, F, and G), and unpaired Student’s t test (C).
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    Figure 2. Hypothalamic vascularity is rapidly and dynamically altered by HFHS diet feeding in association with circulating <t>leptin</t> levels (A) Bodyweight of SC and HFHS diet-fed mice. The red arrow indicates the onset of HFHS-induced hypothalamic hypervascularization in mice (see Figure 1A). n = 4–7 mice per group. (B) mRNA expression of vascular endothelial growth factor A (Vegfa) in the hypothalamus and cortex from mice fed with an SC diet and an HFHS diet at different time points. n = 8 mice per group. (C) <t>Serum</t> <t>leptin</t> levels in mice fed with an SC diet or 14-day HFHS diet. Data are presented as individual mice and mean ± SEM. n = 4–7 mice per group (unpaired t test). (D) Confocal micrographs depicting the MBH vessel profile of SC diet-fed, HFHS diet-fed, and diet-reversed (DR) mice. Data are representative of the cohort depicted in Figure S1G. (E) Linear regression analysis between the length of vessels in the MBH and the body fat mass of mice fed SC, HFHS, DR, and calorie-restricted (CR) diet. The average 24-h food intake of respective groups is shown on the right. n = 6 mice per group. (F) Quantification of the number of VEGF+ cells in the MBH between groups. Data are represented as individual hemisection and mean ± SEM. n = 6 mice per group; 6–8 hemisections/mouse. (G) Quantification of serum leptin levels between groups. n = 6 mice per group. Scale bars, 100 mm (D). *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. n.s., not significant. Statistical tests included two-way ANOVA (A), one-way ANOVA (B, F, and G), and unpaired Student’s t test (C).
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    Effects of Selenov knockout on body weight, tissue fat accumulation, adipocyte histology, and serum lipid profiles and related biomarkers in male mice fed a normal-fat (control) or a high-fat diet from 2- to 6-month old of age. (A) Body weight (n = 10). (B) Upper panel images: magnetic resonance analysis of total body fat mass. Both the vertical (top) and cross (bottom) sections showed increased fat (red color) accumulations by KO and high-fat diet. Lower bar graphs: weights of total fat and individual adipose tissues (n = 10). (C) H&E staining of paraffin-embedded EWAT sections: adipocyte hypertrophy and enlarged lipid droplets by the KO and high-fat diet, scale bar, 20 μm. The image was a representative of five sets of data. (D) Serum concentrations of TC, TG, NEFA, <t>leptin,</t> TNF α , IL6, Mcp1, <t>and</t> <t>adiponectin</t> (n = 6). All graphic data are mean ± SE. Means without sharing a common superscript letter are different (P < 0.05). Abbreviations: BAT, brown adipose tissue; EWAT, epididymis white adipose tissue; HF, high-fat diet; IL6, interleukin 6; KO, knockout; Mcp1, monocyte chemoattractant protein-1; NEFA, non-esterified fat acid; NF, normal-fat diet; TC, total cholesterol; TG, total triglyceride; TNF α , tumor necrosis factor alpha; WT, wild-type. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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    Image Search Results


    A, B, Very low protein (VLP) diet leads to reduced growth and a decrease in serum leptin concentration. Mice maintained on the adequate protein (AP) and VLP diets were assessed daily for percent change in original body weight (A) and serum leptin concentration (B) at 5 weeks after beginning the feeding regimen. A, Results are shown from 1 of 2 independent experiments and consists of 5 mice per group. B, Serum leptin concentration is shown from 6 mice in each group. Error bars represent mean ± SEM. The differences in mean body weights between the VLP and AP groups were statistically significant as follows: P < .001 for day 9 and P < .0001 for days 10–38. C, Mice on the VLP diet show increased susceptibility to influenza infection. Mice maintained on the AP or VLP diets were infected with either A/PR8 or A/Mex influenza and assessed for virus-induced mortality (percent survival). Data represent results from 3 independent experiments.

    Journal: The Journal of infectious diseases

    Article Title: Protein Energy Malnutrition Decreases Immunity and Increases Susceptibility to Influenza Infection in Mice

    doi: 10.1093/infdis/jis527

    Figure Lengend Snippet: A, B, Very low protein (VLP) diet leads to reduced growth and a decrease in serum leptin concentration. Mice maintained on the adequate protein (AP) and VLP diets were assessed daily for percent change in original body weight (A) and serum leptin concentration (B) at 5 weeks after beginning the feeding regimen. A, Results are shown from 1 of 2 independent experiments and consists of 5 mice per group. B, Serum leptin concentration is shown from 6 mice in each group. Error bars represent mean ± SEM. The differences in mean body weights between the VLP and AP groups were statistically significant as follows: P < .001 for day 9 and P < .0001 for days 10–38. C, Mice on the VLP diet show increased susceptibility to influenza infection. Mice maintained on the AP or VLP diets were infected with either A/PR8 or A/Mex influenza and assessed for virus-induced mortality (percent survival). Data represent results from 3 independent experiments.

    Article Snippet: Following the manufacturer’s protocol, serum leptin concentrations were measured using a mouse enzyme-linked immunosorbent assay (ELISA) kit (GenWay Biotech, California).

    Techniques: Concentration Assay, Infection, Virus

    Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) serum leptin; ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.

    Journal: Nutrients

    Article Title: Bifidobacterium animalis ssp. lactis MG741 Reduces Body Weight and Ameliorates Nonalcoholic Fatty Liver Disease via Improving the Gut Permeability and Amelioration of Inflammatory Cytokines

    doi: 10.3390/nu14091965

    Figure Lengend Snippet: Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. ( A ) Fasting blood glucose; ( B ) insulin; ( C ) HOMA-IR; ( D ) serum ALT; ( E ) serum AST; ( F ) serum leptin; ( G ) serum total cholesterol; ( H ) serum HDL-cholesterol; ( I ) serum LDL-cholesterol; ( J ) liver weight; and ( K ) liver triglycerides. Data are presented as the mean ± standard error of the mean ( n = 9). The different letters (a–c) indicate significant differences ( p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.

    Article Snippet: Serum leptin concentration was determined using kits from R&D systems (MOB00B, Minneapolis, MN, USA), and insulin and endotoxin levels were determined with a kit from Thermo Fisher Scientific (EMINS, A39553).

    Techniques:

    Figure 2. Hypothalamic vascularity is rapidly and dynamically altered by HFHS diet feeding in association with circulating leptin levels (A) Bodyweight of SC and HFHS diet-fed mice. The red arrow indicates the onset of HFHS-induced hypothalamic hypervascularization in mice (see Figure 1A). n = 4–7 mice per group. (B) mRNA expression of vascular endothelial growth factor A (Vegfa) in the hypothalamus and cortex from mice fed with an SC diet and an HFHS diet at different time points. n = 8 mice per group. (C) Serum leptin levels in mice fed with an SC diet or 14-day HFHS diet. Data are presented as individual mice and mean ± SEM. n = 4–7 mice per group (unpaired t test). (D) Confocal micrographs depicting the MBH vessel profile of SC diet-fed, HFHS diet-fed, and diet-reversed (DR) mice. Data are representative of the cohort depicted in Figure S1G. (E) Linear regression analysis between the length of vessels in the MBH and the body fat mass of mice fed SC, HFHS, DR, and calorie-restricted (CR) diet. The average 24-h food intake of respective groups is shown on the right. n = 6 mice per group. (F) Quantification of the number of VEGF+ cells in the MBH between groups. Data are represented as individual hemisection and mean ± SEM. n = 6 mice per group; 6–8 hemisections/mouse. (G) Quantification of serum leptin levels between groups. n = 6 mice per group. Scale bars, 100 mm (D). *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. n.s., not significant. Statistical tests included two-way ANOVA (A), one-way ANOVA (B, F, and G), and unpaired Student’s t test (C).

    Journal: Cell metabolism

    Article Title: Obesity-associated hyperleptinemia alters the gliovascular interface of the hypothalamus to promote hypertension.

    doi: 10.1016/j.cmet.2021.04.007

    Figure Lengend Snippet: Figure 2. Hypothalamic vascularity is rapidly and dynamically altered by HFHS diet feeding in association with circulating leptin levels (A) Bodyweight of SC and HFHS diet-fed mice. The red arrow indicates the onset of HFHS-induced hypothalamic hypervascularization in mice (see Figure 1A). n = 4–7 mice per group. (B) mRNA expression of vascular endothelial growth factor A (Vegfa) in the hypothalamus and cortex from mice fed with an SC diet and an HFHS diet at different time points. n = 8 mice per group. (C) Serum leptin levels in mice fed with an SC diet or 14-day HFHS diet. Data are presented as individual mice and mean ± SEM. n = 4–7 mice per group (unpaired t test). (D) Confocal micrographs depicting the MBH vessel profile of SC diet-fed, HFHS diet-fed, and diet-reversed (DR) mice. Data are representative of the cohort depicted in Figure S1G. (E) Linear regression analysis between the length of vessels in the MBH and the body fat mass of mice fed SC, HFHS, DR, and calorie-restricted (CR) diet. The average 24-h food intake of respective groups is shown on the right. n = 6 mice per group. (F) Quantification of the number of VEGF+ cells in the MBH between groups. Data are represented as individual hemisection and mean ± SEM. n = 6 mice per group; 6–8 hemisections/mouse. (G) Quantification of serum leptin levels between groups. n = 6 mice per group. Scale bars, 100 mm (D). *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. n.s., not significant. Statistical tests included two-way ANOVA (A), one-way ANOVA (B, F, and G), and unpaired Student’s t test (C).

    Article Snippet: Serum leptin concentrations determined by a commercial mouse leptin ELISA (Alpco) following the manufacturer’s instructions.

    Techniques: Expressing

    Effects of Selenov knockout on body weight, tissue fat accumulation, adipocyte histology, and serum lipid profiles and related biomarkers in male mice fed a normal-fat (control) or a high-fat diet from 2- to 6-month old of age. (A) Body weight (n = 10). (B) Upper panel images: magnetic resonance analysis of total body fat mass. Both the vertical (top) and cross (bottom) sections showed increased fat (red color) accumulations by KO and high-fat diet. Lower bar graphs: weights of total fat and individual adipose tissues (n = 10). (C) H&E staining of paraffin-embedded EWAT sections: adipocyte hypertrophy and enlarged lipid droplets by the KO and high-fat diet, scale bar, 20 μm. The image was a representative of five sets of data. (D) Serum concentrations of TC, TG, NEFA, leptin, TNF α , IL6, Mcp1, and adiponectin (n = 6). All graphic data are mean ± SE. Means without sharing a common superscript letter are different (P < 0.05). Abbreviations: BAT, brown adipose tissue; EWAT, epididymis white adipose tissue; HF, high-fat diet; IL6, interleukin 6; KO, knockout; Mcp1, monocyte chemoattractant protein-1; NEFA, non-esterified fat acid; NF, normal-fat diet; TC, total cholesterol; TG, total triglyceride; TNF α , tumor necrosis factor alpha; WT, wild-type. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Redox Biology

    Article Title: Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure

    doi: 10.1016/j.redox.2021.102048

    Figure Lengend Snippet: Effects of Selenov knockout on body weight, tissue fat accumulation, adipocyte histology, and serum lipid profiles and related biomarkers in male mice fed a normal-fat (control) or a high-fat diet from 2- to 6-month old of age. (A) Body weight (n = 10). (B) Upper panel images: magnetic resonance analysis of total body fat mass. Both the vertical (top) and cross (bottom) sections showed increased fat (red color) accumulations by KO and high-fat diet. Lower bar graphs: weights of total fat and individual adipose tissues (n = 10). (C) H&E staining of paraffin-embedded EWAT sections: adipocyte hypertrophy and enlarged lipid droplets by the KO and high-fat diet, scale bar, 20 μm. The image was a representative of five sets of data. (D) Serum concentrations of TC, TG, NEFA, leptin, TNF α , IL6, Mcp1, and adiponectin (n = 6). All graphic data are mean ± SE. Means without sharing a common superscript letter are different (P < 0.05). Abbreviations: BAT, brown adipose tissue; EWAT, epididymis white adipose tissue; HF, high-fat diet; IL6, interleukin 6; KO, knockout; Mcp1, monocyte chemoattractant protein-1; NEFA, non-esterified fat acid; NF, normal-fat diet; TC, total cholesterol; TG, total triglyceride; TNF α , tumor necrosis factor alpha; WT, wild-type. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: Respective commercial kits were also used to determine serum concentrations of adiponectin and leptin (Crystal Chem, Downers Grove, IL, USA), interleukin 6 (IL-6) and tumor necrosis factor α (TNFα) (eBioscience, San Diego, CA, USA), and monocyte chemoattractant protein-1 (Mcp1) (BioLengend, San Diego, CA, USA).

    Techniques: Knock-Out, Staining