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infinity cholesterol liquid stable reagent kit  (Thermo Fisher)


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    Structured Review

    Thermo Fisher infinity cholesterol liquid stable reagent kit
    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma <t>cholesterol.</t> ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.
    Infinity Cholesterol Liquid Stable Reagent Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/infinity cholesterol liquid stable reagent kit/product/Thermo Fisher
    Average 98 stars, based on 1 article reviews
    infinity cholesterol liquid stable reagent kit - by Bioz Stars, 2026-06
    98/100 stars

    Images

    1) Product Images from "Dietary depletion of glutamine is atheroprotective"

    Article Title: Dietary depletion of glutamine is atheroprotective

    Journal: bioRxiv

    doi: 10.64898/2026.03.06.710174

    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma cholesterol. ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.
    Figure Legend Snippet: ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma cholesterol. ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.

    Techniques Used: Control, Clinical Proteomics, Concentration Assay



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    Thermo Fisher infinity cholesterol liquid stable reagent kit
    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma <t>cholesterol.</t> ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.
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    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma <t>cholesterol.</t> ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.
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    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma <t>cholesterol.</t> ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.
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    A-B) Overnight fasting insulin, blood glucose, serum triglyceride, <t>cholesterol,</t> non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.
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    A-B) Overnight fasting insulin, blood glucose, serum triglyceride, <t>cholesterol,</t> non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.
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    A-B) Overnight fasting insulin, blood glucose, serum triglyceride, <t>cholesterol,</t> non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.
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    Image Search Results


    ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma cholesterol. ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.

    Journal: bioRxiv

    Article Title: Dietary depletion of glutamine is atheroprotective

    doi: 10.64898/2026.03.06.710174

    Figure Lengend Snippet: ( A ) Experimental design. Apoe -/- male mice were fed WD and received drinking water with no additives (Ctrl) or water supplemented with glutamine (Gln), or alpha-ketoglutarate (AKG) for 8 weeks. ( B ) Oil red O analysis of plaque burden in the aorta with ( C ) representative images of aortas from male mice. Scale bar: 2 mm. ( D ) Plaque area at 7 locations across the aortic root from the first appearance of the aortic valves in (top) male and (bottom) female mice. ( E ) Representative images of aortic root plaques from male and female mice in control (Ctrl) and glutamine (Gln) group. Scale bar: 200 μm. Black dashed line marks representative plaques boundaries. ( F ) Total plaque volume in the aortic root, calculated as the area under the curve from (D). ( G ) Sirius red analysis of plaque collagen content. ( H ) Necrotic core size analysis at the point of peak stenosis. ( I ) Plasma cholesterol. ( J ) Glutamine plasma concentration normalized to sex matched controls. (B, F, G, I, J) Data analyzed using one-way ANOVA with Dunnett’s correction or (H) Kruskal Wallis with Dunn’s correction for post-hoc analysis with N ≥ 13. Error bars represent mean ± SEM or (H) median ± IQR. *** P < 0.001; ** P = 0.001 to 0.01; * P = 0.01 to 0.05; ns, not significant.

    Article Snippet: Plasma cholesterol was analyzed, using Infinity Cholesterol Liquid Stable Reagent kit (Thermo Scientific; cat#: TR13421) and Data-Trol A, Abnormal Control Serum (Thermo Scientific; cat#: TR41001), as an internal standard, according to the manufacturer’s instructions.

    Techniques: Control, Clinical Proteomics, Concentration Assay

    A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

    Journal: bioRxiv

    Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

    doi: 10.64898/2026.01.13.699318

    Figure Lengend Snippet: A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

    Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

    Techniques: Fast Protein Liquid Chromatography

    Quantification of hepatic TAG and DAG (by TLC method), and cholesterol (by infinity assay kit) levels in chow-fed Dp16 male (A-C) and female mice (D-F) and their corresponding WT controls. Sample size: male WT = 10 and Dp16 = 30; female WT = 15 and Dp16 = 10.

    Journal: bioRxiv

    Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

    doi: 10.64898/2026.01.13.699318

    Figure Lengend Snippet: Quantification of hepatic TAG and DAG (by TLC method), and cholesterol (by infinity assay kit) levels in chow-fed Dp16 male (A-C) and female mice (D-F) and their corresponding WT controls. Sample size: male WT = 10 and Dp16 = 30; female WT = 15 and Dp16 = 10.

    Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

    Techniques:

    A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice on HFD. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). C-F) Exacerbated glucose intolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 compared to WT controls on HFD. Exacerbated insulin resistance as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). G-H) The rate of triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

    Journal: bioRxiv

    Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

    doi: 10.64898/2026.01.13.699318

    Figure Lengend Snippet: A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice on HFD. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). C-F) Exacerbated glucose intolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 compared to WT controls on HFD. Exacerbated insulin resistance as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). G-H) The rate of triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

    Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

    Techniques: Fast Protein Liquid Chromatography