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Activation of GPR81 reversed the protective effects of OA‐rich EN on the GPR81‐CTRP6‐p38 pathway and WAT browning without affecting ketogenesis and lactate metabolism in septic mice. Schematic illustration of the experimental design (A). Serum β‐OHB (B) was measured using a ketone meter. Lactate in serum (C) and WAT (D) were measured using a lactate assay kit. Western blot analysis of GPR81, CTRP6, p‐p38, and total p38 protein expression in WAT (E). Representative images of WAT (F). WAT weight (G). Representative H&E and immunohistochemical stained sections of WAT (H). Ratio of adipocytes with cross‐sectional area > 500 μm 2 in WAT (I). Western blot analysis of UCP1 protein expression in WAT (J). N = 8 per group. Data are presented as the mean ± standard error of the mean. * p < 0.05 versus the Control group. # p < 0.05 versus the LPS group. ^ p < 0.05 versus the LPS + OA‐rich EN <t>group.</t> <t>CHBA,</t> <t>3‐chloro‐5‐hydroxybenzoic</t> acid; CTRP6, C1q/tumor necrosis factor‐related protein 6; EN, enteral nutrition; GPR81, G‐protein‐coupled receptor 81; H&E, Hematoxylin–eosin; LPS, lipopolysaccharide; OA, octanoic acid; p‐p38, phosphorylated p38 mitogen‐activated protein kinase; UCP1, uncoupling protein 1; WAT, white adipose tissue; β‐OHB, β‐hydroxybutyrate.
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Activation of GPR81 reversed the protective effects of OA‐rich EN on the GPR81‐CTRP6‐p38 pathway and WAT browning without affecting ketogenesis and lactate metabolism in septic mice. Schematic illustration of the experimental design (A). Serum β‐OHB (B) was measured using a ketone meter. Lactate in serum (C) and WAT (D) were measured using a lactate assay kit. Western blot analysis of GPR81, CTRP6, p‐p38, and total p38 protein expression in WAT (E). Representative images of WAT (F). WAT weight (G). Representative H&E and immunohistochemical stained sections of WAT (H). Ratio of adipocytes with cross‐sectional area > 500 μm 2 in WAT (I). Western blot analysis of UCP1 protein expression in WAT (J). N = 8 per group. Data are presented as the mean ± standard error of the mean. * p < 0.05 versus the Control group. # p < 0.05 versus the LPS group. ^ p < 0.05 versus the LPS + OA‐rich EN group. CHBA, 3‐chloro‐5‐hydroxybenzoic acid; CTRP6, C1q/tumor necrosis factor‐related protein 6; EN, enteral nutrition; GPR81, G‐protein‐coupled receptor 81; H&E, Hematoxylin–eosin; LPS, lipopolysaccharide; OA, octanoic acid; p‐p38, phosphorylated p38 mitogen‐activated protein kinase; UCP1, uncoupling protein 1; WAT, white adipose tissue; β‐OHB, β‐hydroxybutyrate.

Journal: Food Science & Nutrition

Article Title: Octanoic Acid‐Rich Enteral Nutrition Alleviates Sepsis‐Associated Metabolic Disorders by Suppressing White Adipose Tissue Browning in Mice

doi: 10.1002/fsn3.72020

Figure Lengend Snippet: Activation of GPR81 reversed the protective effects of OA‐rich EN on the GPR81‐CTRP6‐p38 pathway and WAT browning without affecting ketogenesis and lactate metabolism in septic mice. Schematic illustration of the experimental design (A). Serum β‐OHB (B) was measured using a ketone meter. Lactate in serum (C) and WAT (D) were measured using a lactate assay kit. Western blot analysis of GPR81, CTRP6, p‐p38, and total p38 protein expression in WAT (E). Representative images of WAT (F). WAT weight (G). Representative H&E and immunohistochemical stained sections of WAT (H). Ratio of adipocytes with cross‐sectional area > 500 μm 2 in WAT (I). Western blot analysis of UCP1 protein expression in WAT (J). N = 8 per group. Data are presented as the mean ± standard error of the mean. * p < 0.05 versus the Control group. # p < 0.05 versus the LPS group. ^ p < 0.05 versus the LPS + OA‐rich EN group. CHBA, 3‐chloro‐5‐hydroxybenzoic acid; CTRP6, C1q/tumor necrosis factor‐related protein 6; EN, enteral nutrition; GPR81, G‐protein‐coupled receptor 81; H&E, Hematoxylin–eosin; LPS, lipopolysaccharide; OA, octanoic acid; p‐p38, phosphorylated p38 mitogen‐activated protein kinase; UCP1, uncoupling protein 1; WAT, white adipose tissue; β‐OHB, β‐hydroxybutyrate.

Article Snippet: 3‐chloro‐5‐hydroxybenzoic acid (CHBA, CAS number: 53984‐36‐4) was obtained from MedChemExpress (China).

Techniques: Activation Assay, Lactate Assay, Western Blot, Expressing, Immunohistochemical staining, Staining, Control

Activation of GPR81 reversed the protective effects of OA‐rich EN on systemic metabolic disorders in septic mice. Percentage change in BW (A). Twenty‐four‐hour EE curve (B) and total daily EE (C) were measured using metabolic cages. Representative H&E stained sections of EDL (D). Grip strength (E) was measured using a digital force gauge. Western blot analysis of MURF‐1 and MAFBx in EDL (F). Fasting blood glucose (G) was measured using a glucometer. Fasting serum insulin (H) was measured by ELISA. The HOMA‐IR index (I). N = 8 per group. Data are presented as the mean ± standard error of the mean. * p < 0.05 versus the Control group. # p < 0.05 versus the LPS group. ^ p < 0.05 versus the LPS + OA‐rich EN group. BW, body weight; CHBA, 3‐chloro‐5‐hydroxybenzoic acid; EDL, extensor digitorum longus; EE, energy expenditure; EN, enteral nutrition; H&E, Hematoxylin–eosin; HOMA‐IR, homeostatic model assessment for insulin resistance; LPS, lipopolysaccharide; MAFBx, muscle atrophy F‐Box; MURF‐1, muscle ring‐finger‐1; OA, octanoic acid.

Journal: Food Science & Nutrition

Article Title: Octanoic Acid‐Rich Enteral Nutrition Alleviates Sepsis‐Associated Metabolic Disorders by Suppressing White Adipose Tissue Browning in Mice

doi: 10.1002/fsn3.72020

Figure Lengend Snippet: Activation of GPR81 reversed the protective effects of OA‐rich EN on systemic metabolic disorders in septic mice. Percentage change in BW (A). Twenty‐four‐hour EE curve (B) and total daily EE (C) were measured using metabolic cages. Representative H&E stained sections of EDL (D). Grip strength (E) was measured using a digital force gauge. Western blot analysis of MURF‐1 and MAFBx in EDL (F). Fasting blood glucose (G) was measured using a glucometer. Fasting serum insulin (H) was measured by ELISA. The HOMA‐IR index (I). N = 8 per group. Data are presented as the mean ± standard error of the mean. * p < 0.05 versus the Control group. # p < 0.05 versus the LPS group. ^ p < 0.05 versus the LPS + OA‐rich EN group. BW, body weight; CHBA, 3‐chloro‐5‐hydroxybenzoic acid; EDL, extensor digitorum longus; EE, energy expenditure; EN, enteral nutrition; H&E, Hematoxylin–eosin; HOMA‐IR, homeostatic model assessment for insulin resistance; LPS, lipopolysaccharide; MAFBx, muscle atrophy F‐Box; MURF‐1, muscle ring‐finger‐1; OA, octanoic acid.

Article Snippet: 3‐chloro‐5‐hydroxybenzoic acid (CHBA, CAS number: 53984‐36‐4) was obtained from MedChemExpress (China).

Techniques: Activation Assay, Staining, Western Blot, Enzyme-linked Immunosorbent Assay, Control