Temperature-Dependent Effects of Eicosapentaenoic Acid (EPA) on Browning of Subcutaneous Adipose Tissue in UCP1 Knockout Male Mice

Figures

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  Figure 1. Body weight and fat percentage, and food intake in WT and UCP1 KO mice fed an HFD or EPA-supplemented diet at ambient and thermoneutral (Thermo) conditions. (A) Percentage of body weight gain, (B) percentage of body fat and (C) food intake. Data are expressed as mean ± standard error of mean (SEM); groups represented with different letter indicate significant difference reported by three-way analysis of variance (ANOVA), p < 0.05, n = 10–12.

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  Figure 2. Effects of UCP1 deficiency and temperature on glucose homeostasis and insulin sensitivity in WT and UCP1 KO mice fed an HFD or EPA-supplemented diet. (A) GTT and area under the curve (AUC) of GTT, (B) ITT, and AUC of ITT and (C) basal fasting serum glucose and insulin levels and HOMA-IR of WT and UCP1 KO mice at ambient and thermoneutral conditions. GTT and ITT were normalized to the lean mass of the mice. Data are expressed as mean ± SEM; groups represented with different letter indicate significant difference reported by three-way ANOVA, p < 0.05, n = 10. Figures with no letters indicate no statistical (ns) differences across the groups.

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  Figure 3. Effects of UCP1 and temperature on serum hormones in WT and UCP1 KO mice fed an HFD or EPA-supplemented diet. (A) Serum levels of adiponectin, (B) leptin, and (C) resistin of mice. Data are expressed as mean ± SEM; groups represented with different letter indicate significant difference reported by three-way-ANOVA, p < 0.05, n = 8.

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  Figure 4. Effects of UCP1 and temperature on thermogenic gene expression levels in the SAT of WT and UCP1 KO mice fed an HFD or EPA-supplemented diet. The gene expression levels for (A) Ucp1, (B) Pgc1α, (C) Cidea, (D) Fgf21, and (E) Bmp8b. For (A), data were analyzed by t-test ** p < 0.01. For (B–E), box plots show the distribution of log2 gene expression level. Data were expressed as mean ± SEM and analyzed by three-way ANOVA with different letters indicating significant difference, p < 0.05, n = 6.

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  Figure 5. Effects of UCP1 and temperature on thermogenic protein expression levels in the SAT of WT and UCP1 KO mice fed an HFD or EPA-supplemented diet. (A) The protein content of UCP1, CIDEA, and FGF21 in the SAT of mice, (B–D) blots were normalized to TBP. Data are expressed as mean ± SEM; figures with no letters indicate no statistical (ns) differences analyzed by three-way ANOVA across the groups, n = 4–5.

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  Figure 6. Effects of UCP1 and temperature on thermogenic, lipid metabolic, and alternative thermogenic gene expression levels in the SAT of WT and UCP1 KO mice fed an HFD or EPA-supplemented diet. The expression levels of genes involved in (A) brown/beige fat biogenesis, (B) lipid metabolism, and (C) alternative thermogenic pathway. Box plots show the distribution of log2 gene expression levels. Groups represented with different letters indicate significant difference reported by three-way-ANOVA, p < 0.05, n = 6.

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  Figure 7. Effects of UCP1 and EPA on thermogenic genes expression and respiration capacity of SAT-derived adipocytes from WT and UCP1 KO mice. (A) The expression levels of thermogenic genes and (B) respiration capacity of differentiated adipocytes treated with vehicle control (Con) or EPA. Data were expressed as mean ± SEM and analyzed by two-way ANOVA with different letters indicating significant difference, p < 0.05, three independent studies.