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Olive leaf extract attenuates obesity in high-fat diet-fed mice by modulating the expression of molecules involved in adipogenesis and thermogenesis.

Shen Y, Song SJ, Keum N, Park T - Evid Based Complement Alternat Med (2014)

Bottom Line: OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice.OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPAR γ , C/EBP α , CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice.Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1 α , and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, Brain Korea 21 PLUS Project, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea.

ABSTRACT
The present study aimed to investigate whether olive leaf extract (OLE) prevents high-fat diet (HFD)-induced obesity in mice and to explore the underlying mechanisms. Mice were randomly divided into groups that received a chow diet (CD), HFD, or 0.15% OLE-supplemented diet (OLD) for 8 weeks. OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice. OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPAR γ , C/EBP α , CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice. Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1 α , and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE. These results suggest that OLE exerts beneficial effects against obesity by regulating the expression of genes involved in adipogenesis and thermogenesis in the visceral adipose tissue of HFD-fed mice.

No MeSH data available.


Related in: MedlinePlus

Effects of OLE on genes regulating adipogenesis in the epididymal adipose tissue of HFD-fed mice. (a) Gene expression of SFRP5, WNT10b, and LRP5, (b) protein levels of β-catenin, (c) mRNA expression of genes involved in the galanin-mediated signaling pathway, (d) protein levels of p-ERK and total ERK, (e) expression of PPARγ2, C/EBPα, and their target genes. Reverse transcriptase-polymerase chain reaction (RT-PCR) data represent the relative density normalized to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Protein levels were normalized to the β-actin level. Data represent the results of three independent experiments (n = 2 or 3 per experiment); P < 0.05 indicates statistical significance. Values are the means ± SEM, n = 8 for each group.
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fig4: Effects of OLE on genes regulating adipogenesis in the epididymal adipose tissue of HFD-fed mice. (a) Gene expression of SFRP5, WNT10b, and LRP5, (b) protein levels of β-catenin, (c) mRNA expression of genes involved in the galanin-mediated signaling pathway, (d) protein levels of p-ERK and total ERK, (e) expression of PPARγ2, C/EBPα, and their target genes. Reverse transcriptase-polymerase chain reaction (RT-PCR) data represent the relative density normalized to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Protein levels were normalized to the β-actin level. Data represent the results of three independent experiments (n = 2 or 3 per experiment); P < 0.05 indicates statistical significance. Values are the means ± SEM, n = 8 for each group.

Mentions: We investigated whether OLE affected HFD-induced activation of adipogenesis in the epididymal adipose tissue of mice. In the present study, we found that OLE significantly upregulated the expression of wingless-type MMTV integration site family, member 10b (WNT10b) (79%, P < 0.05), and low-density lipoprotein receptor-related protein 5 (LRP5) (26%, P < 0.05) and downregulated the expression of secreted frizzled-related protein 5 (SFRP5) (−59%, P < 0.05) in the epididymal adipose tissue of HFD-fed mice (Figure 4(a)). Western blotting of the epididymal adipose tissue of mice revealed a significantly higher protein level of β-catenin (300%, P < 0.05) in OLD-fed mice relative to HFD-fed mice (Figure 4(b)). Furthermore, compared with HFD-fed mice, OLD-fed mice showed significantly lower expression of galanin (−65%, P < 0.05), galanin receptor 1 (GalR1) (−62%, P < 0.05), galanin receptor 2 (GalR2) (−62%, P < 0.05), PKCδ (−74%, P < 0.05), cyclin D (Cyc-D) (−68%, P < 0.05), and E2F1 (−25%, P < 0.05) in the epididymal adipose tissue of mice (Figure 4(c)). OLE supplementation resulted in decreased protein levels of phosphorylated ERK (Thr202/Tyr204) (−38%, P < 0.05) in HFD-fed mice (Figure 4(d)). The mRNA levels of C/EBPα, PPARγ, and its target genes (CD36, FAS, and leptin) were significantly downregulated in OLD-fed mice as compared with those in HFD-fed mice (Figure 4(e)).


Olive leaf extract attenuates obesity in high-fat diet-fed mice by modulating the expression of molecules involved in adipogenesis and thermogenesis.

Shen Y, Song SJ, Keum N, Park T - Evid Based Complement Alternat Med (2014)

Effects of OLE on genes regulating adipogenesis in the epididymal adipose tissue of HFD-fed mice. (a) Gene expression of SFRP5, WNT10b, and LRP5, (b) protein levels of β-catenin, (c) mRNA expression of genes involved in the galanin-mediated signaling pathway, (d) protein levels of p-ERK and total ERK, (e) expression of PPARγ2, C/EBPα, and their target genes. Reverse transcriptase-polymerase chain reaction (RT-PCR) data represent the relative density normalized to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Protein levels were normalized to the β-actin level. Data represent the results of three independent experiments (n = 2 or 3 per experiment); P < 0.05 indicates statistical significance. Values are the means ± SEM, n = 8 for each group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3927866&req=5

fig4: Effects of OLE on genes regulating adipogenesis in the epididymal adipose tissue of HFD-fed mice. (a) Gene expression of SFRP5, WNT10b, and LRP5, (b) protein levels of β-catenin, (c) mRNA expression of genes involved in the galanin-mediated signaling pathway, (d) protein levels of p-ERK and total ERK, (e) expression of PPARγ2, C/EBPα, and their target genes. Reverse transcriptase-polymerase chain reaction (RT-PCR) data represent the relative density normalized to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Protein levels were normalized to the β-actin level. Data represent the results of three independent experiments (n = 2 or 3 per experiment); P < 0.05 indicates statistical significance. Values are the means ± SEM, n = 8 for each group.
Mentions: We investigated whether OLE affected HFD-induced activation of adipogenesis in the epididymal adipose tissue of mice. In the present study, we found that OLE significantly upregulated the expression of wingless-type MMTV integration site family, member 10b (WNT10b) (79%, P < 0.05), and low-density lipoprotein receptor-related protein 5 (LRP5) (26%, P < 0.05) and downregulated the expression of secreted frizzled-related protein 5 (SFRP5) (−59%, P < 0.05) in the epididymal adipose tissue of HFD-fed mice (Figure 4(a)). Western blotting of the epididymal adipose tissue of mice revealed a significantly higher protein level of β-catenin (300%, P < 0.05) in OLD-fed mice relative to HFD-fed mice (Figure 4(b)). Furthermore, compared with HFD-fed mice, OLD-fed mice showed significantly lower expression of galanin (−65%, P < 0.05), galanin receptor 1 (GalR1) (−62%, P < 0.05), galanin receptor 2 (GalR2) (−62%, P < 0.05), PKCδ (−74%, P < 0.05), cyclin D (Cyc-D) (−68%, P < 0.05), and E2F1 (−25%, P < 0.05) in the epididymal adipose tissue of mice (Figure 4(c)). OLE supplementation resulted in decreased protein levels of phosphorylated ERK (Thr202/Tyr204) (−38%, P < 0.05) in HFD-fed mice (Figure 4(d)). The mRNA levels of C/EBPα, PPARγ, and its target genes (CD36, FAS, and leptin) were significantly downregulated in OLD-fed mice as compared with those in HFD-fed mice (Figure 4(e)).

Bottom Line: OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice.OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPAR γ , C/EBP α , CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice.Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1 α , and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, Brain Korea 21 PLUS Project, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea.

ABSTRACT
The present study aimed to investigate whether olive leaf extract (OLE) prevents high-fat diet (HFD)-induced obesity in mice and to explore the underlying mechanisms. Mice were randomly divided into groups that received a chow diet (CD), HFD, or 0.15% OLE-supplemented diet (OLD) for 8 weeks. OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice. OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPAR γ , C/EBP α , CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice. Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1 α , and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE. These results suggest that OLE exerts beneficial effects against obesity by regulating the expression of genes involved in adipogenesis and thermogenesis in the visceral adipose tissue of HFD-fed mice.

No MeSH data available.


Related in: MedlinePlus