Olive leaf extract attenuates obesity in high-fat diet-fed mice by modulating the expression of molecules involved in adipogenesis and thermogenesis
Ying Shen1, Su Jin Song1, Narae Keum1
1Department 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.
Insights
Olive leaf extract (OLE) combats high-fat diet (HFD)-induced obesity by reducing weight gain and fat accumulation. It achieves this by regulating genes involved in fat production and energy expenditure in mice.
Area of Science:
- Nutritional Science
- Metabolic Research
- Obesity Studies
Background:
- High-fat diets (HFD) are a primary driver of obesity.
- Understanding molecular mechanisms behind diet-induced obesity is crucial.
- Natural compounds offer potential therapeutic strategies for obesity management.
Purpose of the Study:
- To determine if olive leaf extract (OLE) can prevent obesity induced by a high-fat diet (HFD) in mice.
- To elucidate the molecular mechanisms by which OLE may exert anti-obesity effects.
- To investigate OLE's impact on adipogenesis and thermogenesis pathways.
Main Methods:
- Mice were fed a standard chow diet (CD), HFD, or HFD supplemented with 0.15% OLE (OLD) for 8 weeks.
- Body weight, visceral fat-pad weights, and plasma lipid levels were measured.
- Gene expression analysis of adipogenic and thermogenic markers in epididymal adipose tissue was performed.
Main Results:
- OLE supplementation significantly reduced body weight gain and visceral fat-pad weights compared to HFD alone.
- OLE reversed the HFD-induced changes in signaling molecules and key adipogenic genes (e.g., PPARγ, C/EBPα, leptin).
- OLE normalized the expression of thermogenic and mitochondrial biogenesis genes (e.g., SIRT1, PGC1α, UCP1, TFAM) downregulated by HFD.
Conclusions:
- Olive leaf extract demonstrates efficacy in preventing HFD-induced obesity in mice.
- OLE acts by modulating gene expression related to adipogenesis and thermogenesis in visceral adipose tissue.
- These findings highlight OLE as a potential dietary intervention for obesity management.
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