Abstract
BackgroundThe effect of pomegranate vinegar (PV) on adiposity was investigated in high-fat diet (HF)-induced obese rats.MethodsThe rats were divided into 5 groups and treated with HF with PV or acetic acid (0, 6.5 or 13% w/w) for 16 weeks. Statistical analyses were performed by the Statistical Analysis Systems package, version 9.2.ResultsCompared to control, PV supplementation increased phosphorylation of AMP-activated protein kinase (AMPK), leading to changes in mRNA expressions: increases for hormone sensitive lipase and mitochondrial uncoupling protein 2 and decreases for sterol regulatory element binding protein-1c (SREBP-1c) and peroxisome proliferator-activated receptorγ (PPARγ) in adipose tissue; increases for PPARα and carnitinepalmitoyltransferase-1a (CPT-1a) and decrease for SREBP-1c in the liver. Concomitantly, PV reduced increases of body weight (p = 0.048), fat mass (p = 0.033), hepatic triglycerides (p = 0.005), and plasma triglycerides (p = 0.001).ConclusionsThese results suggest that PV attenuates adiposity through the coordinated control of AMPK, which leads to promotion of lipolysis in adipose tissue and stimulation of fatty acid oxidation in the liver.
Highlights
The effect of pomegranate vinegar (PV) on adiposity was investigated in high-fat diet (HF)-induced obese rats
We investigated the role of AMP-activated protein kinase (AMPK) protein and its downstream effectors with a focus on the coordinated control of lipid metabolism between the liver and adipose tissue
Daily calorie intake was not different among the groups, both AH and VL supplementation significantly suppressed body weight increases induced by a high-fat diet (p = 0.048)
Summary
The effect of pomegranate vinegar (PV) on adiposity was investigated in high-fat diet (HF)-induced obese rats. AMP-activated protein kinase (AMPK) is regarded as important as it senses the cellular energy status and Dietary acetic acid is metabolized to acetyl-CoA with the production of AMP [4], which, in vitro, results in the elevation of the AMP/ATP ratio and subsequent phosphorylation of AMPK [5]. Based on these findings, previous studies found that dietary acetic acid suppressed body fat accumulation in animals by regulating genes for energy consumption and fatty acid oxidation enzymes in liver [6]. Little information is available on the coordinated control of lipid metabolism through the phosphorylation of each AMPK protein and its downstream effectors in the liver and adipose tissue
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