Abstract
Phyllodulcin is a natural sweetener found in Hydrangea macrophylla var. thunbergii. This study investigated whether phyllodulcin could improve metabolic abnormalities in high-fat diet (HFD)-induced obese mice. Animals were fed a 60% HFD for 6 weeks to induce obesity, followed by 7 weeks of supplementation with phyllodulcin (20 or 40 mg/kg body weight (b.w.)/day). Stevioside (40 mg/kg b.w./day) was used as a positive control. Phyllodulcin supplementation reduced subcutaneous fat mass, levels of plasma lipids, triglycerides, total cholesterol, and low-density lipoprotein cholesterol and improved the levels of leptin, adiponectin, and fasting blood glucose. In subcutaneous fat tissues, supplementation with stevioside or phyllodulcin significantly decreased mRNA expression of lipogenesis-related genes, including CCAAT/enhancer-binding protein α (C/EBPα), peroxisome proliferator activated receptor γ (PPARγ), and sterol regulatory element-binding protein-1C (SREBP-1c) compared to the high-fat group. Phyllodulcin supplementation significantly increased the expression of fat browning-related genes, including PR domain containing 16 (Prdm16), uncoupling protein 1 (UCP1), and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), compared to the high-fat group. Hypothalamic brain-derived neurotrophic factor-tropomyosin receptor kinase B (BDNF-TrkB) signaling was upregulated by phyllodulcin supplementation. In conclusion, phyllodulcin is a potential sweetener that could be used to combat obesity by regulating levels of leptin, fat browning-related genes, and hypothalamic BDNF-TrkB signaling.
Highlights
The worldwide prevalence of obesity has more than doubled since 1980
Stevioside supplementation decreased food intake compared to the HF group (p < 0.001), but phyllodulcin supplementation did not have the same effect
Phyllodulcin improved the levels of fasting blood glucose (FBG) and blood lipids, including TG, TC, and Low-density lipoprotein (LDL). These results suggest that phyllodulcin supplementation may reduce subcutaneous fat, leptin levels, and metabolic abnormalities, including those related to blood glucose and lipids, by regulating the expression of both lipogenesis-related genes and browning-related genes
Summary
The worldwide prevalence of obesity has more than doubled since 1980. World Health Organization (WHO) in 2014, more than 1.9 billion adults were overweight and over 600 million were obese [1]. Obesity involves alterations in hormone production and metabolism, and it is a condition that results from an imbalance between energy intake and energy output. Intake of high-energy foods that contain large amounts of fats and sugars has dramatically increased over the past several decades [3,5]. This change in dietary habits is thought to be a key driver of the increasing prevalence of obesity
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