Jin Heegu, Oh Hyun-Ji, Nah Seung-Yeol, Lee Boo-Yong
Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Gyeonggi, Republic of Korea.
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.
J Ginseng Res. 2022 May;46(3):454-463. doi: 10.1016/j.jgr.2021.10.003. Epub 2021 Oct 13.
Gintonin-enriched fraction (GEF), a non-saponin fraction of ginseng, is a novel glycolipoprotein rich in hydrophobic amino acids. GEF has recently been shown to regulate lipid metabolism and browning in adipocytes; however, the mechanisms underlying its effects on energy metabolism and whether it affects sarcopenic obesity are unclear. We aimed to evaluate the effects of GEF on skeletal muscle atrophy in high-fat diet (HFD)-induced obese mice.
To examine the effect of GEF on sarcopenic obesity, 4-week-old male ICR mice were used. The mice were divided into four groups: chow diet (CD), HFD, HFD supplemented with 50 mg/kg/day GEF, or 150 mg/kg/day GEF for 6 weeks. We analyzed body mass gain and grip strength, histological staining, western blot analysis, and immunofluorescence to quantify changes in sarcopenic obesity-related factors.
GEF inhibited body mass gain while HFD-fed mice gained 22.7 ± 2.0 g, whereas GEF-treated mice gained 14.3 ± 1.2 g for GEF50 and 11.8 ± 1.6 g for GEF150 by downregulating adipogenesis and inducing lipolysis and browning in white adipose tissue (WAT). GEF also enhanced mitochondrial biogenesis threefold in skeletal muscle. Furthermore, GEF-treated skeletal muscle exhibited decreased expression of muscle-specific atrophic genes, and promoted myogenic differentiation and increased muscle mass and strength in a dose-dependent manner ( < 0.05).
These findings indicate that GEF may have potential uses in preventing sarcopenic obesity by promoting energy expenditure and attenuating skeletal muscle atrophy.
人参富含ginsenoside的组分（GEF）是一种人参的非皂苷组分，是一种富含疏水氨基酸的新型糖脂蛋白。最近研究表明，GEF可调节脂肪细胞中的脂质代谢和褐变；然而，其对能量代谢的影响机制以及是否影响肌肉减少性肥胖尚不清楚。我们旨在评估GEF对高脂饮食（HFD）诱导的肥胖小鼠骨骼肌萎缩的影响。
为了研究GEF对肌肉减少性肥胖的影响，使用4周龄雄性ICR小鼠。将小鼠分为四组：正常饮食（CD）组、HFD组、补充50mg/kg/天GEF的HFD组或补充150mg/kg/天GEF的HFD组，持续6周。我们分析了体重增加和握力、组织学染色、蛋白质免疫印迹分析和免疫荧光，以量化肌肉减少性肥胖相关因素的变化。
GEF抑制体重增加，HFD喂养的小鼠体重增加22.7±2.0g，而GEF处理的小鼠中，GEF50组体重增加14.3±1.2g，GEF150组体重增加11.8±1.6g，这是通过下调白色脂肪组织（WAT）中的脂肪生成并诱导脂肪分解和褐变实现的。GEF还使骨骼肌中的线粒体生物发生增加了三倍。此外，GEF处理的骨骼肌中肌肉特异性萎缩基因的表达降低，并以剂量依赖性方式促进肌源性分化，增加肌肉质量和力量（P<0.05）。
这些发现表明，GEF可能通过促进能量消耗和减轻骨骼肌萎缩来预防肌肉减少性肥胖。
