Park Jeong-Eun, Oh Suk-Heung, Cha Youn-Soo
Department of Food Science and Human Nutrition, Chonbuk National University, Jeonju, Republic of Korea; Jeonju Makgeolli Research Center, Chonbuk National University, Jeonju, Republic of Korea.
J Sci Food Agric. 2014 Sep;94(12):2514-20. doi: 10.1002/jsfa.6588. Epub 2014 Feb 26.
Kimchi is a traditional fermented food in Korea that contains various unique microorganisms. Diverse bacteria are involved in the process of Kimchi fermentation and the healthful advantages; one of the major species is Lactobacillus. We investigated whether lactic acid bacteria isolated from Kimchi (KLAB) are capable of reducing intracellular lipid accumulation by downregulating the expression of adipogenesis and lipogenesis promoting genes in differentiating 3T3-L1 cells.
KLAB (Lactobacillus brevis OPK-3) mediated dose-dependent inhibition of adipocyte differentiation, intracellular triglyceride accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity. The expression of transcription factors such as peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α involved in adipogenesis was markedly decreased by the KLAB treatment. Terminal adipogenic marker, e.g. adipocyte fatty acid binding protein (aP2), lipoprotein lipase, liver X receptor α, leptin and GPDH were significantly downregulated by KLAB treatment compared to untreated control. Moreover, cytokine genes, such as tumor necrosis factor-α and interleukin-6 mRNA expressions level were also decreased, whereas adiponectin mRNA level was upregulated by KLAB.
These results suggest that the KLAB inhibits lipid accumulation in the differentiating adipocyte through downregulating the expression of adipogenic transcription factors and other specific genes involved in lipid metabolism.
泡菜是韩国的一种传统发酵食品,含有多种独特的微生物。多种细菌参与泡菜发酵过程及其健康益处;其中主要的一种是乳酸菌。我们研究了从泡菜中分离出的乳酸菌(KLAB)是否能够通过下调分化的3T3-L1细胞中脂肪生成和脂肪生成促进基因的表达来减少细胞内脂质积累。
KLAB(短乳杆菌OPK-3)介导了对脂肪细胞分化、细胞内甘油三酯积累和甘油-3-磷酸脱氢酶(GPDH)活性的剂量依赖性抑制。KLAB处理显著降低了参与脂肪生成的转录因子如过氧化物酶体增殖物激活受体γ和CCAAT/增强子结合蛋白α的表达。与未处理的对照相比,KLAB处理显著下调了终末脂肪生成标志物,如脂肪细胞脂肪酸结合蛋白(aP2)、脂蛋白脂肪酶、肝脏X受体α、瘦素和GPDH。此外,KLAB还降低了细胞因子基因如肿瘤坏死因子-α和白细胞介素-6的mRNA表达水平,而上调了脂联素的mRNA水平。
这些结果表明,KLAB通过下调脂肪生成转录因子和其他参与脂质代谢的特定基因的表达来抑制分化中的脂肪细胞中的脂质积累。