Department of Biochemistry, CSIR - Central Food Technological Research Institute, Mysore, Karnataka, 570 020, India.
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, Uttar Pradesh, 201002, India.
Mol Nutr Food Res. 2024 Apr;68(8):e2200660. doi: 10.1002/mnfr.202200660. Epub 2024 Mar 29.
The identification of novel therapeutic agents capable of modulating lipid metabolism holds a promising potential in combating obesity and its associated complications. This study is conducted to evaluate the lipid lowering effect of dietary taurine administration on high-fat fed C57BL6 mice and to study the mechanism by which taurine impacts lipid metabolism.
C57BL6 mice are grouped into four (n = 6): i) normal diet (ND), ii) a high-fat diet (HFD), iii) HFD + orlistat (STD), iv) HFD + taurine (TAU) group for 12 weeks. The results show that taurine administration for 12 weeks reduces high fat-induced weight gain, and liver weight when compared with HFD fed mice. It also improves serum biochemical parameters like total cholesterol and triglycerides. Sirtuin 1 (SIRT1) activity, Nicotinamide adenine dinucleotide (NAD) levels, SIRT1 mRNA, and protein expression are increased in HFD + TAU diet group as compared to HFD group. Taurine treatment suppresses the expression of lipogenic genes (sterol regulatory element binding protein 1c [SREBP1c], fatty acid synthase [FAS], Peroxisome proliferator-activated receptor gamma [PPARγ]) and increases the expression of β-oxidation (peroxisome proliferator-activated receptor alpha [PPARα], liver x receptor beta [LXRβ], peroxisome proliferator-activated receptor gamma coactivator 1-alpha [PGC1α], AMP-activated protein kinase [AMPK]) and lipolytic (forkhead box protein O1 [FOXO1]) genes. Further, taurine mitigates hepatic inflammation by suppressing nuclear factor kappa B (NF-κB) gene expression and pro-inflammatory cytokine markers (IL-6, IL-1β, and TNFα).
Taurine exerts lipid lowering effects through activating SIRT1/AMPK/FOXO1 signaling pathways and regulating their downstream targets.
鉴定能够调节脂质代谢的新型治疗剂在治疗肥胖及其相关并发症方面具有很大的潜力。本研究旨在评估膳食牛磺酸对高脂肪喂养的 C57BL6 小鼠的降血脂作用,并研究牛磺酸影响脂质代谢的机制。
将 C57BL6 小鼠分为四组(n = 6):i)正常饮食(ND)组,ii)高脂肪饮食(HFD)组,iii)HFD+奥利司他(STD)组,iv)HFD+牛磺酸(TAU)组,喂养 12 周。结果显示,与 HFD 喂养的小鼠相比,牛磺酸给药 12 周可降低高脂肪诱导的体重增加和肝脏重量。它还改善了血清生化参数,如总胆固醇和甘油三酯。与 HFD 组相比,HFD+TAU 饮食组的 Sirtuin 1(SIRT1)活性、烟酰胺腺嘌呤二核苷酸(NAD)水平、SIRT1 mRNA 和蛋白表达增加。牛磺酸处理可抑制脂肪生成基因(固醇调节元件结合蛋白 1c [SREBP1c]、脂肪酸合成酶 [FAS]、过氧化物酶体增殖物激活受体 γ [PPARγ])的表达,并增加β-氧化(过氧化物酶体增殖物激活受体 α [PPARα]、肝 X 受体 β [LXRβ]、过氧化物酶体增殖物激活受体 γ 共激活因子 1-α [PGC1α]、AMP 激活的蛋白激酶 [AMPK])和脂肪分解(叉头框蛋白 O1 [FOXO1])基因的表达。此外,牛磺酸通过抑制核因子 kappa B(NF-κB)基因表达和促炎细胞因子标志物(IL-6、IL-1β和 TNFα)来减轻肝炎症。
牛磺酸通过激活 SIRT1/AMPK/FOXO1 信号通路及其下游靶点发挥降血脂作用。