Boone-Villa Daniel, Aguilera-Méndez Asdrubal, Miranda-Cervantes Adriana, Fernandez-Mejia Cristina
Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México , Instituto Nacional de Pediatría, Mexico City, Mexico .
J Med Food. 2015 Oct;18(10):1150-6. doi: 10.1089/jmf.2014.0170. Epub 2015 Apr 2.
Several studies have shown that pharmacological concentrations of biotin decrease hyperlipidemia. The molecular mechanisms by which pharmacological concentrations of biotin modify lipid metabolism are largely unknown. Adipose tissue plays a central role in lipid homeostasis. In the present study, we analyzed the effects of biotin supplementation in adipose tissue on signaling pathways and critical proteins that regulate lipid metabolism, as well as on lipolysis. In addition, we assessed serum fatty acid concentrations. Male BALB/cAnN Hsd mice were fed a control or a biotin-supplemented diet (control: 1.76 mg biotin/kg; supplemented: 97.7 mg biotin/kg diet) over 8 weeks postweaning. Compared with the control group, biotin-supplemented mice showed an increase in the levels of adipose guanosine 3',5'-cyclic monophosphate (cGMP) (control: 30.3±3.27 pmol/g wet tissue; supplemented: 49.5±3.44 pmol/g wet tissue) and of phosphorylated forms of adenosine 5'-monophosphate-activated protein kinase (AMPK; 65.2%±1.06%), acetyl-coenzyme A (CoA), carboxylase-1 (196%±68%), and acetyl-CoA carboxylase-2 (78.1%±18%). Serum fatty acid concentrations were decreased (control: 1.12±0.04 mM; supplemented: 0.91±0.03 mM), and no change in lipolysis was found (control: 0.29±0.05 μmol/mL; supplemented: 0.33±0.08 μmol/mL). In conclusion, 8 weeks of dietary biotin supplementation increased adipose tissue cGMP content and protein expression of the active form of AMPK and of the inactive forms of acetyl-CoA carboxylase-1 and acetyl-CoA carboxylase-2. Serum fatty acid levels fell, and no change in lipolysis was observed. These findings provide insight into the effects of biotin supplementation on adipose tissue and support its use in the treatment of dyslipidemia.
多项研究表明，药理浓度的生物素可降低高脂血症。药理浓度的生物素改变脂质代谢的分子机制在很大程度上尚不清楚。脂肪组织在脂质稳态中起核心作用。在本研究中，我们分析了在脂肪组织中补充生物素对调节脂质代谢的信号通路和关键蛋白以及对脂肪分解的影响。此外，我们评估了血清脂肪酸浓度。在断奶后的8周内，给雄性BALB/cAnN Hsd小鼠喂食对照饮食或补充生物素的饮食（对照：1.76毫克生物素/千克；补充：97.7毫克生物素/千克饮食）。与对照组相比，补充生物素的小鼠脂肪组织中环磷酸鸟苷（cGMP）水平升高（对照：30.3±3.27皮摩尔/克湿组织；补充：49.5±3.44皮摩尔/克湿组织），腺苷5'-单磷酸激活蛋白激酶（AMPK）的磷酸化形式（65.2%±1.06%）、乙酰辅酶A（CoA）羧化酶-1（196%±68%）和乙酰辅酶A羧化酶-2（78.1%±18%）也升高。血清脂肪酸浓度降低（对照：1.12±0.04毫摩尔/升；补充：0.91±0.03毫摩尔/升），且未发现脂肪分解有变化（对照：0.29±0.05微摩尔/毫升；补充：0.33±0.08微摩尔/毫升）。总之，8周的饮食生物素补充增加了脂肪组织cGMP含量以及AMPK活性形式和乙酰辅酶A羧化酶-1及乙酰辅酶A羧化酶-2非活性形式的蛋白表达。血清脂肪酸水平下降，且未观察到脂肪分解有变化。这些发现为补充生物素对脂肪组织的影响提供了见解，并支持其在治疗血脂异常中的应用。
