Tong J, Zhu M J, Underwood K R, Hess B W, Ford S P, Du M
Department of Animal Science and Interdepartmental Molecular and Cellular Life Sciences Program, University of Wyoming, Laramie 82071, USA.
J Anim Sci. 2008 Jun;86(6):1296-305. doi: 10.2527/jas.2007-0794. Epub 2008 Mar 14.
Marbling, or i.m. fat, is an important factor determining beef quality. Both adipogenesis and hypertrophy of existing adipocytes contribute to enhanced marbling. We hypothesized that the fetal stage is important for the formation of i.m. adipocytes and that AMP-activated protein kinase (AMPK) has a key role in adipogenesis during this stage. The objective of this study was to assess the role of AMPK in adipogenesis in fetal sheep muscle and 3T3-L1 cells. Nonpregnant ewes were randomly assigned to a control (Con, 100% of NRC recommendations, n = 7) or overfed (OF, 150% of NRC, n = 7) diet from 60 d before to 75 d after conception, when the ewes were killed. The fetal LM was collected at necropsy for biochemical analyses. The activity of AMPK was less in the fetal muscle of OF sheep. The expression of peroxisome proliferator-activated receptor (PPAR)gamma, a marker of adipogenesis, was greater in OF fetal muscle compared with Con fetal muscle. To further show the role of AMPK in adipogenesis, we used 3T3-L1 cells. The 3T3-L1 cells were incubated in a standard adipogenic medium for 24 h and 10 d. Activation of AMPK by 5-aminoimidazole-4-car-boxamide-1-beta-d-ribonucleoside dramatically inhibited the expression of PPARgamma and reduced the presence of adipocytes after 10 d of differentiation. Inhibition of AMPK by compound C enhanced the expression of PPARgamma. In conclusion, these data show that AMPK activity is inversely related to adipogenesis in fetal sheep muscle and 3T3-L1 cells.
大理石花纹，即肌内脂肪，是决定牛肉品质的一个重要因素。现存脂肪细胞的脂肪生成和肥大都有助于增加大理石花纹。我们推测胎儿期对肌内脂肪细胞的形成很重要，并且AMP激活的蛋白激酶（AMPK）在这个阶段的脂肪生成中起关键作用。本研究的目的是评估AMPK在胎羊肌肉和3T3-L1细胞脂肪生成中的作用。未怀孕的母羊在受孕前60天至受孕后75天被随机分配到对照组（Con，100%的NRC推荐量，n = 7）或过量饲喂组（OF，150%的NRC，n = 7），之后将母羊处死。在尸检时收集胎儿的腰大肌进行生化分析。OF组绵羊胎儿肌肉中AMPK的活性较低。过氧化物酶体增殖物激活受体（PPAR）γ是脂肪生成的标志物，其在OF组胎儿肌肉中的表达高于Con组胎儿肌肉。为了进一步证明AMPK在脂肪生成中的作用，我们使用了3T3-L1细胞。将3T3-L（此处原文有误，应为3T3-L1）细胞在标准成脂培养基中培养24小时和培养10天。用5-氨基咪唑-4-甲酰胺-1-β-D-核糖核苷激活AMPK可显著抑制PPARγ的表达，并在分化10天后减少脂肪细胞的数量。用化合物C抑制AMPK可增强PPARγ的表达。总之，这些数据表明AMPK活性与胎羊肌肉和3T3-L1细胞中的脂肪生成呈负相关。
