Szkudelski Tomasz, Szkudelska Katarzyna
a Department of Animal Physiology and Biochemistry , Poznan University of Life Sciences , Poznan , Poland.
Arch Physiol Biochem. 2017 Feb;123(1):43-49. doi: 10.1080/13813455.2016.1227853. Epub 2016 Sep 22.
Adipose tissue plays a key role in energy homeostasis. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an important intracellular energy sensor. Effects of activation of AMPK by aminomidazole-4-carboxamide ribonucleotide (AICAR) on lipolysis in the rat adipocytes were determined in the presence of 3 or 12 mM glucose. Response to epinephrine or dibutyryl-cAMP was higher in the presence of 12 mM glucose. AICAR decreased lipolysis, also when glucose was replaced by alanine or succinate and without decrease in cAMP levels. AICAR attenuated epinephrine-induced decrease in adenosine triphosphate (ATP) levels, reduced glucose uptake and lactate release. These results indicate that short-term activation of AMPK by AICAR in the rat adipocytes inhibits lipolysis, due to changes in the final, followed by protein kinase A (PKA), steps of the lipolytic cascade and improves intracellular energy status. Similar effects of AICAR were observed in the presence of 3 and 12 mM glucose, which indicates that the AMPK system is operative at high glucose concentrations.
脂肪组织在能量平衡中起关键作用。单磷酸腺苷（AMP）激活的蛋白激酶（AMPK）是一种重要的细胞内能量传感器。在3或12 mM葡萄糖存在的情况下，测定了氨基咪唑-4-甲酰胺核糖核苷酸（AICAR）激活AMPK对大鼠脂肪细胞脂解的影响。在12 mM葡萄糖存在时，对肾上腺素或二丁酰环磷腺苷（dibutyryl-cAMP）的反应更高。当葡萄糖被丙氨酸或琥珀酸替代且环磷腺苷水平未降低时，AICAR也会减少脂解。AICAR减弱了肾上腺素诱导的三磷酸腺苷（ATP）水平降低，减少了葡萄糖摄取和乳酸释放。这些结果表明，AICAR在大鼠脂肪细胞中短期激活AMPK会抑制脂解，这是由于脂解级联反应的最终步骤（随后是蛋白激酶A（PKA））发生了变化，并改善了细胞内能量状态。在3和12 mM葡萄糖存在的情况下观察到了AICAR的类似作用，这表明AMPK系统在高葡萄糖浓度下也起作用。
