Department of Biochemistry, Medical University of Gdansk, Debinki 1, 80-211, Gdansk, Poland.
Mol Cell Biochem. 2010 Dec;345(1-2):181-8. doi: 10.1007/s11010-010-0571-x. Epub 2010 Aug 19.
Successful treatment of obesity and related diseases by chronic food restriction requires the understanding of the effect of such nutritional therapy on the expression of genes which have been implicated to be involved in some diseases associated with obesity. The purpose of this study was to examine the effect of chronic food restriction and chronic food restriction/refeeding on lipogenic enzymes, especially the expression of genes encoding the stearoyl-CoA desaturase 1 (Scd1) and elongase6 (Elovl6) in rat liver and adipose tissue. We found that both chronic food restriction and chronic food restriction/refeeding caused increased expression of the Scd1 and Elovl6 genes in both the liver and adipose tissue. The increase was more pronounced in case of chronic food restriction/refeeding (several-fold increase) than that in chronic food restriction alone (two to threefold increase). Essentially, similar results were obtained when the expression of fatty acid synthase, acetyl-CoA carboxylase, ATP-citrate lyase, and malic enzyme genes was studied. Moreover, we found that chronic food restriction and short-term fasting exert opposite effects on the expression of lipogenic enzymes genes. The increased expression of the genes encoding Scd1, Elovl6, and other key lipogenic enzymes may favor fat storage after chronic food restriction/refeeding and may be part of the molecular mechanism by which food restriction/refeeding increases body weight and enhances susceptibility to insulin resistance.
慢性食物限制治疗肥胖症和相关疾病的成功需要理解这种营养疗法对涉及与肥胖相关的某些疾病的基因表达的影响。本研究的目的是研究慢性食物限制和慢性食物限制/再喂养对脂肪生成酶的影响，特别是编码硬脂酰辅酶 A 去饱和酶 1（Scd1）和延伸酶 6（Elovl6）的基因在大鼠肝脏和脂肪组织中的表达。我们发现，慢性食物限制和慢性食物限制/再喂养都会导致肝脏和脂肪组织中 Scd1 和 Elovl6 基因的表达增加。与慢性食物限制相比，慢性食物限制/再喂养引起的增加更为明显（增加几倍）（增加 2-3 倍）。本质上，当研究脂肪酸合酶、乙酰辅酶 A 羧化酶、ATP-柠檬酸裂解酶和苹果酸酶基因的表达时，也得到了类似的结果。此外，我们发现慢性食物限制和短期禁食对脂肪生成酶基因的表达有相反的影响。编码 Scd1、Elovl6 和其他关键脂肪生成酶的基因的表达增加可能有利于慢性食物限制/再喂养后的脂肪储存，并且可能是食物限制/再喂养增加体重和增强胰岛素抵抗易感性的分子机制的一部分。
