Tsujita Takahiro
Division of Medical Bioscience, Department of Bioscience, Integrated Center for Sciences, Ehime University, Toon, Japan.
J Nutr Sci Vitaminol (Tokyo). 2006 Feb;52(1):47-53. doi: 10.3177/jnsv.52.47.
The level of free fatty acid (FFA) in plasma is increased by diabetes. The increase in plasma FFA levels accompanied the stimulation of basal lipolysis (i.e. lipolysis in the absence of lipolytic agents) in fat cells. Injection of streptozotocin with rats resulted in a significant increase in basal FFA production (5.5 fold) in fat cells. However, basal glycerol production in fat cells was increased only 1.5 fold by streptozotocin-induced diabetes, implying that FFA re-esterification in fat cells was decreased by streptozotocin-induced diabetes. The FFA re-esterification in fat cells was also decreased by 1 d of fasting. Although basal lipolysis was increased by streptozotocin-induced diabetes or 1-d fasting, neutral triacylglycerol lipase activity and the immunoreactive HSL protein content in fat cells from streptozotocin-induced diabetic rats or 1-d fasting rats were not significantly changed. Although beta-blockers inhibited lipolysis induced by norepinephrine at a concentration of 10(-4) M, it failed to inhibit the basal lipolysis and FFA re-esterification in fat cells from streptozotocin-induced diabetic rats. Nor did insulin or H-89, another antilipolytic agent, affect basal lipolysis or FFA re-esterification in fat cells from streptozotocin-induced diabetic rats. These results indicate that basal FFA production may be induced by a decrease of re-esterification of FFA in diabetic rats and is not affected by antilipolytic agents such as insulin, beta-blockers or H-89.
糖尿病会使血浆中游离脂肪酸（FFA）水平升高。血浆FFA水平的升高伴随着脂肪细胞基础脂解作用（即在无脂解剂情况下的脂解作用）的增强。给大鼠注射链脲佐菌素会导致脂肪细胞基础FFA生成量显著增加（5.5倍）。然而，链脲佐菌素诱导的糖尿病仅使脂肪细胞基础甘油生成量增加1.5倍，这意味着链脲佐菌素诱导的糖尿病会使脂肪细胞中FFA的再酯化作用减弱。禁食1天也会使脂肪细胞中FFA的再酯化作用减弱。尽管链脲佐菌素诱导的糖尿病或禁食1天会使基础脂解作用增强，但链脲佐菌素诱导的糖尿病大鼠或禁食1天大鼠的脂肪细胞中，中性三酰甘油脂肪酶活性和免疫反应性激素敏感脂肪酶（HSL）蛋白含量并未显著改变。尽管β受体阻滞剂在浓度为10⁻⁴ M时可抑制去甲肾上腺素诱导的脂解作用，但它无法抑制链脲佐菌素诱导的糖尿病大鼠脂肪细胞中的基础脂解作用和FFA再酯化作用。胰岛素或另一种抗脂解剂H - 89也不会影响链脲佐菌素诱导的糖尿病大鼠脂肪细胞中的基础脂解作用或FFA再酯化作用。这些结果表明，基础FFA生成可能是由糖尿病大鼠中FFA再酯化作用的减弱所诱导，且不受胰岛素、β受体阻滞剂或H - 89等抗脂解剂的影响。
