Jamal Z, Saggerson E D
Department of Biochemistry, University College London, U.K.
Biochem J. 1988 May 15;252(1):293-6. doi: 10.1042/bj2520293.
Diabetic rats were used as a source of brown-adipose-tissue mitochondria 2 days after a single subcutaneous injection of streptozotocin (100 mg/kg). Diabetes caused an 80% decrease in carnitine-dependent oxidation of palmitoyl-CoA and a 50-60% decrease in overt carnitine palmitoyltransferase activity. An additional lesion in brown-adipose-tissue mitochondrial oxidative capacity was also indicated, since diabetes increased by 30-50% the rate of oxidation under uncoupled conditions of several respiratory substrates (i.e. malate + palmitoylcarnitine, malate + pyruvate, succinate, NNN'N'-tetramethyl-p-phenylenediamine + ascorbate). This decrease in mitochondrial function was accompanied by an approx. 30% decrease in the abundance of cytochromes (a + a3) and total cytochromes b.
单次皮下注射链脲佐菌素（100 mg/kg）2天后，将糖尿病大鼠作为棕色脂肪组织线粒体的来源。糖尿病导致棕榈酰辅酶A的肉碱依赖性氧化减少80%，明显的肉碱棕榈酰转移酶活性降低50 - 60%。还表明棕色脂肪组织线粒体氧化能力存在额外损伤，因为糖尿病使几种呼吸底物在解偶联条件下（即苹果酸+棕榈酰肉碱、苹果酸+丙酮酸、琥珀酸、N，N，N'，N'-四甲基对苯二胺+抗坏血酸）的氧化速率提高了30 - 50%。线粒体功能的这种下降伴随着细胞色素（a + a3）和总细胞色素b丰度约30%的降低。
