Expression of mRNAs encoding uncoupling proteins in human skeletal muscle - Effects of obesity and diabetes
Expression of mRNAs encoding uncoupling proteins in human skeletal muscle - Effects of obesity and diabetes
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DOI：
10.2337/diabetes.47.12.1935
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发表时间：
1998-12-01
期刊：
影响因子：
7.7
通讯作者：
Garvey, WT
中科院分区：
文献类型：
--
作者：
Bao, S;Kennedy, A;Garvey, WT
为了探索解偶联蛋白 (UCP) 家族在人类肥胖和糖尿病中的潜在作用，我们使用逆转录聚合酶链式反应来量化人类骨骼肌中 UCP mRNA 的表达。 UCP2 以及 UCP3 的短 (UCP3S) 和长 (UCP3L) 形式的 mRNA 水平在个体中高度相关，表明这些 UCP 的基因转录可能受到共同机制的协调调节。在正常耐糖个体中，肌肉 UCP2 mRNA 水平仅与体脂百分比和 BMI 呈正相关（两者的 r = 0.6 且 P < 0.05）。 UCP3S mRNA 水平还与体脂百分比呈正相关（r = 0.52，P < 0.05），而 UCP3L mRNA 则随着肥胖程度的增加而增加（0.05 < P < 0.1）。然而，UCP mRNA 水平与静息代谢率不相关。 2 型糖尿病中 UCP3S 和 UCP3L mRNA 水平（P < 0.05）和 UCP2 mRNA 水平（P = 0.09）增加了 1.8 至 2.7 倍，这种效应无法用肥胖来解释。胰岛素敏感型和胰岛素抵抗型非糖尿病亚组之间的 UCP2、UCP3S 或 UCP3L mRNA 水平没有发现显着差异。我们的结论是：1）编码 UCP2 和 UCP3 的骨骼肌 mRNA 水平在个体之间相关，并且可能受到协调调节； 2) UCP3表达不受UCP3L和UCP3S形式mRNA的差异影响的调节； 3) UCP mRNA 表达在肌肉中随着肥胖而增加，但与静息代谢率或胰岛素抵抗无关，并且在 2 型糖尿病患者中增加。
To explore the potential role of the uncoupling protein (UCP) family in human obesity and diabetes, we have used the reverse transcription-polymerase chain reaction to quantify UCP mRNA expression in human skeletal muscle. Levels of mRNA for UCP2, and for both short (UCP3S) and long (UCP3L) forms of UCP3, were highly correlated in individuals, indicating that gene transcription of these UCPs may be coordinately regulated by common mechanisms. In normal glucose-tolerant individuals, muscle UCP2 mRNA levels mere positively correlated with percentage of body fat and with BMI (r = 0.6 and P < 0.05 for both). UCP3S mRNA levels were also positively correlated with percentage of body fat (r = 0.52, P < 0.05), and UCP3L mRNA tended to increase as a function of obesity (0.05 < P < 0.1). UCP mRNA levels, however were not correlated with resting metabolic rate. UCP3S and UCP3L mRNA levels (P < 0.05) and the UCP2 mRNA level (P = 0.09) were increased by 1.8- to 2.7-fold in type 2 diabetes, an effect that could not be explained by obesity. No significant difference was found for UCP2, UCP3S, or UCP3L mRNA levels between insulin-sensitive and insulin-resistant nondiabetic subgroups. We conclude that 1) skeletal muscle mRNA levels encoding UCP2 and UCP3 are correlated among individuals and may be coordinately regulated; 2) UCP3 expression is not regulated by differential effects on UCP3L and UCP3S forms of the mRNA; and 3) UCP mRNA expression tends to increase in muscle as a function of obesity but not of resting metabolic rate or insulin resistance, and is increased in patients with type 2 diabetes.