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本文引用的文献

1
Multiple environmental and genetic factors influence skeletal muscle PGC-1alpha and PGC-1beta gene expression in twins.多种环境和遗传因素影响双胞胎骨骼肌中PGC-1α和PGC-1β基因的表达。
J Clin Invest. 2004 Nov;114(10):1518-26. doi: 10.1172/JCI21889.
2
Genetic variation near the hepatocyte nuclear factor-4 alpha gene predicts susceptibility to type 2 diabetes.肝细胞核因子-4α基因附近的遗传变异可预测2型糖尿病易感性。
Diabetes. 2004 Apr;53(4):1141-9. doi: 10.2337/diabetes.53.4.1141.
3
A common polymorphism in the upstream promoter region of the hepatocyte nuclear factor-4 alpha gene on chromosome 20q is associated with type 2 diabetes and appears to contribute to the evidence for linkage in an ashkenazi jewish population.位于20号染色体上的肝细胞核因子4α基因上游启动子区域的一种常见多态性与2型糖尿病相关，并且似乎为阿什肯纳兹犹太人群体中的连锁证据提供了支持。
Diabetes. 2004 Apr;53(4):1134-40. doi: 10.2337/diabetes.53.4.1134.
4
Acquired and inherited lipodystrophies.获得性和遗传性脂肪营养不良。
N Engl J Med. 2004 Mar 18;350(12):1220-34. doi: 10.1056/NEJMra025261.
5
Genetics of diabetes.糖尿病的遗传学
Rev Endocr Metab Disord. 2004 Mar;5(1):25-36. doi: 10.1023/B:REMD.0000016122.84105.75.
6
Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.2型糖尿病患者胰岛素抵抗后代的线粒体活性受损。
N Engl J Med. 2004 Feb 12;350(7):664-71. doi: 10.1056/NEJMoa031314.
7
PPARgamma coactivator 1beta/ERR ligand 1 is an ERR protein ligand, whose expression induces a high-energy expenditure and antagonizes obesity.过氧化物酶体增殖物激活受体γ共激活因子1β/雌激素相关受体配体1是一种雌激素相关受体蛋白配体，其表达可诱导高能量消耗并对抗肥胖。
Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12378-83. doi: 10.1073/pnas.2135217100. Epub 2003 Oct 6.
8
Suppression of beta cell energy metabolism and insulin release by PGC-1alpha.PGC-1α对β细胞能量代谢和胰岛素释放的抑制作用。
Dev Cell. 2003 Jul;5(1):73-83. doi: 10.1016/s1534-5807(03)00170-9.
9
Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1.胰岛素抵抗和糖尿病患者氧化代谢相关基因的协同下调：PGC1和NRF1的潜在作用。
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8466-71. doi: 10.1073/pnas.1032913100. Epub 2003 Jun 27.
10
PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes.参与氧化磷酸化的PGC-1α反应性基因在人类糖尿病中协同下调。
Nat Genet. 2003 Jul;34(3):267-73. doi: 10.1038/ng1180.

2型糖尿病的基因与病理生理学：远不止是兰德尔循环的再次上演。

Genes and pathophysiology of type 2 diabetes: more than just the Randle cycle all over again.

作者信息

Shuldiner Alan R, McLenithan John C

机构信息

Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

出版信息

J Clin Invest. 2004 Nov;114(10):1414-7. doi: 10.1172/JCI23586.

DOI:10.1172/JCI23586
PMID:15545992
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC525752/
Abstract

The Randle cycle, which has been invoked to explain the reciprocal relationship between fatty acid oxidation and glucose oxidation, has long been implicated as a potential mechanism for hyperglycemia and type 2 diabetes mellitus (T2DM). Now genetic, functional genomic, and transgenic approaches have identified PPARgamma coactivators (PGC-1alpha and PGC-1beta) as key regulators of mitochondrial number and function. They regulate adaptive thermogenesis as well as glucose and fat oxidation in muscle and fat tissue, gluconeogenesis in liver, and even glucose-regulated insulin secretion in beta cells. PGC-1alpha and PGC-1beta mRNA levels and the mitochondrial genes they regulate are decreased in muscle of people with prediabetes and T2DM. A new report indicates that PGC-1alpha and PGC-1beta mRNA levels decrease with age in individuals with a genetic variant in PGC-1alpha, and these decreases correlate with alterations in whole-body glucose and fatty acid oxidation. These findings provide insights into how aging modifies genetic susceptibility to alterations in oxidative phosphorylation and T2DM.

摘要

兰德尔循环一直被用来解释脂肪酸氧化与葡萄糖氧化之间的相互关系，长期以来一直被认为是高血糖和2型糖尿病（T2DM）的潜在机制。现在，遗传学、功能基因组学和转基因方法已将过氧化物酶体增殖物激活受体γ共激活因子（PGC-1α和PGC-1β）确定为线粒体数量和功能的关键调节因子。它们调节适应性产热以及肌肉和脂肪组织中的葡萄糖和脂肪氧化、肝脏中的糖异生，甚至β细胞中葡萄糖调节的胰岛素分泌。糖尿病前期和T2DM患者肌肉中PGC-1α和PGC-1β的mRNA水平及其调节的线粒体基因均降低。一项新报告表明，携带PGC-1α基因变异的个体中，PGC-1α和PGC-1β的mRNA水平会随年龄增长而降低，且这些降低与全身葡萄糖和脂肪酸氧化的改变相关。这些发现为衰老如何改变氧化磷酸化改变和T2DM的遗传易感性提供了见解。