期刊
NATURE
卷 576, 期 7785, 页码 51-60出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41586-019-1797-8
关键词
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资金
- German Federal Ministry of Health
- Ministry of Culture and Science of the state North Rhine-Westphalia
- German Federal Ministry of Education and Research
- European Funds for Regional Development [EFRE-0400191]
- EUREKA Eurostars-2 [E! 113230 DIA-PEP]
- German Science Foundation [CRC/SFB 1116/2 B12]
- US Public Health Service [R01 DK-113984, R01 DK114793, R01 DK116774, R01 DK119968, P30 DK-045735]
Obesity and type 2 diabetes are the most frequent metabolic disorders, but their causes remain largely unclear. Insulin resistance, the common underlying abnormality, results from imbalance between energy intake and expenditure favouring nutrient-storage pathways, which evolved to maximize energy utilization and preserve adequate substrate supply to the brain. Initially, dysfunction of white adipose tissue and circulating metabolites modulate tissue communication and insulin signalling. However, when the energy imbalance is chronic, mechanisms such as inflammatory pathways accelerate these abnormalities. Here we summarize recent studies providing insights into insulin resistance and increased hepatic gluconeogenesis associated with obesity and type 2 diabetes, focusing on data from humans and relevant animal models.
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