期刊
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 18, 期 1, 页码 1-9出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2006.03.013
关键词
fructose; liver; obesity; diabetes; stress-activated protein kinases
资金
- NIDDK NIH HHS [DK47416] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK047416, R29DK047416] Funding Source: NIH RePORTER
Organisms reprogram metabolic pathways to adapt to changes in nutrient availability. This requires that nutrient-based stimuli are sensed, signals are transmitted, and highly specific responses are engaged. We propose that in the liver, the mitogen-activated protein kinase, c-jun N-terminal kinase (JNK), links excessive nutrient metabolism with impaired insulin regulation of glucose production. The liver, by virtue of its anatomic position and selective regulatory features, buffers and is highly responsive to changes in nutrient delivery. In particular, sugars such as sucrose and fructose uniquely regulate and are selectively metabolized by the liver. We propose that when hepatic fructose uptake exceeds requirements for glycogen and energy (hepatic sugar excess), the JNK-signaling pathway is engaged as part of the adaptive response. (c) 2007 Elsevier Inc. All rights reserved.
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