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Articles in PresS, published online ahead of print March 5, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00017.2002
Submitted on January 15, 2002
Accepted on February 27, 2002
1 Medicine, Fukui Medical University, Fukui, Japan
2 Medicine, Stanford University, Stanford, CA, USA
3 Psychiatry, Stanford University, Stanford, CA, USA
4 Psychiatry, Stanford University, Stanford, CA, USA; MIRECC, VA Palo Alto Health Care System, Palo Alto, CA, USA
5 Medicine, Stanford University, Stanford, CA, USA; GRECC, VA Palo Alto Health Care System, Palo Alto, CA, USA
* To whom correspondence should be addressed. E-mail: jinya{at}fmsrsa.fukui-med.ac.jp.
Starvation induces many biochemical and histological changes in the heart; however, the molecular events underlying these changes have not been fully elucidated. To explore the molecular response of the heart to starvation, microarray analysis was performed together with biochemical and histological investigations. Serum free fatty acids increased 2-fold in both 16h- and 48h-fasted mice, and cardiac triglyceride content increased 3-fold and 6-fold in 16h- and 48h-fasted mice, respectively. Electron microscopy showed numerous lipid droplets in hearts of 48h-fasted mice, while fewer numbers of droplets were seen in hearts from 16h-fasted mice. Expression of 11,000 cardiac genes was screened by microarrays. More than 50 and 150 known genes were detected by differential expression analysis after 16h- and 48h-fast, respectively. Genes for fatty acid oxidation and gluconeogenesis were increased, and genes for glycolysis were decreased. Many other genes for metabolism, signaling/cell cycle, cytoskeleton, and tissue antigens were affected by fasting. These data provide a broad perspective of the molecular events occurring physiologically in the heart in response to starvation.
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