Hypothalamic Neuropeptide Y (NPY) Controls Hepatic VLDL-Triglyceride Secretion in Rats via the Sympathetic Nervous System
- Eveline Bruinstroop1⇓,
- Lei Pei2,3,
- Mariëtte T. Ackermans4,
- Ewout Foppen1,2,
- Anke J. Borgers1,
- Joan Kwakkel1,
- Anneke Alkemade1,
- Eric Fliers1 and
- Andries Kalsbeek1,2
- 1Department of Endocrinology and Metabolism, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
- 2Department of Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Science, Amsterdam, the Netherlands
- 3Department of Neurobiology, Tongji Medical College of Huazhong University of Science and Technology, Hubei, China
- 4Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
- Corresponding author: Eveline Bruinstroop, .
Excessive secretion of triglyceride-rich very low-density lipoproteins (VLDL-TG) contributes to diabetic dyslipidemia. Earlier studies have indicated a possible role for the hypothalamus and autonomic nervous system in the regulation of VLDL-TG. In the current study, we investigated whether the autonomic nervous system and hypothalamic neuropeptide Y (NPY) release during fasting regulates hepatic VLDL-TG secretion. We report that, in fasted rats, an intact hypothalamic arcuate nucleus and hepatic sympathetic innervation are necessary to maintain VLDL-TG secretion. Furthermore, the hepatic sympathetic innervation is necessary to mediate the stimulatory effect of intracerebroventricular administration of NPY on VLDL-TG secretion. Since the intracerebroventricular administration of NPY increases VLDL-TG secretion by the liver without affecting lipolysis, its effect on lipid metabolism appears to be selective to the liver. Together, our findings indicate that the increased release of NPY during fasting stimulates the sympathetic nervous system to maintain VLDL-TG secretion at a postprandial level.
This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db11-1142/-/DC1.
- Received August 17, 2011.
- Accepted January 13, 2012.
- © 2012 by the American Diabetes Association.
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