Acute high-fat diet paradigms link galanin to triglycerides and their transport and metabolism in muscle

被引:73
作者
Leibowitz, SF
Dourmashkin, JT
Chang, GQ
Hill, JO
Gayles, EC
Fried, SK
Wang, J
机构
[1] Rockefeller Univ, Lab Behav Neurobiol, New York, NY 10021 USA
[2] Univ Colorado, Ctr Hlth Sci, Denver, CO 80260 USA
[3] Rutgers State Univ, New Brunswick, NJ 08901 USA
关键词
dietary fat; fat oxidation; muscle lipoprotein lipase; paraventricular nucleus;
D O I
10.1016/j.brainres.2004.02.030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To compare the effects of acute exposure to dietary fat to those of chronic exposure, Sprague-Dawley rats were given a high-fat diet (50% fat) or moderate-fat diet (25% fat) for I day, 2 h or 3 weeks. With measurements of various parameters, the high-fat diet for 21 days produced the expected changes of: (1) a significant increase in total caloric intake and dissected fat pad weights; (2) a rise in leptin and the metabolites, triglycerides (TG), non-esterified fatty acids and glucose; (3) an increase in muscle beta-hydroxyacyl-CoA dehydrogenase (HADH) and adipose lipoprotein lipase (aLPL) activity, along with a decrease in LPL activity in muscle (mLPL); and (4) elevated galanin (GAL) expression and peptide levels in the anterior region of the paraventricular nucleus (PVN), with no change in the arcuate nucleus. The acute 1-day or 2-h high-fat diet similarly increased circulating lipids, HADH activity and PVN GAL mRNA but stimulated rather than suppressed mLPL activity. These effects occurred in the absence of a change in total caloric intake, fat pad weights, and adipose-related measures, suggesting that they resulted more from the rise in dietary fat from 25% to 50% than from increased adiposity or hyperphagia. Moreover, PVN GAL mRNA in the different groups was consistently and positively correlated with the specific measures of TG levels and both HADH and mLPL activity, linking it to metabolic processes related to the transport and capacity for oxidation of TG in muscle, rather than adipose tissue. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:168 / 178
页数:11
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