Biochemical and Biophysical Research Communications
Dietary polyunsaturated fatty acids enhance hepatic AMP-activated protein kinase activity in rats
Section snippets
Materials and methods
All animal studies were approved by the Institutional Animal Care and Use Committee of the Pennington Biomedical Research Center. Male Sprague–Dawley rats (Harlan Sprague–Dawley, Indianapolis, IN; 120–130 g) were housed in a temperature- and light-controlled environment, and adapted to a 3 h per day (09:00–12:00) meal-feeding regimen using a high-glucose, fat-free diet (80% dextrose) formulated according to AIN-93-G diet (Dyets; Bethlehem, PA). After a 7-day adaptation period, the rats were
Effect of a high-glucose meal on AMPK and ACC phosphorylation, AMPK activity, and FAS and CPT-1 mRNA
Rats were trained for 7 days to consume a high-glucose, fat-free diet during a single daily meal of 3 h duration (09:00–12:00 AM). AMPK activity and phosphorylation were assayed prior to the meal (21 h fasting) and 5 h after the food was introduced. As shown in Figs. 1A and C, the ingestion of high-glucose diet decreased the phosphorylation of AMPK by 80% from its pre-meal value, whereas AMPK protein abundance was unchanged. The decrease in P-AMPK was associated with a concomitant reduction in
Discussion
The results suggest that the ingestion of PUFA causes changes in AMPK activity that could account for PUFA’s previously described effects on hepatic lipid metabolism and gene expression. Thus, the ingestion of a meal enriched in PUFA resulted in a much smaller decrease in AMPK phosphorylation and activity than did comparable glucose-rich meals or a glucose-rich meal supplemented with triolein. In addition, changes in ACC phosphorylation and FAS and CPT-1 mRNA abundance in the latter groups were
Acknowledgments
The authors thank Amanda K. Shirah and Xiaochun Xi for their technical assistance and Dr. A. Zuberi for critical reading of the manuscript. This work was supported by NIH Grants RO1 DK 053872 (T.W.G.), DK 064156 (T.W.G.), DK 19514 (N.B.R.), DK 49147 (N.B.R.), and a grant from the Juvenile Diabetes Foundation (N.B.R.).
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