Abstract | BACKGROUND: METHODS: The purpose of this study was to determine if chronic activation of AMPK prevented an increase in GPAT1 activity in rats fed a high fat diet. Rats were fed a control (C), or a high fat (HF) diet (60% fat) for 6 weeks and injected with saline or a daily aminoimidazole carboxamide ribnucleotide ( AICAR) dose of 0.5 mg/g body weight. RESULTS: Chronic AMPK activation by AICAR injections resulted in a significant reduction in hepatic triglyceride accumulation in both the C and HF fed animals (C, 5.5±0.7; C+AICAR, 2.7 ±0.3; HF, 21.8±3.3; and HF+AICAR, 8.0±1.8 mg/g liver). HF feeding caused an increase in total GPAT and GPAT1 activity, which was not affected by chronic AMPK activation (GPAT1 activity vs. C, C+AICAR, 92±19%; HF, 186±43%; HF+AICAR, 234±62%). Markers of oxidative capacity, including citrate synthase activity and cytochrome c abundance, were not affected by chronic AICAR treatment. Interestingly, HF feeding caused a significant increase in long chain acyl-CoA dehydrogenase or LCAD (up 66% from C), a marker of fatty acid oxidation capacity. CONCLUSIONS: These results suggest that chronic AMPK activation limits hepatic triglyceride accumulation independent of a reduction in total GPAT1 activity.
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Authors | Bradley S Henriksen, Mary E Curtis, Natasha Fillmore, Brandon R Cardon, David M Thomson, Chad R Hancock |
Journal | Diabetology & metabolic syndrome
(Diabetol Metab Syndr)
Vol. 5
Pg. 29
( 2013)
ISSN: 1758-5996 [Print] England |
PMID | 23725555
(Publication Type: Journal Article)
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