A high-fat diet decreases AMPK activity in multiple tissues in the absence of hyperglycemia or systemic inflammation in rats

Consumption of a high-fat diet (HFD) in experimental animal models initiates a series of molecular events and outcomes, including insulin resistance and obesity, that mimic the metabolic syndrome in humans. The relationship among, and order of, the molecular events linking a diet high in fat to path...

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Bibliographic Details
Published in:Journal of physiology and biochemistry 2013-06, Vol.69 (2), p.165-175
Main Authors: Lindholm, Christopher R., Ertel, Rebecca L., Bauwens, Jake D., Schmuck, Eric G., Mulligan, Jacob D., Saupe, Kurt W.
Format: Article
Language:English
Subjects:
Adipose Tissue, Brown - metabolism
Adipose Tissue, White - metabolism
AMP-Activated Protein Kinases - metabolism
Animal Physiology
Animals
Biomedical and Life Sciences
Biomedicine
Diet, High-Fat
Dietary Fats
Human Physiology
Hyperglycemia - metabolism
Inflammation - metabolism
Inflammation - pathology
Male
Obesity - metabolism
Obesity - pathology
Organ Specificity
Original Paper
Rats
Rats, Sprague-Dawley
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Summary:Consumption of a high-fat diet (HFD) in experimental animal models initiates a series of molecular events and outcomes, including insulin resistance and obesity, that mimic the metabolic syndrome in humans. The relationship among, and order of, the molecular events linking a diet high in fat to pathologies is often unclear. In the present study, we provide several novel insights into the relationship between a HFD and AMP-activated protein kinase (AMPK), a key regulator of cellular metabolism and whole-body energy balance. HFD substantially decreased the activities of both isoforms of AMPK in white adipose tissue, heart, and liver. These decreases in AMPK activity occurred in the absence of decreased AMPK transcription, systemic inflammation, hyperglycemia, or elevated levels of free fatty acids. The HFD-induced decrease in AMPK activity was associated with systemic insulin resistance and hyperleptinemia. In blood, >98 % of AMPK activity was localized in agranulocytes as the α1 isoform. In contrast to the solid tissues studied, AMPK activities were not altered by HFD in granulocytes or agranulocytes. We conclude that HFD-induced obesity causes a broad, non-tissue, or isoform-specific lowering of AMPK activity. Given the central position AMPK plays in whole-body energy balance, this decreased AMPK activity may play a previously unrecognized role in obesity and its associated pathologies.
ISSN:1138-7548
1877-8755
DOI:10.1007/s13105-012-0199-2