Early skeletal muscle adaptations to short-term high-fat diet in humans before changes in insulin sensitivity
Autor: | Kevin P. Davy, Matthew W. Hulver, Angela S. Anderson, Kimberly R. Haynie, Brenda M. Davy, Madlyn I. Frisard, Ryan P. McMillan, Nabil E. Boutagy, Kristin L. Osterberg |
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Rok vydání: | 2015 |
Předmět: |
medicine.medical_specialty
Meal Nutrition and Dietetics Cholesterol business.industry Endocrinology Diabetes and Metabolism digestive oral and skin physiology Medicine (miscellaneous) Skeletal muscle Inflammation Metabolism medicine.disease Obesity chemistry.chemical_compound Endocrinology Insulin resistance Postprandial medicine.anatomical_structure chemistry Internal medicine medicine medicine.symptom business |
Zdroj: | Obesity. 23:720-724 |
ISSN: | 1930-7381 |
DOI: | 10.1002/oby.21031 |
Popis: | Objective The purpose of this investigation was to understand the metabolic adaptations to a short-term (5 days), isocaloric, high-fat diet (HFD) in healthy, young males. Methods Two studies were undertaken with 12 subjects. Study 1 investigated the effect of the HFD on skeletal muscle substrate metabolism and insulin sensitivity. Study 2 assessed the metabolic and transcriptional responses in skeletal muscle to the transition from a fasted to fed state using a high-fat meal challenge before and after 5 days of the HFD. Results Study 1 showed no effect of a HFD on skeletal muscle metabolism or insulin sensitivity in fasting samples. Study 2 showed that a HFD elicits significant increases in fasting serum endotoxin and disrupts the normal postprandial excursions of serum endotoxin, as well as metabolic and transcriptional responses in skeletal muscle. These effects after 5 days of the HFD were accompanied by an altered fasting and postprandial response in the ratio of phosphorylated- to total-p38 protein. These changes all occurred in the absence of alterations in insulin sensitivity. Conclusions Our findings provide evidence for early biological adaptations to high-fat feeding that proceed and possibly lead to insulin resistance. |
Databáze: | OpenAIRE |
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