Reversing diet-induced metabolic dysregulation by diet switching leads to altered hepatic de novo lipogenesis and glycerolipid synthesis
| Autor: | David P De Souza, Dedreia Tull, Brunda Nijagal, Steven Hamley, Malcolm J. McConville, Clinton R. Bruce, Ahrathy Selathurai, Greg M. Kowalski, Sean O'Callaghan, Joachim Kloehn |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
Blood Glucose
Male 0301 basic medicine medicine.medical_specialty Adipose tissue 030209 endocrinology & metabolism Carbohydrate metabolism Biology Diet High-Fat Weight Gain Article Diglycerides Mice 03 medical and health sciences 0302 clinical medicine Insulin resistance Weight loss Internal medicine Glucose Intolerance Hyperinsulinemia medicine Animals Obesity Triglycerides Diacylglycerol kinase Multidisciplinary Lipogenesis Fatty Acids medicine.disease Dietary Fats Mice Inbred C57BL 030104 developmental biology Endocrinology Liver Glycolipids medicine.symptom Energy Intake Weight gain |
| Zdroj: | Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/srep27541 |
| Popis: | In humans, low-energy diets rapidly reduce hepatic fat and improve/normalise glycemic control. Due to difficulties in obtaining human liver, little is known about changes to the lipid species and pathway fluxes that occur under these conditions. Using a combination of stable isotope and targeted metabolomic approaches we investigated the acute (7–9 days) hepatic effects of switching high-fat high-sucrose diet (HFD) fed obese mice back to a chow diet. Upon the switch, energy intake was reduced, resulting in reductions of fat mass and hepatic triacyl- and diacylglycerol. However, these parameters were still elevated compared to chow fed mice, thus representing an intermediate phenotype. Nonetheless, glucose intolerance and hyperinsulinemia were completely normalized. The diet reversal resulted in marked reductions in hepatic de novo lipogenesis when compared to the chow and HFD groups. Compared with HFD, glycerolipid synthesis was reduced in the reversal animals, however it remained elevated above that of chow controls, indicating that despite experiencing a net loss in lipid stores, the liver was still actively esterifying available fatty acids at rates higher than that in chow control mice. This effect likely promotes the re-esterification of excess free fatty acids released from the breakdown of adipose depots during the weight loss period. |
| Databáze: | OpenAIRE |
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