Abstract
Background & AimsDietary saturated fatty acids contribute to the development of fatty liver and have pathogenic link to systemic inflammation. We investigated the effects of dietary fat towards the pathogenesis of non-alcoholic fatty liver disease by longitudinal in vivo magnetic resonance spectroscopy (MRS) and in vitro liquid chromatography coupled with mass spectrometry (LC-MS).MethodsAll measurements were performed on rats fed with high fat diet (HFD) and chow diet for twenty four weeks. Longitudinal MRS measurements were performed at the 12th, 18th and 24th weeks. Liver tissues were analyzed by LC-MS, histology and gene transcription studies after terminal in vivo experiments.ResultsLiver fat content of HFD rats for all ages was significantly (P<0.05) higher compared to their respective chow diet fed rats. Unsaturation indices estimated from MRS and LC-MS data of chow diet fed rats were significantly higher (P<0.05) than HFD fed rats. The concentration of triglycerides 48∶1, 48∶2, 50∶1, 50∶2, 50∶3, 52∶1, 52∶2, 52∶3, 54∶3 and 54∶2 was significantly higher (P<0.05) in HFD rats. The concentration for some polyunsaturated triglycerides 54∶7, 56∶8, 56∶7, 58∶11, 58∶10, 58∶9, 58∶8 and 60∶10 was significantly higher (P<0.05) in chow diet fed rats compared to HFD rats. Lysophospholipid concentrations including LPC and LPE were higher in HFD rats at 24 weeks indicating the increased risk of diabetes. The expression of CD36, PPARα, SCD1, SREBF1 and UCP2 were significantly upregulated in HFD rats.ConclusionsWe demonstrated the early changes in saturated and unsaturated lipid composition in fatty liver by in vivo MRS and ex vivo LC-MS. The higher LPC concentration in HFD rats indicated a higher risk of developing diabetes. Early metabolic perturbations causing changes in lipid composition can be evaluated by the unsaturation index and correlated to the non alcoholic fatty liver disease.
Highlights
Non alcoholic fatty liver disease (NAFLD) results from an imbalance between lipid availability and lipid disposal
The accumulated lipids induce oxidative stress, resulting in production of cytokines and reactive oxygen species which in turn activate apoptosis thereby initiating a sequence of disease events from steatosis to nonalcoholic steatohepatitis (NASH), which progress into fibrosis and cirrhosis [1,2,3,4,5]
Plasma glucose and insulin concentrations calculated by the area under the curve from 0–120 mins were significantly (P,0.001) higher in high fat diet (HFD) fed rats compared to chow diet fed rats
Summary
Non alcoholic fatty liver disease (NAFLD) results from an imbalance between lipid availability (from circulating lipid uptake or de novo lipogenesis) and lipid disposal (via fatty acid oxidation or triglyceride-rich lipoprotein secretion). Hepatic steatosis causes insulin resistance which may act as pathogenic link between obesity and its metabolic complications [6,7]. Many patients suffering from metabolic syndrome involving obesity, dyslipidemia, hypertension, insulin-resistant type-2 diabetes mellitus and atherosclerotic cardiovascular disease are associated with NAFLD [1,2,3,4,5]. Saturated fatty acids are poorly oxidized compared to unsaturated fat and are more likely to accumulate in insulin resistant tissues [13]. We investigated the effects of dietary fat towards the pathogenesis of non-alcoholic fatty liver disease by longitudinal in vivo magnetic resonance spectroscopy (MRS) and in vitro liquid chromatography coupled with mass spectrometry (LC-MS)
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