Abstract
High-fat diet (HFD) consumption can lead to Non-Alcoholic Fatty Liver Disease (NAFLD), which is characterized by hepatic triglycerides accumulation and is directly associated with the prevalence of obesity in worldwide. Insulin resistance underlies the genesis of both obesity and NAFLD. These mecanisms can be regulated by microRNAs, such as miR-122 and Let-7 in the liver. Therefore, the aim of the present study was to investigate a possible connection between insulin resistance, obesity, NAFLD development and alterations in miR-122 and Let-7 expression in mice fed a HFD.
Highlights
Insulin resistance underlies the genesis of obesity and Non-Alcoholic Fatty Liver Disease (NAFLD)
It was observed that lipid accumulation appears on the first day of high-fat diet (HFD) (HF1), even after glycogen reduction in this tissue that occurred in HF3
We showed here that HFD consumption could alter miRNA expression pattern that may drive alterations in whole body homeostasis and disrupt metabolic syndrome phenotype since the first day of exposure
Summary
Insulin resistance underlies the genesis of obesity and NAFLD. Studies have shown that high-fat diet (HFD) consumption can lead to these conditions, and as the mechanism has not been fully elucidated microRNAs expression has been linked as possible regulators of those events. Let-7 is an important hepatic miR and recent studies have been showing that it is involved with glucose homeostasis and insulin sensitivity.
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