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Liver protein profiles in insulin receptor-knockout mice reveal novel molecules involved in the diabetes pathophysiology. | LitMetric

AI Article Synopsis

  • The liver plays a key role in managing glucose levels and lipid balance, regulated by hormones, nutrients, and nerve signals, particularly through insulin's influence on various metabolic processes.
  • Research utilizing insulin receptor-knockout and heterozygous mouse models aimed to understand metabolic liver disease associated with diabetes by examining liver protein patterns through advanced proteomic techniques.
  • Findings revealed significant changes in protein expression related to insulin resistance and liver health, highlighting new potential biomarkers that could help predict diabetes risk and complications.

Article Abstract

Liver has a principal role in glucose regulation and lipids homeostasis. It is under a complex control by substrates such as hormones, nutrients, and neuronal impulses. Insulin promotes glycogen synthesis, lipogenesis, and lipoprotein synthesis and inhibits gluconeogenesis, glycogenolysis, and VLDL secretion by modifying the expression and enzymatic activity of specific molecules. To understand the pathophysiological mechanisms leading to metabolic liver disease, we analyzed liver protein patterns expressed in a mouse model of diabetes by proteomic approaches. We used insulin receptor-knockout (IR(-/-)) and heterozygous (IR(+/-)) mice as a murine model of liver metabolic dysfunction associated with diabetic ketoacidosis and insulin resistance. We evaluated liver fatty acid levels by microscopic examination and protein expression profiles by orthogonal experimental strategies using protein 2-DE MALDI-TOF/TOF and peptic nLC-MS/MS shotgun profiling. Identified proteins were then loaded into Ingenuity Pathways Analysis to find possible molecular networks. Twenty-eight proteins identified by 2-DE analysis and 24 identified by nLC-MS/MS shotgun were differentially expressed among the three genotypes. Bioinformatic analysis revealed a central role of high-mobility group box 1/2 and huntigtin never reported before in association with metabolic and related liver disease. A different modulation of these proteins in both blood and hepatic tissue further suggests their role in these processes. These results provide new insight into pathophysiology of insulin resistance and hepatic steatosis and could be useful in identifying novel biomarkers to predict risk for diabetes and its complications.

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http://dx.doi.org/10.1152/ajpendo.00447.2014DOI Listing

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