Abstract
ObjectiveTo investigate the effect of silibinin on the protein expression profile of white adipose tissue (WAT) in obese mice by using Tandem Mass Tag (TMT) and liquid chromatography-tandem mass spectrometry (LC-MS/MS).MethodsAccording to experimental requirements, 36 C57BL/6JC mice were randomly divided into normal diet group (WC group), high fat diet group (WF group), and high fat diet + silibinin group (WS group). WS group was intragastrically administered with 54 mg/kg body weight of silibinin, and the WC group and the WF group were intragastrically administered with equal volume of normal saline. Serum samples were collected to detect fasting blood glucose and blood lipids. IPGTT was used to measure the blood glucose value at each time point and calculate the area under the glucose curve. TMT combined with LC-MS/MS were used to study the expression of WAT, and its cellular processes, biological processes, corresponding molecular functions, and related network molecular mechanisms were analyzed by bioinformatics. Finally, RT-PCR and LC-MS/MS were used to detect the mRNA and protein expressions of FABP5, Plin4, GPD1, and AGPAT2, respectively.ResultsAlthough silibinin did not reduce the mice's weight, it did improve glucose metabolism. In addition, silibinin decreased the concentration of TC, TG, and LDL-C and increased the concentration of HDL-C in the serum of mice. In the WF/WS group, 182 differentially expressed proteins were up-regulated and 159 were down-regulated. While in the WS/WF group, 362 differentially expressed proteins were up-regulated and 176 were down-regulated. Further analysis found that these differential proteins are mainly distributed in the peroxisome proliferation-activated receptor (PPAR), lipolysis of fat cells, metabolism of glycerides, oxidative phosphorylation, and other signaling pathways, and participate in cell processes and lipid metabolism through catalysis and integration functions. Specifically, silibinin reduced the expression of several key factors such as FABP5, Plin4, GPD1, and AGPTA2.ConclusionHigh fat diet (HFD) can increase the expression of lipid synthesis and transport-related proteins and reduce mitochondrial related proteins, thereby increasing lipid synthesis, reducing energy consumption, and improving lipid metabolism in vivo. Silibinin can reduce lipid synthesis, increase energy consumption, and improve lipid metabolism in mice in vivo.
Highlights
Obesity is a chronic metabolic disease caused by heredity, lifestyle, environment, and other factors, and the imbalance between energy intake and consumption was the root cause
We selected some of them for detailed introduction: Fatty acid-binding proteins (FABPs) are a kind of lipid chaperone protein that can regulate fatty acid transport, signal transduction, and nuclear transcription (Gan et al, 2015), which is closely related to obesity, type-2 diabetes, cardiovascular disease, tumor, fatty liver, and other diseases (Senolt et al, 2010; Kawaguchi et al, 2016; Thompson et al, 2018)
FABPs expression is regulated by various factors such as peroxisome proliferator-activated receptor gamma (PPARg), free fatty acid (FFA), insulin, and long-chain fatty acids (Liu et al, 2007), which can promote FFA transport to lipid droplets, leading to lipid deposition in adipose tissue (Holmes and Cox, 2012)
Summary
Obesity is a chronic metabolic disease caused by heredity, lifestyle, environment, and other factors, and the imbalance between energy intake and consumption was the root cause. Excess energy is stored in fat cells in the form of TG and promotes the increase in size and number of fat cells and reduces lipid toxicity. It will become dysfunctional when WAT storage exceeds its threshold (Brestoff and Artis, 2015). Lipids will be deposited in the liver, pancreas, and other important organs, leading to chronic inflammation and occurrence of diabetes, insulin resistance, cardiovascular disease, obesity, and other diseases, which can further aggravate adipose tissue function (Ibarretxe et al, 2016). It is of great significance to intervene in lipid synthesis and reduce fat inflammation to prevent the occurrence of obesity-related complications (Hubler and Kennedy, 2016)
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