关键词： 1,5-AG, 1,5-anhydroglucitol 2-AAA, 2-aminoadipic acid 2-DGE, two-dimensional gel electrophoresis ABCC8, ATP binding cassette subfamily C member 8 ADA, American Diabetes Association AhR, aromatic hydrocarbon receptor BA, bile acid BCAA, branched-chain amino acid BCKAs, branched chain keto acids Biomarkers CE, cholesterol ester CFL1, cofilin-1 CRP, C reactive protein CYP450, cytochrome P450 DAG, diacylglycerol DPP-4, dipeptyl peptidase 4 EASD, European Association for the Study of Diabetes FA, fatty acid FFA, free fatty acid FMT, fecal microbiota transplantation FTO, fat mass and obesity-associated GAS5, growth arrest-specific transcript 5 GC–MS/MS, gas chromatography-tandem mass spectrometry GLP-1, glucagon-like peptide 1 GLP-1R, glucagon-like peptide 1 receptor GSIS, glucose-stimulated insulin secretion GWAS, genome-wide association study Glycolipid metabolism disorder HGF, hepatocyte growth factor HMG-CoA, hydroxymethylglutaryl-coenzyme A HMGCR, 3-hydroxy-methylglutaryl coenzyme A reductase HPLC, high performance liquid chromatography HbA1C, glycylated hemoglobin IL-1ra, interleukin-1 receptor antagonist IMP, imidazole propionate IR, insulin resistance JNK, c-Jun-N-terminal-kinase KCNJ11, potassium inwardly rectifying channel subfamily J member 11 L-GPC, linoleoyl-glycerophosphocholine LC-MS/MS, liquid chromatography-tandem mass spectrometry LPC, lysophosphatidylcholine LPE, lysophosphatidylethanolamines LPS, lipopolysaccharide MAPK, mitogen-activated protein kinase MASP, mannose-binding lectin-associated serine protease 1 MATE1, multidrug and toxin extrusion protein 1 MDR1, multidrug resistance mutation 1 MGT, magnesium transporter MS, Mass Spectrometry Mechanism study Multi-omics NK, natural killer NMR, nuclear magnetic resonance OCT, organic cationic transporter OGTT, oral glucose tolerance test PC-PL, phosphatidylcholine-plasmalogen PE, phosphatidylethanolamines PNPLA3, patatin-like phospholipase domain-containing protein 3 PPAR, peroxisome proliferator-activated receptor PTBP1, polypyrimidine tract-binding protein 1 PTP, protein tyrosine phosphatase RNS, reactive nitrogen species ROS, reactive oxygen species SCFA, short-chain fatty acid SLC30A8, solute carrier family 30 member 8 SLC47A1, solute carrier family 47 member 1 SLC5A2, solute carrier family 5 member 2 SM, sphingomyelin SNP, single-nucleotide polymorphism SSPG, steady-state plasma glucose SUR1, sulfonylurea receptor 1 T2DM, type 2 diabetes mellitus TAG, triacylglycerol TCA, tricarboxylic acid TCF7L2, transcription factor 7-like 2 TF, transcription factor TMA, trimethylamine TMAO, trimethylamine oxide TNF-α, tumor necrosis factor alpha TOF-MS, time-of-flight mass spectrum TUG1, taurine upregulated gene 1 USP20, ubiquitin-specificpeptidase 20 WBC, white blood cell circRNA, circular RNA hADCS, human adipose-derived stem cells hsCRP, high-sensitivity C-reactive protein lnc-BATE1, brown adipose tissue enriched long non-coding RNA 1 lncRNA SHGL, lncRNA suppressor of hepatic gluconeogenesis and lipogenesis lncRNA, long non-coding RNA mRNA, messenger RNAs mTORC1, mechanistic target of rapamycin complex 1 miRNA, micro RNA ncRNA, non-coding RNA t-PA, tissue plasminogen activator α-HB, α-hydroxybutyrate

来  源：   DOI：10.1016/j.csbj.2022.10.030   PDF(Pubmed)

Abstract：
Glycolipid metabolism disorder are major threats to human health and life. Genetic, environmental, psychological, cellular, and molecular factors contribute to their pathogenesis. Several studies demonstrated that neuroendocrine axis dysfunction, insulin resistance, oxidative stress, chronic inflammatory response, and gut microbiota dysbiosis are core pathological links associated with it. However, the underlying molecular mechanisms and therapeutic targets of glycolipid metabolism disorder remain to be elucidated. Progress in high-throughput technologies has helped clarify the pathophysiology of glycolipid metabolism disorder. In the present review, we explored the ways and means by which genomics, transcriptomics, proteomics, metabolomics, and gut microbiomics could help identify novel candidate biomarkers for the clinical management of glycolipid metabolism disorder. We also discuss the limitations and recommended future research directions of multi-omics studies on these diseases.
摘要：
糖脂代谢紊乱是威胁人类健康和生命的主要因素。遗传,环境,心理,细胞，和分子因素有助于其发病机制。一些研究表明，神经内分泌轴功能障碍，胰岛素抵抗，氧化应激，慢性炎症反应，肠道菌群失调是与其相关的核心病理联系。然而,糖脂代谢紊乱的潜在分子机制和治疗靶点仍有待阐明。高通量技术的进展有助于阐明糖脂代谢紊乱的病理生理学。在本次审查中，我们探索了基因组学的方法和方法，转录组学，蛋白质组学，代谢组学，和肠道微生物可以帮助识别新的候选生物标志物，用于糖脂代谢紊乱的临床管理。我们还讨论了这些疾病的多组学研究的局限性和建议的未来研究方向。
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