Recent decades have witnessed the rapid increase in morbidity of metabolic associated fatty liver disease (MAFLD), also known as non-alcoholic fatty liver disease, worldwide(13.48% in Africa, 25% in Asia, 23.71% in Europe, 31.79% in Middle East, 24.13% in North America, and 30.45% in South America). As the leading cause of chronic liver disease, MAFLD exhibits the spectrum from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), with outcomes of fibrosis/cirrhosis and hepatocellular carcinoma. Interestingly, accumulating proofs highlight the prevalence of MAFLD in the population suffering from endocrine disorders with metabolic dysregulation, such as metabolic syndrome (MetS) components (obesity, hyperinsulinemia, type 2 diabetes), polycystic ovary syndrome (PCOS), and hypothyroidism. The occurrence of MAFLD reciprocally enhances the risk of endocrine-based metabolic dysregulation, such as insulin resistance, type 2 diabetes, and dyslipidemia. Except for the common etiologies of Western diet and sedentary lifestyle, multiple genetic and epigenetic factors play important roles in the interaction of endocrine disorders and MAFLD. For example, TCF7L2 CT/TT genotype predisposes both diabetes and MAFLD through beta-cell dysfunction, insulin resistance, and reduced incretin effect. Deacetylase inhibition upregulates the GLP-1 receptor expression to ameliorate MAFLD. High-level miR-103 serves as the molecular link between insulin resistance and MAFLD.
It is suggested to be reciprocal causation between metabolism-related endocrine disorders and MAFLD. Various mutations and single nucleotide polymorphisms (SNPs) associated with endocrine disorders confer a high risk of MAFLD. DNA (e.g., methylation), RNA (e.g., m6A RNA methylation), and histone (e.g., methylation, acetylation) modification reflect another layer of mechanisms underlying the interaction of endocrine disorders and MAFLD. Moreover, different kinds of non-coding RNAs (e.g., miRNA, piRNA, lncRNA, circRNA) demonstrate deep involvement in the cross-talk of MAFLD and endocrine disorders. This Research Topic aims to fully investigate the interaction, with the exploration of its genetic and epigenetic basis.
We welcome submissions of Original Research articles, Brief Reports, Reviews, Systematic Reviews, and Meta-analyses focusing on, but not limited to, the following themes:
• Impact of metabolism-related endocrine disorders on the incidence, morbidity, histopathology, natural course, complications, and therapeutic strategy of MAFLD.
• Role of MAFLD in the prevalence, progression, outcome, and treatment response of endocrine disorders.
• Variants and mutations that underlie the interaction of MAFLD spectrum and endocrine disorders.
• Profile, characteristics, and mechanisms of DNA, RNA, and histone modification mediating the crosstalk between endocrine disorders and MAFLD.
• Signalling and regulation, together with predictive and/or diagnostic value, of ncRNAs in the interaction of different endocrine disorders and MAFLD.
Recent decades have witnessed the rapid increase in morbidity of metabolic associated fatty liver disease (MAFLD), also known as non-alcoholic fatty liver disease, worldwide(13.48% in Africa, 25% in Asia, 23.71% in Europe, 31.79% in Middle East, 24.13% in North America, and 30.45% in South America). As the leading cause of chronic liver disease, MAFLD exhibits the spectrum from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), with outcomes of fibrosis/cirrhosis and hepatocellular carcinoma. Interestingly, accumulating proofs highlight the prevalence of MAFLD in the population suffering from endocrine disorders with metabolic dysregulation, such as metabolic syndrome (MetS) components (obesity, hyperinsulinemia, type 2 diabetes), polycystic ovary syndrome (PCOS), and hypothyroidism. The occurrence of MAFLD reciprocally enhances the risk of endocrine-based metabolic dysregulation, such as insulin resistance, type 2 diabetes, and dyslipidemia. Except for the common etiologies of Western diet and sedentary lifestyle, multiple genetic and epigenetic factors play important roles in the interaction of endocrine disorders and MAFLD. For example, TCF7L2 CT/TT genotype predisposes both diabetes and MAFLD through beta-cell dysfunction, insulin resistance, and reduced incretin effect. Deacetylase inhibition upregulates the GLP-1 receptor expression to ameliorate MAFLD. High-level miR-103 serves as the molecular link between insulin resistance and MAFLD.
It is suggested to be reciprocal causation between metabolism-related endocrine disorders and MAFLD. Various mutations and single nucleotide polymorphisms (SNPs) associated with endocrine disorders confer a high risk of MAFLD. DNA (e.g., methylation), RNA (e.g., m6A RNA methylation), and histone (e.g., methylation, acetylation) modification reflect another layer of mechanisms underlying the interaction of endocrine disorders and MAFLD. Moreover, different kinds of non-coding RNAs (e.g., miRNA, piRNA, lncRNA, circRNA) demonstrate deep involvement in the cross-talk of MAFLD and endocrine disorders. This Research Topic aims to fully investigate the interaction, with the exploration of its genetic and epigenetic basis.
We welcome submissions of Original Research articles, Brief Reports, Reviews, Systematic Reviews, and Meta-analyses focusing on, but not limited to, the following themes:
• Impact of metabolism-related endocrine disorders on the incidence, morbidity, histopathology, natural course, complications, and therapeutic strategy of MAFLD.
• Role of MAFLD in the prevalence, progression, outcome, and treatment response of endocrine disorders.
• Variants and mutations that underlie the interaction of MAFLD spectrum and endocrine disorders.
• Profile, characteristics, and mechanisms of DNA, RNA, and histone modification mediating the crosstalk between endocrine disorders and MAFLD.
• Signalling and regulation, together with predictive and/or diagnostic value, of ncRNAs in the interaction of different endocrine disorders and MAFLD.
