Glucose homeostasis is strictly regulated to guarantee energy supply to vital organs and tissues, and thus normal “whole body” function. Genetic and/or environmental disruption of glucose metabolism can lead to cellular dysfunctions and diseases in experimental in vitro and in vivo models, while abnormalities of glucose homeostasis occur in several common endocrine/metabolic disorders, such as diabetes mellitus, the metabolic syndrome, and obesity. Hormones, adipokines, nutrients, and other biologically active molecules can influence glucose metabolism by stimulating or inhibiting key enzymes that are directly involved in glucose-related metabolic pathways, and in recent decades, intensive work has been devoted to elucidating the molecular and cellular mechanisms underpinning this. Both ubiquitous and tissue-specific transcription factors, such as PPAR?, ChREBP, FOXO1, and PDX-1 among many others, have been identified to be key, and their activities have been shown to be modulated by post-translational modifications, as well as by non-genomic cross-talk with phosphatases or kinases, such as ERK1/2, PKC and AMPK. In addition, accumulating evidences emphasize important regulatory roles of non-coding RNAs, which, by regulating gene expression at transcriptional and post-transcriptional levels, may functionally impact on different steps of the regulation of glucose metabolism, including DNA sequestration of transcription factors, and control of mRNA decay. Despite major advancements in the field, however, the molecular mechanisms underlying the interplay between nuclear factors that directly activate transcription of metabolic target genes, and other molecules that are typically involved in the control of glucose pathways, have been only partly elucidated. For example, little is known about the transcriptional regulation of genes, such as the liver piruvate kinase gene, lipasin gene, and even the ChREBP gene in response to food intake, while controversial results have been obtained about the role of ChREBP in pancreatic beta cells. Tissue-specific factors may functionally interact with ubiquitous transcription factors, such as ATF3 and HMGA1, among others, to regulate metabolism, and these cooperations have been only partly investigated. In addition, even if some small non-coding RNAs, such as mIR 33, 34, and 194, as well as long non-coding RNAs, such as lncRNA-H19, E-33, and Meg3 have been described to influence glucose metabolism, very little is known about the role of many other identified non-coding RNAs putatively relevant within this scenario.
This Research Topic highlights the need to further expand our understanding on the pathophysiology of glucose metabolism with the aim to fill gaps in the current knowledge, and to reconcile or refute controversial observations in the field.
Potential contributions may include, but are not limited to: transcriptional, post-transcriptional, and post-translational regulation of glucose metabolism; regulation of glucose metabolism by hormones, cytokines, nutrients, and other bioactive molecules; insulin signaling and glucose metabolism.
Glucose homeostasis is strictly regulated to guarantee energy supply to vital organs and tissues, and thus normal “whole body” function. Genetic and/or environmental disruption of glucose metabolism can lead to cellular dysfunctions and diseases in experimental in vitro and in vivo models, while abnormalities of glucose homeostasis occur in several common endocrine/metabolic disorders, such as diabetes mellitus, the metabolic syndrome, and obesity. Hormones, adipokines, nutrients, and other biologically active molecules can influence glucose metabolism by stimulating or inhibiting key enzymes that are directly involved in glucose-related metabolic pathways, and in recent decades, intensive work has been devoted to elucidating the molecular and cellular mechanisms underpinning this. Both ubiquitous and tissue-specific transcription factors, such as PPAR?, ChREBP, FOXO1, and PDX-1 among many others, have been identified to be key, and their activities have been shown to be modulated by post-translational modifications, as well as by non-genomic cross-talk with phosphatases or kinases, such as ERK1/2, PKC and AMPK. In addition, accumulating evidences emphasize important regulatory roles of non-coding RNAs, which, by regulating gene expression at transcriptional and post-transcriptional levels, may functionally impact on different steps of the regulation of glucose metabolism, including DNA sequestration of transcription factors, and control of mRNA decay. Despite major advancements in the field, however, the molecular mechanisms underlying the interplay between nuclear factors that directly activate transcription of metabolic target genes, and other molecules that are typically involved in the control of glucose pathways, have been only partly elucidated. For example, little is known about the transcriptional regulation of genes, such as the liver piruvate kinase gene, lipasin gene, and even the ChREBP gene in response to food intake, while controversial results have been obtained about the role of ChREBP in pancreatic beta cells. Tissue-specific factors may functionally interact with ubiquitous transcription factors, such as ATF3 and HMGA1, among others, to regulate metabolism, and these cooperations have been only partly investigated. In addition, even if some small non-coding RNAs, such as mIR 33, 34, and 194, as well as long non-coding RNAs, such as lncRNA-H19, E-33, and Meg3 have been described to influence glucose metabolism, very little is known about the role of many other identified non-coding RNAs putatively relevant within this scenario.
This Research Topic highlights the need to further expand our understanding on the pathophysiology of glucose metabolism with the aim to fill gaps in the current knowledge, and to reconcile or refute controversial observations in the field.
Potential contributions may include, but are not limited to: transcriptional, post-transcriptional, and post-translational regulation of glucose metabolism; regulation of glucose metabolism by hormones, cytokines, nutrients, and other bioactive molecules; insulin signaling and glucose metabolism.
