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The Section seeks to present novel, ground-breaking preclinical studies on molecular aspects of type 1 and type 2 diabetes aimed to increase understanding of fundamental aspects of each disease process, and potential therapies. The section will thus focus on fundamental research into the biology of systems and disease-relevant tissues, including, but not limited to, pancreatic islet and enteroendocrine (L, K, I) cells, “classical” insulin target tissues (liver, muscle, adipose tissue etc), and non-classical tissues (brain, immune system etc). Studies describing technologies advances in this area are also particularly welcome. Clinical research studies or epidemiological studies do not fall within the scope of this section.  

Research on the following themes will be particularly welcome:

• Basic metabolism and metabolic regulation. Inter-relationships between different metabolic fuels and the resulting effects on diabetes-relevant phenotypes (fatty acid, amino acid and glucose metabolism);

• Systems level regulation of glucose metabolism and inter-organ and inter-cellular communication. Integration of basic metabolism with diabetes-relevant cellular functions: β-cells, skeletal muscle, hepatic gluconeogenesis etc (adipose-liver, gut-brain etc). The microbiome and its interaction with these systems;

• Control of feeding and satiety and its relationship to tissue damage in type 2 diabetes. Role and regulation of neural circuits (hypothalamus, hind brain etc);

• β cell failure (dysfunction, apoptosis, ER stress, altered proliferation etc ) in type 1 and type 2 diabetes. Relationship with obesity and fuel exceess. Immune mechanisms of pancreatic β cell destruction in type 1 diabetes, and its targeting by immune therapies. Immunomodulation and immunometabolism;

• Functional genomics, genetic models of gene function/dysfunction in mouse and other model organisms including non-mammalian species (Yeast, C. elegans, Drosophila, zebrafish etc). Modelling genetic variants associated with diabetes (GWAS etc.);

• Control of adipose tissue development and differentiation, insulin action, adipokine production;

• Disease complications: metabolism of liver and kidney: nephropathy, neuropathy, retinopathy. Bone loss in diabetes;

• Receptor-ligand interactions and trafficking, particularly of receptors central to normal glucose homeostasis, e.g. insulin, GLP-1, relevant neurotransmitters. The molecular basis of receptor bias. Intracellular signalling (Ca2 , cAMP, phosphorylation cascades);

• Omics: transcriptomics, proteomics, metabolomics (MS-MS etc) lipidomics, RNAomics of plasma and tissues. Biomarkers of disease

• Intracellular organelle function and stasis: e.g. secretory granule dynamic, exocytosis and mitochondrial biology; autophagy, apoptosis; transmembrane transporters and molecular motors;

• Epigenetics and genomics: chromatin landscape, enhancer biology, genome stability, metabolism:epigenome interactions. Roles and regulation of non-coding RNAs;

• Translational models, e.g. high throughput screens of credible targets; 

Technological advances pertinent to the field including:

• Genome editing (CRISPR etc)

• Metabolomics, lipidomics, metabolic flux profiling, metabolic modelling. ChiPSeq, RNASeq, mass spectometry, etc;

• Discovery and characterization of pharmacological tools and agents that are of use in the study or treatment of diabetes and related disorders;

• In vivo and in vitro imaging (novel probes, approaches); optogenetics, pharmacogenetcs and related technologies (DREADs, acoustic sensors etc); super-resolution microscopy (PALM STORM, SIM etc) and analytical tools. Imaging mass cytometry, CyTOF etc;

• Transplantation and new sources of transplantable tissues: Stem cell therapies, directed differentiation (e.g. iPSC to β cell conversion). Tissue encapsulation;

• Devices for hormone release in vivo (“artificial pancreas”);

• Single cell omic approaches and analyses;

• Computational biology, “big data”, machine learning and its applications. Data archiving and tissue atlases. 

Frontiers in Endocrinology is member of the Committee on Publication Ethics.


  • Short name

    Front. Endocrinol.

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    PubMed, MEDLINE, PubMed Central (PMC), Scopus, Web of Science Science Citation Index Expanded (SCIE), Google Scholar, DOAJ, CrossRef, Chemical Abstracts Service (CAS), Embase, Semantic Scholar, Ulrich's Periodicals Directory, CLOCKSS, EBSCO, OpenAIRE, Zetoc


    All published articles receive a PMCID


Diabetes: Molecular Mechanisms welcomes submissions of the following article types: Addendum, Correction, Editorial, Erratum, General Commentary, Hypothesis & Theory, Methods, Mini Review, Opinion, Original Research, Perspective, Review, Systematic Review, Technology and Code.

All manuscripts must be submitted directly to the section Diabetes: Molecular Mechanisms, where they are peer-reviewed by the Associate and Review Editors of the specialty section.

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