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Novel biomarkers for a personalized managemnet of Type II Diabetes [islet]

ABSTRACT: Novel biomarkers for a personalized managemnet of Type II Diabetes [islet]

PROVIDER: PRJNA589525 | ENA |

REPOSITORIES: ENA

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Novel biomarkers for a personalized managemnet of Type II Diabetes [islet]

Project description:Quantitative measurement of circulating metabolites may help to identify tissue specific metabolic pathways that are modulated by or causal for a disease condition. The aim of the study was to explore associations between plasma lipid concentrations and gene expression in pancreatic β-cells and insulin target tissues in a mouse model of pre-diabetes to uncover molecular mechanisms and biomarkers of diabetes susceptibility.

2021-11-24 | GSE140369 | GEO

Novel biomarkers for a personalized managemnet of Type II Diabetes

Project description:Novel biomarkers for a personalized managemnet of Type II Diabetes

| PRJNA691535 | ENA

Novel biomarkers for a personalized managemnet of Type II Diabetes [adipose, liver, muscle]

Project description:Novel biomarkers for a personalized managemnet of Type II Diabetes [adipose, liver, muscle]

| PRJNA691542 | ENA

Novel biomarkers for a personalized managemnet of Type II Diabetes [adipose, liver, muscle]

2021-11-24 | GSE164672 | GEO

transcriptional profile of islet EVs for diabetes genes

Project description:Identification of transcriptional profile of several genes involved in diabetes in islet-derived extracellular vesicles (Evs). Recently, EVs are identified as a new mechanism in cell-to-cell communication by transfer of protein and genic information (mRNA, microRNA). Their role is under investigation in immunology, stem cell and cancer, but not in islets and diabetes. The aim of this experiment is to identify mRNA transcripts (in particular, mRNA transcripts involved in diabetes pathophysiology) present in islet Evs.

2012-08-02 | E-MEXP-3695 | biostudies-arrayexpress

Personalized Dietary Management in Type 2 Diabetes

Project description:Personalized Dietary Management in Type 2 Diabetes

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Islet Sympathetic Innervation and Islet Neuropathology in Patients with Type 1 Diabetes

Project description:Dysregulation of glucagon secretion in type 1 diabetes (T1D) involves hypersecretion during postprandial states, but insufficient secretion during hypoglycemia. The sympathetic nervous system regulates glucagon secretion. To investigate islet sympathetic innervation in T1D, sympathetic tyrosine hydroxylase (TH) axons were analyzed in control non-diabetic organ donors, non-diabetic islet autoantibody-positive individuals (AAb), and age-matched persons with T1D. Islet TH axon numbers and density were significantly decreased in AAb compared to T1D with no significant differences observed in exocrine TH axon volume or lengths between groups. TH axons were in close approximation to islet α-cells in T1D individuals with long-standing diabetes. Islet RNA-sequencing and qRT-PCR analyses identified significant alterations in noradrenalin degradation, α-adrenergic signaling, cardiac b-adrenergic signaling, catecholamine biosynthesis, and additional neuropathology pathways. The close approximation of TH axons at islet α-cells supports a model for sympathetic efferent neurons directly regulating glucagon secretion. Sympathetic islet innervation and intrinsic adrenergic signaling pathways could be novel targets for improving glucagon secretion in T1D.

2021-08-09 | GSE181674 | GEO

Novel biomarkers for a personalized managemnet of Type II Diabetes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-24 | GSE164673 | GEO

Circulating Metabolites in Progression to Islet Autoimmunity and Type 1 Diabetes

Project description:<h4><strong>AIMS/HYPOTHESIS: </strong>Metabolic dysregulation may precede the onset of type 1 diabetes. However, these metabolic disturbances and their specific role in disease initiation remain poorly understood. In this study, we examined whether children who progress to type 1 diabetes have a circulatory polar metabolite profile distinct from that of children who later progress to islet autoimmunity but not type 1 diabetes and a matched control group.</h4><h4><strong>METHODS: </strong>We analysed polar metabolites from 415 longitudinal plasma samples in a prospective cohort of children in three study groups: those who progressed to type 1 diabetes; those who seroconverted to one islet autoantibody but not to type 1 diabetes; and an antibody-negative control group. Metabolites were measured using two-dimensional GC high-speed time of flight MS.</h4><h4><strong>RESULTS: </strong>In early infancy, progression to type 1 diabetes was associated with downregulated amino acids, sugar derivatives and fatty acids, including catabolites of microbial origin, compared with the control group. Methionine remained persistently upregulated in those progressing to type 1 diabetes compared with the control group and those who seroconverted to one islet autoantibody. The appearance of islet autoantibodies was associated with decreased glutamic and aspartic acids.</h4><h4><strong>CONCLUSIONS/INTERPRETATION: </strong>Our findings suggest that children who progress to type 1 diabetes have a unique metabolic profile, which is, however, altered with the appearance of islet autoantibodies. Our findings may assist with early prediction of the disease.</h4>

2022-01-19 | MTBLS802 | MetaboLights

Transcriptional changes underlying progression from islet autoantibody positivity to type 1 diabetes

Project description:Type 1 diabetes (T1D) usually has a preclinical phase identified by the presence of circulating autoantibodies to pancreatic islet antigens, and most young children who have multiple autoantibodies progress to diabetes within 10 years. While autoantibodies denote underlying islet autoimmunity, how this process is initiated and then progresses to clinical diabetes on a background of genetic susceptibility is not clearly understood. We analysed gene expression by RNA-seq in four types of immune cells from five genetically at-risk children with islet autoantibodies who progressed to diabetes in ≤ 3 years (‘progressors’) and in five at-risk children matched for sex, age and HLA who had not progressed to diabetes (‘non-progressors’).

2022-03-09 | GSE185190 | GEO

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