Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Differential effects on β-cell mass by disruption of Bardet–Biedl syndrome or Alstrom syndrome genes

22 Oct 2015

Abstract excerpt

Rare genetic syndromes characterized by early-onset type 2 diabetes have revealed the importance of pancreatic β-cells in genetic susceptibility to diabetes. However, the role of genetic regulation of β-cells in disorders that are also characterized by highly penetrant obesity, a major additional risk factor, is unclear. In this study, we investigated the contribution of genes associated with two obesity...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Genetic and Kidney Cyst Diseases
Share to Genetic Syndromes and Imprinting
Share to Pancreatic function and diabetes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26494903
DOI: 10.1093/hmg/ddv447

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Differential effects on β-cell mass by disruption of Bardet–Biedl syndrome or Alstrom syndrome genesPMID 26494903Read ↗

Exocrine pancreas proteases regulate β-cell proliferation in zebrafish ciliopathy models and in murine systems.Semantic proximity Read ↗

Genomic knockout of <i>alms1</i> in zebrafish recapitulates Alström syndrome and provides insight into metabolic phenotypesSemantic proximity Read ↗

Alström syndrome: insights into the pathogenesis of metabolic disorders.Semantic proximity Read ↗

Assignment of Functional Relevance to Genes at Type 2 Diabetes-Associated Loci Through Investigation of β-Cell Mass Deficits.Semantic proximity Read ↗

Bardet‐Biedl syndrome: A focus on genetics, mechanisms and metabolic dysfunctionSemantic proximity Read ↗

Ciliary dysfunction impairs beta-cell insulin secretion and promotes development of type 2 diabetes in rodents.Semantic proximity Read ↗

Psammomys Obesus, a Model for Environment-Gene Interactions in Type 2 DiabetesSemantic proximity Read ↗

Subcellular Localization of ALMS1 Supports Involvement of Centrosome and Basal Body Dysfunction in the Pathogenesis of Obesity, Insulin Resistance, and Type 2 DiabetesSemantic proximity Read ↗

Regulation of intracellular signaling and neuron function by Bardet-Biedl Syndrome proteins in patient-specific iPSC-derived neuronsSemantic proximity Read ↗

Knockdown of the Alström syndrome-associated gene Alms1 in 3T3-L1 preadipocytes impairs adipogenesis but has no effect on cell-autonomous insulin action.Semantic proximity Read ↗

Whole organism transcriptome analysis of zebrafish models of Bardet-Biedl Syndrome and Alström Syndrome provides mechanistic insight into shared and divergent phenotypes.Semantic proximity Read ↗

A δ-cell subpopulation with a pro-β-cell identity confers efficient age-independent recovery in a zebrafish model of diabetesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.