GSE78183: Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers Elovl2 as a novel regulator of glucose-induced insulin secretion

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GROUP CONDITION SAMPLES
pancreatic islets
GSM2068892 GSM2068893 GSM2068894 GSM2068895 GSM2068896 GSM2068897 GSM2068898 GSM2068899 GSM2068947 GSM2068948 GSM2068949 GSM2068950 GSM2068951 GSM2068952 GSM2068953 GSM2068954 GSM2069000 GSM2069001 GSM2069002 GSM2069003 GSM2069004 GSM2069005 GSM2069006 GSM2069055 GSM2069056 GSM2069057 GSM2069058 GSM2069059 GSM2069060 GSM2069061 GSM2069062 GSM2069108 GSM2069109 GSM2069110 GSM2069111 GSM2069112 GSM2069113 GSM2069114 GSM2069115 GSM2069162 GSM2069163 GSM2069164 GSM2069165 GSM2069166 GSM2069167 GSM2069168 GSM2069169 GSM2069176 GSM2069177
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Description

Submission Date: Feb 22, 2016

Summary: Defective insulin secretion by pancreatic β cells underlies the development of type 2 diabetes (T2D). High fat diet-fed mice are commonly used to study diabetes progression, but studies are usually limited to a single strain, such as C57Bl/6J. Here, we use a systems biology approach to integrate large phenotypic and islet transcriptomic data sets from six commonly used strains fed a high fat or regular chow diet to identify genes associated with glucose intolerance and insulin secretion. One of these genes is Elovl2, encoding very long chain fatty acid elongase 2. ELOVL2 is responsible for the synthesis of the polyunsaturated fatty acid, docosahexaenoic acid (DHA). We show that DHA rescues glucose-induced insulin secretion and cytosolic Ca2+ influx impaired by glucolipotoxicity, and that Elovl2 over-expression is able to restore the insulin secretion defect under these conditions. We propose that increased endogenous DHA levels resulting from Elovl2 up-regulation counteracts the insulin secretion defect associated with glucolipotoxicity. Although we focus our experimental validation on Elovl2, the comprehensive data set and integrative network model we used to identify this candidate gene represents an important novel resource to dissect the molecular aetiology of β cell failure in murine models.

GEO Accession ID: GSE78183

PMID: 28377873

Description

Submission Date: Feb 22, 2016

Summary: Defective insulin secretion by pancreatic β cells underlies the development of type 2 diabetes (T2D). High fat diet-fed mice are commonly used to study diabetes progression, but studies are usually limited to a single strain, such as C57Bl/6J. Here, we use a systems biology approach to integrate large phenotypic and islet transcriptomic data sets from six commonly used strains fed a high fat or regular chow diet to identify genes associated with glucose intolerance and insulin secretion. One of these genes is Elovl2, encoding very long chain fatty acid elongase 2. ELOVL2 is responsible for the synthesis of the polyunsaturated fatty acid, docosahexaenoic acid (DHA). We show that DHA rescues glucose-induced insulin secretion and cytosolic Ca2+ influx impaired by glucolipotoxicity, and that Elovl2 over-expression is able to restore the insulin secretion defect under these conditions. We propose that increased endogenous DHA levels resulting from Elovl2 up-regulation counteracts the insulin secretion defect associated with glucolipotoxicity. Although we focus our experimental validation on Elovl2, the comprehensive data set and integrative network model we used to identify this candidate gene represents an important novel resource to dissect the molecular aetiology of β cell failure in murine models.

GEO Accession ID: GSE78183

PMID: 28377873

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