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
GSM2068878 GSM2068879 GSM2068880 GSM2068881 GSM2068882 GSM2068883 GSM2068933 GSM2068934 GSM2068935 GSM2068936 GSM2068937 GSM2068938 GSM2068983 GSM2068984 GSM2068985 GSM2068986 GSM2068987 GSM2068988 GSM2069038 GSM2069039 GSM2069040 GSM2069041 GSM2069042 GSM2069043 GSM2069091 GSM2069092 GSM2069093 GSM2069094 GSM2069095 GSM2069096 GSM2069146 GSM2069147 GSM2069148 GSM2069149 GSM2069150 GSM2069151
GSM2068872 GSM2068873 GSM2068874 GSM2068875 GSM2068876 GSM2068877 GSM2068927 GSM2068928 GSM2068929 GSM2068930 GSM2068931 GSM2068932 GSM2068982 GSM2068989 GSM2068995 GSM2068999 GSM2069007 GSM2069008 GSM2069037 GSM2069044 GSM2069050 GSM2069054 GSM2069063 GSM2069064 GSM2069090 GSM2069097 GSM2069103 GSM2069107 GSM2069116 GSM2069117 GSM2069145 GSM2069152 GSM2069157 GSM2069161 GSM2069170 GSM2069171 GSM2069172 GSM2069173 GSM2069174 GSM2069175
GSM2068920 GSM2068921 GSM2068922 GSM2068923 GSM2068924 GSM2068925 GSM2068926 GSM2068971 GSM2068972 GSM2068973 GSM2068974 GSM2068975 GSM2068976 GSM2068977 GSM2068978 GSM2069027 GSM2069028 GSM2069029 GSM2069030 GSM2069031 GSM2069032 GSM2069033 GSM2069034 GSM2069081 GSM2069082 GSM2069083 GSM2069084 GSM2069085 GSM2069086 GSM2069087 GSM2069088 GSM2069136 GSM2069137 GSM2069138 GSM2069139 GSM2069140 GSM2069141 GSM2069142 GSM2069143 GSM2069195 GSM2069196 GSM2069197 GSM2069198 GSM2069199 GSM2069200 GSM2069201 GSM2069206 GSM2069207 GSM2069208 GSM2069209
GSM2068884 GSM2068885 GSM2068886 GSM2068887 GSM2068888 GSM2068889 GSM2068890 GSM2068891 GSM2068939 GSM2068940 GSM2068941 GSM2068942 GSM2068943 GSM2068944 GSM2068945 GSM2068946 GSM2068990 GSM2068991 GSM2068992 GSM2068993 GSM2068994 GSM2068996 GSM2068997 GSM2068998 GSM2069045 GSM2069046 GSM2069047 GSM2069048 GSM2069049 GSM2069051 GSM2069052 GSM2069053 GSM2069098 GSM2069099 GSM2069100 GSM2069101 GSM2069102 GSM2069104 GSM2069105 GSM2069106 GSM2069153 GSM2069154 GSM2069155 GSM2069156 GSM2069158 GSM2069159 GSM2069160
GSM2068912 GSM2068913 GSM2068914 GSM2068915 GSM2068916 GSM2068917 GSM2068918 GSM2068919 GSM2068963 GSM2068964 GSM2068965 GSM2068966 GSM2068967 GSM2068968 GSM2068969 GSM2068970 GSM2069017 GSM2069018 GSM2069019 GSM2069020 GSM2069021 GSM2069023 GSM2069024 GSM2069025 GSM2069071 GSM2069072 GSM2069073 GSM2069074 GSM2069075 GSM2069077 GSM2069078 GSM2069079 GSM2069126 GSM2069127 GSM2069128 GSM2069129 GSM2069130 GSM2069132 GSM2069133 GSM2069134 GSM2069185 GSM2069186 GSM2069187 GSM2069188 GSM2069189 GSM2069191 GSM2069192 GSM2069193
GSM2068900 GSM2068901 GSM2068902 GSM2068903 GSM2068904 GSM2068905 GSM2068955 GSM2068956 GSM2068957 GSM2068979 GSM2068980 GSM2068981 GSM2069009 GSM2069016 GSM2069022 GSM2069026 GSM2069035 GSM2069036 GSM2069065 GSM2069070 GSM2069076 GSM2069080 GSM2069089 GSM2069118 GSM2069125 GSM2069131 GSM2069135 GSM2069144 GSM2069178 GSM2069184 GSM2069190 GSM2069194 GSM2069202 GSM2069203 GSM2069204 GSM2069205
GSM2068906 GSM2068907 GSM2068908 GSM2068909 GSM2068910 GSM2068911 GSM2068958 GSM2068959 GSM2068960 GSM2068961 GSM2068962 GSM2069010 GSM2069011 GSM2069012 GSM2069013 GSM2069014 GSM2069015 GSM2069066 GSM2069067 GSM2069068 GSM2069069 GSM2069119 GSM2069120 GSM2069121 GSM2069122 GSM2069123 GSM2069124 GSM2069179 GSM2069180 GSM2069181 GSM2069182 GSM2069183
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
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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