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Replacing SNAP-25b with SNAP-25a expression results in metabolic disease
Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the solubleN-ethylmaleimide–sensitive factor attachment protein (SNARE) complex mediating fast Ca2+-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this p...
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| Published in: | Proceedings of the National Academy of Sciences - PNAS 2015-08, Vol.112 (31), p.E4326-E4335 |
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| container_issue | 31 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Valladolid-Acebes, Ismael Daraio, Teresa Brismar, Kerstin Harkany, Tibor Ögren, Sven Ove Hökfelt, Tomas G. M. Bark, Christina |
| description | Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the solubleN-ethylmaleimide–sensitive factor attachment protein (SNARE) complex mediating fast Ca2+-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process. Here we explore the hypothesis that minor alterations in the machinery mediating regulated membrane fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabetes. Thus, we used a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a. These SNAP-25b–deficient mice were exposed to either a control or a high-fat/high-sucrose diet. Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b–deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. Our SNAP-25b–deficient mouse may represent a diabesity model. |
| doi_str_mv | 10.1073/pnas.1511951112 |
| format | article |
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Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b–deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. 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M.</creatorcontrib><creatorcontrib>Bark, Christina</creatorcontrib><title>Replacing SNAP-25b with SNAP-25a expression results in metabolic disease</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the solubleN-ethylmaleimide–sensitive factor attachment protein (SNARE) complex mediating fast Ca2+-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process. Here we explore the hypothesis that minor alterations in the machinery mediating regulated membrane fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabetes. Thus, we used a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a. These SNAP-25b–deficient mice were exposed to either a control or a high-fat/high-sucrose diet. Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b–deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. Our SNAP-25b–deficient mouse may represent a diabesity model.</description><subject>Adipocytes - metabolism</subject><subject>Adipocytes - pathology</subject><subject>Adipose Tissue, White - metabolism</subject><subject>Adipose Tissue, White - pathology</subject><subject>Adiposity</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight</subject><subject>Dyslipidemias - pathology</subject><subject>Energy Intake</subject><subject>Energy Metabolism</subject><subject>Feeding Behavior</subject><subject>Female</subject><subject>Homeostasis</subject><subject>Hormones</subject><subject>Hyperglycemia</subject><subject>Hypertrophy</subject><subject>Hypothalamus - metabolism</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Leptin - blood</subject><subject>Lipids</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Medicin och hälsovetenskap</subject><subject>Metabolic Diseases - blood</subject><subject>Metabolic Diseases - metabolism</subject><subject>Mice, Obese</subject><subject>Neurotransmitters</subject><subject>Phenotype</subject><subject>PNAS Plus</subject><subject>Proteins</subject><subject>Receptors, Leptin - metabolism</subject><subject>Rodents</subject><subject>Synaptosomal-Associated Protein 25 - deficiency</subject><subject>Synaptosomal-Associated Protein 25 - metabolism</subject><issn>0027-8424</issn><issn>1091-6490</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNpdkc1v1DAQxS0EosvCmRMoEhcuacceJ7YvSFVVaKWKVnycLcfxtl6ycbATCv89Tne7tBxG_pjfe3r2EPKawiEFgUdDb9IhrShVuSh7QhYUFC1rruApWQAwUUrO-AF5kdIaAFQl4Tk5YHUWCM4W5OyLGzpjfX9dfP18fFWyqilu_XhzfzKF-z1El5IPfZHXqRtT4fti40bThM7bovXJmeRekmcr0yX3arcuyfePp99OzsqLy0_nJ8cXpa2oHEuBFhCxEUIyiaucwjSSClczSyUDaHJmhJXIQVurBG0RlePYKCEFMnC4JGrrm27dMDV6iH5j4h8djM_70Ord_Q8_l05OU6Si5qLGrP2w1WZg41rr-jGa7rHFo07vb_R1-KV5hZxhnQ3e7wxi-Dm5NOqNT9Z1neldmJKmAhgoxnLWJXn3H7oOU-zz19xRUlRQz9TRlrIxpBTdah-Ggp4nrOcJ638Tzoq3D9-w5-9HmoFiB8zKvR1lGqk-5cjmZ7zZIus0hvjAgte5z_Ev33Kzqg</recordid><startdate>20150804</startdate><enddate>20150804</enddate><creator>Valladolid-Acebes, Ismael</creator><creator>Daraio, Teresa</creator><creator>Brismar, Kerstin</creator><creator>Harkany, Tibor</creator><creator>Ögren, Sven Ove</creator><creator>Hökfelt, Tomas G. M.</creator><creator>Bark, Christina</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>20150804</creationdate><title>Replacing SNAP-25b with SNAP-25a expression results in metabolic disease</title><author>Valladolid-Acebes, Ismael ; Daraio, Teresa ; Brismar, Kerstin ; Harkany, Tibor ; Ögren, Sven Ove ; Hökfelt, Tomas G. 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M.</au><au>Bark, Christina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Replacing SNAP-25b with SNAP-25a expression results in metabolic disease</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2015-08-04</date><risdate>2015</risdate><volume>112</volume><issue>31</issue><spage>E4326</spage><epage>E4335</epage><pages>E4326-E4335</pages><issn>0027-8424</issn><issn>1091-6490</issn><eissn>1091-6490</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Reviewers included: J.K.E., University of Texas Southwestern Medical Center; J.M.F., The Rockefeller University; and M.H.T., Institute for Diabetes and Obesity, Helmholtz Center Munich.</notes><notes>Contributed by Tomas G. M. Hökfelt, June 22, 2015 (sent for review February 11, 2015; reviewed by Joel K. Elmquist, Jeffrey M. Friedman, and Matthias H. Tschöp)</notes><notes>Author contributions: I.V.-A. and C.B. designed research; I.V.-A., T.D., and C.B. performed research; K.B., T.H., T.G.M.H., and C.B. contributed new reagents/analytic tools; I.V.-A., T.D., K.B., T.H., S.O.Ö., T.G.M.H., and C.B. analyzed data; and I.V.-A., T.G.M.H., and C.B. wrote the paper.</notes><abstract>Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the solubleN-ethylmaleimide–sensitive factor attachment protein (SNARE) complex mediating fast Ca2+-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process. Here we explore the hypothesis that minor alterations in the machinery mediating regulated membrane fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabetes. Thus, we used a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a. These SNAP-25b–deficient mice were exposed to either a control or a high-fat/high-sucrose diet. Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b–deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. Our SNAP-25b–deficient mouse may represent a diabesity model.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>26195742</pmid><doi>10.1073/pnas.1511951112</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes - metabolism Adipocytes - pathology Adipose Tissue, White - metabolism Adipose Tissue, White - pathology Adiposity Animals Biological Sciences Blood Glucose - metabolism Body Weight Dyslipidemias - pathology Energy Intake Energy Metabolism Feeding Behavior Female Homeostasis Hormones Hyperglycemia Hypertrophy Hypothalamus - metabolism Insulin - metabolism Insulin Secretion Leptin - blood Lipids Liver - metabolism Liver - pathology Male Medicin och hälsovetenskap Metabolic Diseases - blood Metabolic Diseases - metabolism Mice, Obese Neurotransmitters Phenotype PNAS Plus Proteins Receptors, Leptin - metabolism Rodents Synaptosomal-Associated Protein 25 - deficiency Synaptosomal-Associated Protein 25 - metabolism |
| title | Replacing SNAP-25b with SNAP-25a expression results in metabolic disease |
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