@article{Heiker-2014-ID6,
  title     = {Identification of genetic loci associated with different responses to
               high-fat diet-induced obesity in C57{BL}/6N and C57{BL}/6J substrains.},
  abstract  = {We have recently demonstrated that C57{BL}/6{NT}ac and C57{BL}/6{JR}j
               substrains are significantly different in their response to high-fat
               diet-induced obesity ({DIO}). The C57{BL}/6{JR}j substrain seems to be
               protected from {DIO} and genetic differences between C57{BL}/6J and
               C57{BL}/6N substrains at 11 single nucleotide polymorphism ({SNP}) loci
               have been identified. To define genetic variants as well as differences in
               parameters of glucose homeostasis and insulin sensitivity between
               C57{BL}/6{NT}ac and C57{BL}/6{JR}j substrains that may explain the
               different response to {DIO}, we analyzed 208 first backcross ({BC}1)
               hybrids of C57{BL}/6{NT}ac and C57{BL}/6{JR}j [(C57{BL}/6{NT}ac ×
               C57{BL}/6{JR}j)F1 × C57{BL}/6{NT}ac] mice. Body weight, epigonadal and
               subcutaneous fat mass, circulating leptin, as well as parameters of glucose
               metabolism were measured after 10 wk of high-fat diet ({HFD}). Genetic
               profiling of {BC}1 hybrids were performed using TaqMan {SNP} genotyping
               assays. Furthermore, to assess whether {SNP} polymorphisms could affect
               m{RNA} level, we carried out gene expression analysis in murine liver
               samples. Human subcutaneous adipose tissue was used to verify murine data
               of {SNAP}29. We identified four sex-specific variants that are associated
               with the extent of {HFD}-induced weight gain and fat depot mass. {BC}1
               hybrids carrying the combination of risk or beneficial alleles exhibit the
               phenotypical extremes of the parental strains. Murine and human {SC}
               expression analysis revealed Snap29 as strongest candidate. Our data
               indicate an important role of these loci in responsiveness to {HFD}-induced
               obesity and suggest genes of the synaptic vesicle release system such as
               Snap29 being involved in the regulation of high-fat {DIO}.},
  author    = {Heiker, John T and Kunath, Anne and Kosacka, Joanna and Flehmig, Gesine and
               Knigge, Anja and Kern, Matthias and Stumvoll, Michael and Kovacs, Peter and
               Blüher, Matthias and Klöting, Nora},
  volume    = {46},
  number    = {11},
  pages     = {377--84},
  year      = {2014},
  month     = {6},
  url       = {http://www.pubmed.org/24692188},
  pmid      = {24692188},
  doi       = {10.1152/physiolgenomics.00014.2014},
  keywords  = {Animals, Humans, Mice, Male, Adipose Tissue, Alleles, Body Weight, Diet,
               High-Fat, Female, Genetic Loci, Genotype, Glucose, Leptin, Mice, Inbred
               C57{BL}, Middle Aged, Obesity, Polymorphism, Single Nucleotide, Vesicular
               Transport Proteins, Weight Gain},
  file      = {FULLTEXT:pdfs/000/000/000000006.pdf:PDF}
}

{"_id":"26CiiRWRSx2Wzxvv4","bibbaseid":"heiker-kunath-kosacka-flehmig-knigge-kern-stumvoll-kovacs-etal-identificationofgeneticlociassociatedwithdifferentresponsestohighfatdietinducedobesityinc57bl6nandc57bl6jsubstrains-2014","authorIDs":[],"author_short":["Heiker, J. T","Kunath, A.","Kosacka, J.","Flehmig, G.","Knigge, A.","Kern, M.","Stumvoll, M.","Kovacs, P.","Blüher, M.","Klöting, N."],"bibdata":{"bibtype":"article","type":"article","title":"Identification of genetic loci associated with different responses to high-fat diet-induced obesity in C57BL/6N and C57BL/6J substrains.","abstract":"We have recently demonstrated that C57BL/6NTac and C57BL/6JRj substrains are significantly different in their response to high-fat diet-induced obesity (DIO). The C57BL/6JRj substrain seems to be protected from DIO and genetic differences between C57BL/6J and C57BL/6N substrains at 11 single nucleotide polymorphism (SNP) loci have been identified. To define genetic variants as well as differences in parameters of glucose homeostasis and insulin sensitivity between C57BL/6NTac and C57BL/6JRj substrains that may explain the different response to DIO, we analyzed 208 first backcross (BC1) hybrids of C57BL/6NTac and C57BL/6JRj [(C57BL/6NTac × C57BL/6JRj)F1 × C57BL/6NTac] mice. Body weight, epigonadal and subcutaneous fat mass, circulating leptin, as well as parameters of glucose metabolism were measured after 10 wk of high-fat diet (HFD). Genetic profiling of BC1 hybrids were performed using TaqMan SNP genotyping assays. Furthermore, to assess whether SNP polymorphisms could affect mRNA level, we carried out gene expression analysis in murine liver samples. Human subcutaneous adipose tissue was used to verify murine data of SNAP29. We identified four sex-specific variants that are associated with the extent of HFD-induced weight gain and fat depot mass. BC1 hybrids carrying the combination of risk or beneficial alleles exhibit the phenotypical extremes of the parental strains. Murine and human SC expression analysis revealed Snap29 as strongest candidate. Our data indicate an important role of these loci in responsiveness to HFD-induced obesity and suggest genes of the synaptic vesicle release system such as Snap29 being involved in the regulation of high-fat DIO.","author":[{"propositions":[],"lastnames":["Heiker"],"firstnames":["John","T"],"suffixes":[]},{"propositions":[],"lastnames":["Kunath"],"firstnames":["Anne"],"suffixes":[]},{"propositions":[],"lastnames":["Kosacka"],"firstnames":["Joanna"],"suffixes":[]},{"propositions":[],"lastnames":["Flehmig"],"firstnames":["Gesine"],"suffixes":[]},{"propositions":[],"lastnames":["Knigge"],"firstnames":["Anja"],"suffixes":[]},{"propositions":[],"lastnames":["Kern"],"firstnames":["Matthias"],"suffixes":[]},{"propositions":[],"lastnames":["Stumvoll"],"firstnames":["Michael"],"suffixes":[]},{"propositions":[],"lastnames":["Kovacs"],"firstnames":["Peter"],"suffixes":[]},{"propositions":[],"lastnames":["Blüher"],"firstnames":["Matthias"],"suffixes":[]},{"propositions":[],"lastnames":["Klöting"],"firstnames":["Nora"],"suffixes":[]}],"volume":"46","number":"11","pages":"377–84","year":"2014","month":"6","url":"http://www.pubmed.org/24692188","pmid":"24692188","doi":"10.1152/physiolgenomics.00014.2014","keywords":"Animals, Humans, Mice, Male, Adipose Tissue, Alleles, Body Weight, Diet, High-Fat, Female, Genetic Loci, Genotype, Glucose, Leptin, Mice, Inbred C57BL, Middle Aged, Obesity, Polymorphism, Single Nucleotide, Vesicular Transport Proteins, Weight Gain","file":"FULLTEXT:pdfs/000/000/000000006.pdf:PDF","bibtex":"@article{Heiker-2014-ID6,\n title = {Identification of genetic loci associated with different responses to\n high-fat diet-induced obesity in C57{BL}/6N and C57{BL}/6J substrains.},\n abstract = {We have recently demonstrated that C57{BL}/6{NT}ac and C57{BL}/6{JR}j\n substrains are significantly different in their response to high-fat\n diet-induced obesity ({DIO}). The C57{BL}/6{JR}j substrain seems to be\n protected from {DIO} and genetic differences between C57{BL}/6J and\n C57{BL}/6N substrains at 11 single nucleotide polymorphism ({SNP}) loci\n have been identified. To define genetic variants as well as differences in\n parameters of glucose homeostasis and insulin sensitivity between\n C57{BL}/6{NT}ac and C57{BL}/6{JR}j substrains that may explain the\n different response to {DIO}, we analyzed 208 first backcross ({BC}1)\n hybrids of C57{BL}/6{NT}ac and C57{BL}/6{JR}j [(C57{BL}/6{NT}ac ×\n C57{BL}/6{JR}j)F1 × C57{BL}/6{NT}ac] mice. Body weight, epigonadal and\n subcutaneous fat mass, circulating leptin, as well as parameters of glucose\n metabolism were measured after 10 wk of high-fat diet ({HFD}). Genetic\n profiling of {BC}1 hybrids were performed using TaqMan {SNP} genotyping\n assays. Furthermore, to assess whether {SNP} polymorphisms could affect\n m{RNA} level, we carried out gene expression analysis in murine liver\n samples. Human subcutaneous adipose tissue was used to verify murine data\n of {SNAP}29. We identified four sex-specific variants that are associated\n with the extent of {HFD}-induced weight gain and fat depot mass. {BC}1\n hybrids carrying the combination of risk or beneficial alleles exhibit the\n phenotypical extremes of the parental strains. Murine and human {SC}\n expression analysis revealed Snap29 as strongest candidate. Our data\n indicate an important role of these loci in responsiveness to {HFD}-induced\n obesity and suggest genes of the synaptic vesicle release system such as\n Snap29 being involved in the regulation of high-fat {DIO}.},\n author = {Heiker, John T and Kunath, Anne and Kosacka, Joanna and Flehmig, Gesine and\n Knigge, Anja and Kern, Matthias and Stumvoll, Michael and Kovacs, Peter and\n Blüher, Matthias and Klöting, Nora},\n volume = {46},\n number = {11},\n pages = {377--84},\n year = {2014},\n month = {6},\n url = {http://www.pubmed.org/24692188},\n pmid = {24692188},\n doi = {10.1152/physiolgenomics.00014.2014},\n keywords = {Animals, Humans, Mice, Male, Adipose Tissue, Alleles, Body Weight, Diet,\n High-Fat, Female, Genetic Loci, Genotype, Glucose, Leptin, Mice, Inbred\n C57{BL}, Middle Aged, Obesity, Polymorphism, Single Nucleotide, Vesicular\n Transport Proteins, Weight Gain},\n file = {FULLTEXT:pdfs/000/000/000000006.pdf:PDF}\n}\n\n","author_short":["Heiker, J. 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