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@ARTICLE{Wolff:141735,
      author       = {G. Wolff$^*$ and A. E. Taranko$^*$ and I. Meln$^*$ and J.
                      Weinmann$^*$ and T. Sijmonsma and S. Lerch and D. Heide$^*$
                      and A. T. Billeter and D. Tews and D. Krunic$^*$ and P.
                      Fischer-Posovszky and B. P. Müller-Stich and S. Herzig and
                      D. Grimm and M. Heikenwälder$^*$ and W. W. Kao and A.
                      Vegiopoulos$^*$},
      title        = {{D}iet-dependent function of the extracellular matrix
                      proteoglycan {L}umican in obesity and glucose homeostasis.},
      journal      = {Molecular metabolism},
      volume       = {19},
      issn         = {2212-8778},
      address      = {Oxford [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2018-02004},
      pages        = {97-106},
      year         = {2019},
      note         = {EA:A171LA:A171},
      abstract     = {Extracellular matrix remodeling is required for adipose
                      expansion under increased caloric intake. In turn, inhibited
                      expandability due to aberrant collagen deposition promotes
                      insulin resistance and progression towards the metabolic
                      syndrome. An emerging role for the small leucine-rich
                      proteoglycan Lumican in metabolically driven nonalcoholic
                      fatty liver disease sparks an interest in further
                      understanding its role in diet-induced obesity and metabolic
                      complications.Whole body ablation of Lumican (Lum-/-) gene
                      and adeno-associated virus-mediated over-expression were
                      used in combination with control or high fat diet to assess
                      energy balance, glucose homeostasis as well as adipose
                      tissue health and remodeling.Lumican was found to be
                      particularly enriched in the stromal cells isolated from
                      murine gonadal white adipose tissue. Likewise murine and
                      human visceral fat showed a robust increase in Lumican as
                      compared to fat from the subcutaneous depot. Lumican null
                      female mice exhibited moderately increased fat mass,
                      decreased insulin sensitivity and increased liver
                      triglycerides in a diet-dependent manner. These changes
                      coincided with inflammation in adipose tissue and no overt
                      effects in adipose expandability, i.e. adipocyte formation
                      and hypertrophy. Lumican over-expression in visceral fat and
                      liver resulted in improved insulin sensitivity and glucose
                      clearance.These data indicate that Lumican may represent a
                      functional link between the extracellular matrix, glucose
                      homeostasis, and features of the metabolic syndrome.},
      cin          = {A171 / W210 / F180},
      ddc          = {610},
      cid          = {I:(DE-He78)A171-20160331 / I:(DE-He78)W210-20160331 /
                      I:(DE-He78)F180-20160331},
      pnm          = {323 - Metabolic Dysfunction as Risk Factor (POF3-323)},
      pid          = {G:(DE-HGF)POF3-323},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30409703},
      doi          = {10.1016/j.molmet.2018.10.007},
      url          = {https://inrepo02.dkfz.de/record/141735},
}