Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Pinent, M; Prokesch, A; Hackl, H; Voshol, PJ; Klatzer, A; Walenta, E; Panzenboeck, U; Kenner, L; Trajanoski, Z; Hoefler, G; Bogner-Strauss, JG.
Adipose triglyceride lipase and hormone-sensitive lipase are involved in fat loss in JunB-deficient mice.
Endocrinology. 2011; 152(7):2678-2689 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Hoefler Gerald
Kenner Lukas
Panzenboeck Ute
Prokesch Andreas

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Number of Figures: 6
| | | | | |
Proteins of the activator protein-1 family are known to have roles in many physiological processes such as proliferation, apoptosis, and inflammation. However, their role in fat metabolism has yet to be defined in more detail. Here we study the impact of JunB deficiency on the metabolic state of mice. JunB knockout (JunB-KO) mice show markedly decreased weight gain, reduced fat mass, and a low survival rate compared with control mice. If fed a high-fat diet, the weight gain of JunB-KO mice is comparable to control mice and the survival rate improves dramatically. Along with normal expression of adipogenic marker genes in white adipose tissue (WAT) of JunB-KO mice, this suggests that adipogenesis per se is not affected by JunB deficiency. This is supported by in vitro data, because neither JunB-silenced 3T3-L1 cells nor mouse embryonic fibroblasts from JunB-KO mice show a change in adipogenic potential. Interestingly, the key enzymes of lipolysis, adipose triglyceride lipase and hormone-sensitive lipase, were significantly increased in WAT of fasted JunB-KO mice. Concomitantly, the ratio of plasma free fatty acids per gram fat mass was increased, suggesting an elevated lipolytic rate under fasting conditions. Furthermore, up-regulation of TNFα and reduced expression of perilipin indicate that this pathway is also involved in increased lipolytic rate in these mice. Additionally, JunB-KO mice are more insulin sensitive than controls and show up-regulation of lipogenic genes in skeletal muscle, indicating a shuttling of energy substrates from WAT to skeletal muscle. In summary, this study provides valuable insights into the impact of JunB deficiency on the metabolic state of mice.
Find related publications in this database (using NLM MeSH Indexing)
3T3-L1 Cells -
Adipocytes, White - cytology Adipocytes, White - metabolism
Adiposity -
Animals -
Carrier Proteins -
Crosses, Genetic -
Dietary Fats - administration & dosage
Gene Expression Regulation -
Growth Disorders - diet therapy Growth Disorders - genetics Growth Disorders - metabolism Growth Disorders - mortality
Insulin Resistance -
Lipase - genetics Lipase - metabolism
Lipolysis -
Male -
Mice -
Mice, Knockout -
Muscle, Skeletal - metabolism
Phosphoproteins - genetics Phosphoproteins - metabolism
Protein Isoforms - genetics Protein Isoforms - physiology
Proto-Oncogene Proteins c-jun - genetics Proto-Oncogene Proteins c-jun - physiology
Sterol Esterase - genetics Sterol Esterase - metabolism
Survival Analysis -
Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism

© Med Uni Graz Impressum