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  • 1
    Publication Date: 1993-01-01
    Description: Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Shargill, N S -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):87-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678183" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipose Tissue/physiology/*physiopathology ; Animals ; Blood Glucose/metabolism ; Blotting, Northern ; Diabetes Mellitus, Experimental/physiopathology ; Glucose Clamp Technique ; Homeostasis ; Immunoglobulin G/genetics/pharmacology ; Insulin/pharmacology ; Insulin Infusion Systems ; Insulin Resistance/*genetics ; Male ; Mice ; Mice, Obese ; Obesity/chemically induced/*genetics/*physiopathology ; RNA/genetics/isolation & purification ; RNA, Messenger/*biosynthesis/isolation & purification ; Rats ; Rats, Zucker ; Receptors, Cell Surface/genetics/physiology ; Receptors, Tumor Necrosis Factor ; Recombinant Fusion Proteins/pharmacology ; Reference Values ; Sodium Glutamate ; Tumor Necrosis Factor-alpha/biosynthesis/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1996-12-20
    Description: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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