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The potential function of syndecans in triglyceride metabolism are explored and it is found that syndecan-1 and syndecan-4 are expressed by adipocytes in adipose tissue and by 3T3-L1 adipocytes and are shed as soluble ectodomains in the extracellular space by insulin-stimulated 3T3-L1 adipocytes. The studies have shown that syndecan extodomains, shed by adipocytes in response to insulin, are physiological extracellular chaperons for lipoprotein lipase as it translocates from its site of synthesis to its site of action.

The identification of robust alpha oxidation of unbranched long chain fatty acids in a mammalian cell line and the obligatory sequential ordered alpha oxidation of fatty acids prior to their delta9 desaturation is studied. The results show that proximal peroxisomal fatty acids are an important metabolic determinant of the lipid content in the differentiating adipocyte.

The identification of robust alpha oxidation of unbranched long chain fatty acids in a mammalian cell line and the obligatory sequential ordered alpha oxidation of fatty acids prior to their delta9 desaturation is studied. The results show that proximal peroxisomal fatty acids are an important metabolic determinant of the lipid content in the differentiating adipocyte.

Lipid rafts are detergent-insoluble membrane domains that play a key role in signal transduction by the T-cell antigen receptor. Proteome analysis revealed the presence of amidosulfobetaine-soluble signal transducing, integral membrane, cytoskeletal, heat shock, and GTP-binding proteins in rafts prepared from Jurkat cells. Several of these proteins were recruited to rafts by CD3/CD28 costimulation. Of particular interest is the inducible association of activated IkappaB kinase complexes with raft vesicles that could be captured with anti-flotillin-1 antibodies. Following amidosulfobetaine solubilization, flotillin-beta and IKKbeta underwent reciprocal co-immunoprecipitation. Treatment of Jurkat cells with methyl-beta-cyclodextrin disrupted the assembly and activation of this raft complex and also interfered in CD3/ CD28-induced activation of a NF-kappaB response element in the IL-2 promoter.