Anti-ST3GAL5 (aa 31-117) polyclonal antibody

AIMS: The association between central obesity and insulin resistance reflects the properties of visceral adipose tissue. Our aim was to gain further insight into this association by analysing the lipid composition of subcutaneous and omental adipose tissue in obese women with and without insulin resistance. METHODS: Subcutaneous and omental adipose tissue and serum were obtained from 29 obese non-diabetic women, 13 of whom were hyperinsulinemic. Histology, lipid and gene profiling were performed. RESULTS: In omental adipose tissue of obese, insulin-resistant women, adipocyte hypertrophy and macrophage infiltration were accompanied by an increase in G(M3) ganglioside and its synthesis enzyme ST3GAL5; in addition, phosphatidylethanolamine (PE) lipids were increased and their degradation enzyme, phosphatidylethanolamine methyl transferase (PEMT), decreased. ST3GAL5 was expressed predominantly in adipose stromovascular cells and PEMT in adipocytes. Insulin resistance was also associated with an increase in PE lipids in serum. INTERPRETATION: The relevance of these findings to insulin resistance in humans is supported by published mouse studies, in which adipocyte G(M3) ganglioside, increased by the inflammatory cytokine tumour necrosis factor-alpha, impaired insulin action and PEMT was required for adipocyte lipid storage. Thus in visceral adipose tissue of obese humans, an increase in G(M3) ganglioside secondary to inflammation may contribute to insulin resistance and a decrease in PEMT may be a compensatory response to adipocyte hypertrophy.

The existence and treatment of rectal cancer are important for the function of defecation and the quality of life. However, the precise mechanisms of rectal carcinogenesis remain unclear. To screen the overexpressed gene in rectal carcinoma, we performed suppressive subtractive hybridization (SSH) on rectal carcinoma cells and the corresponding normal rectal cells. A total of 64 recombinant clones were subjected to DNA sequencing analysis, and 9 known genes were found to overexpressed in the tumors compared with those of the normal tissues. The genes are ST3 beta-galactoside alpha-2,3-sialyltransferase (ST3GAL5), interferon-induced transmembrane protein 3 (IFITM3), platelet-derived growth factor A-associated protein 1 (PDAP1), AlkB alkylating repair homolog 3 (ALKBH3), nucleoside diphosphate linked moiety X (Nudix)-type motif 14 (NUDT14), calponin 2 (CNN2), mitogen-activated protein kinase 14 (MAPK14), aconitase 1 (ACO1), and selenophosphate synthetase 1 (SEPHS1). The expression profiles of the genes were further confirmed in rectal carcinoma cells and the corresponding normal rectal cells of 12 patients by quantitative real-time RT-PCR. Our results revealed that ST3GAL5, IFITM3, PDAP1, ALKBH3, NUDT14, CNN2, MAPK14, ACO1, and SEPHS1 may be involved in rectal carcinogenesis.