Glycoprotein biosynthesis during inflammation in normal and streptozotocin-induced diabetic rats.

Extracellular glycoproteins play an important role in wound healing; yet little is known about glycoprotein biosynthesis and its regulation by insulin in inflammation. Using [1-14C] fucose as a marker, glycoprotein biosynthesis was studied in carrageenan-induced granuloma from diabetic and control rats. Fucose incorporation into glycoproteins was followed for 24 h after an intraperitoneal injection of the label. Radioactivity in trichloroacetic acid precipitable serum glycoproteins and saline-soluble and insoluble glycoproteins was assessed in five-, seven-, and ten-day-old granuloma tissues. Fucose incorporation was higher in soluble glycoproteins (P less than 0.01) at all points in controls than in diabetic granulomas, and peak incorporation was reached in both groups on the seventh day. Incorporation of fucose into insoluble glycoproteins was higher in normals on the seventh day than in diabetics. Liver-, kidney-, and intestine-soluble glycoproteins showed a maximum incorporation on the seventh day, but no difference was noted between diabetic and normal rats. Incorporation of fucose in insoluble glycoproteins showed a gradual decline with the age of granuloma in all tissues from both groups, with the exception of the kidney. In the kidney, fucosylation of insoluble glycoproteins was decreased (P less than 0.01) in diabetics compared to controls. These results indicate an active phase of biosynthesis, with an increase in glycosylation during inflammation that is probably insulin dependent.