Organogenesis of the colon in rats

Colonic organogenesis in rats was studied using light microscopic techniques for the demonstration of mucosubstances, glycogen, and connective tissue fibers. Crypts began as intraepithelial spaces which were in continuity with the colonic lumen. The cells forming the floors of these spaces invaded the nonsulfated acid glycosaminoglycan-rich mesenchyme as the basement membrane became discontinuous. As the diameter of the colon increased, the crypts lengthened and the lamina propria thickened until a layer of collagen and sulfated acid glycosaminoglycans formed at the bases of the crypts and the basement membrane was reestablished. The circular layer of the muscularis externa developed first, then the longitudinal layer, and finally the muscularis mucosae. Three types of mucous cells arose in these newly formed crypts. The initial epithelial cell type contained glycogen and gave rise to cells with apical coats of nonsulfated acid glycoproteins. This cell type was followed by the appearance of cells at the bases of the crypts containing nonsulfated acid glycoproteins. As the crypts lengthened, the goblet cells near the base contained nonsulfated and/or sulfated acid glycoproteins. Closer to and on the surface, the cells contained sulfated acid glycoproteins, a mixture of sulfated acid and neutral glycoproteins, or just neutral glycoproteins. Striated-border cells appeared intermingled with the mucous cells close to the bases of the crypts and continued onto the surface. A comparison was made between regeneration following placement of a surgical lesion in adult rats and events in organogenesis of the colon.     

Gluconeogenesis in the liver of arthritic rats

The gluconeogenic response in the liver from rats with chronic arthritis to various substrates and the effects of glucagon were investigated. The experimental technique used was the isolated liver perfusion. Hepatic gluconeogenesis in arthritic rats was generally lower than in normal rats. The difference between normal and arthritic rats depended on the gluconeogenic substrate. In the absence of glucagon the following sequence of decreasing differences was found: alanine (-71.8 per cent) reverse similarglutamine (-71.7 per cent)>pyruvate (-60 per cent)>lactate+pyruvate (-44.9 per cent)>xylitol (n.s.=non-significant) reverse similarglycerol (n.s.). For most substrates glucagon increased hepatic gluconeogenesis in both normal and arthritic rats. The difference between normal and arthritic rats, however, tended to diminish, as revealed by the data of the following sequence: alanine (-48.9 per cent) reverse similarpyruvate (-47.6 per cent)>glutamine (-33.8 per cent)>glycerol (n.s.) reverse similarlactate+pyruvate (n.s.) reverse similarxylitol (n.s.). The causes for the reduced hepatic gluconeogenesis in arthritic rats are probably related to: (a) lower activities of key enzymes catalyzing most probably steps preceding phosphoenolpyruvate (e.g. phosphoenolpyruvate carboxykinase, pyruvate carboxylase, etc. ); (b) a reduced availability of reducing equivalents in the cytosol; (c) specific differences in the situations induced by hormones or by the individual substrates. Since glycaemia is almost normal in chronically arthritic rats, it seems that lower gluconeogenesis is actually adapted to the specific needs of these animals.