As examples, suppressed osteoblast activity and reduced bone formation rates during diabetes were increased in vivo by oral administration of non-antimicrobial TCs (82, 85); evidence suggests that an increase in steady-state levels of type I procollagen mRNA and accelerated collagen synthesis provides one mechanism by which TCs counteract the loss of collagen (or atrophy) which occurs as a complication of diabetes in bone and other tissues such as skin (86). The gene discussed is COL1A2; the disease is diabetes mellitus.