The Contribution of Alcohol Dehydrogenase 3 to the Development of Alcoholic Osteoporosis in Mice.

CONCLUSIONS: The Adh3-/- control mice exhibited a high turnover of osteoporosis since osteoclastogenesis dominated osteoblastogenesis; however, bone resorption was not enhanced after CAC. In comparison, CAC lead to alcoholic osteoporosis in WT mice, accompanied by increased mRNA levels of ADH3. Hence, ADH3 can prevent osteoporosis development in normal ADH genotypes with no alcohol ingestion. However, ADH3 contributes to the development of alcoholic osteoporosis under CAC by participating in alcohol metabolism, increasing metabolic toxicity, and lowering GSNO reducing activity. PMID: 30568058 [PubMed - in process]

https://www.ncbi.nlm.nih.gov/pubmed/30568058?dopt=Abstract

Source: Journal of Nippon Medical School - December 21, 2018 Category: Universities & Medical Training Authors: Okuda T, Naruo M, Iijima O, Igarashi T, Katsuyama M, Maruyama M, Akimoto T, Ohno Y, Haseba T Tags: J Nippon Med Sch Source Type: research