After bariatric surgery (BS), there is an increased risk of bone health issues due to restricted nutrient intake, malabsorption, insufficient supplement adherence, and reduced mechanical loading from significant weight loss. We aimed to provide a review of the current understanding of post-BS human physiology and the relevant animal models employed to investigate bone metabolism. Muscle-derived signals influence bone metabolism through mechanisms beyond just mechanical forces, highlighting the relevance of skeletal muscle as an endocrine organ to regulate bone health. BS patients often have high parathyroid hormone (PTH) due to calcium and vitamin D deficiency, which inhibits bone formation. Bone, muscle, and fat tissues communicate via cytokines, and myostatin negatively affects bone by increasing sclerostin, Dickkopf-1, and nuclear factor kappa β ligand, leading to higher bone resorption. Moreover, BS leads to changes in gastrointestinal signaling and gut peptides like glucagon-like peptides (GLP)-1 and peptide YY (PYY). Additionally, exercise may impact bone hormonal signaling, potentially lowering sclerostin and linking mechanical loading to osteoporosis. Nevertheless, there remains limited evidence regarding the association between bone remodeling and changes in these proteins post-BS. As outlined, future studies are required to validate findings from preclinical models and to adequately test these hypotheses in humans, especially regarding a better understanding of cytokines, ghrelin, sclerostin, PTH, cholecystokinin, GLP-1, and PYY physiology, their roles in obesity and BS, and their therapeutic potentials.
Borges et al. (2026) studied this question.