Adiponectin signalling in bone homeostasis, with age and in disease

Abstract

Adiponectin is the most abundant circulating adipokine and is primarily involved in glucose metabolism and insulin resistance. Within the bone, osteoblasts and osteoclasts express the adiponectin receptors, however, there are conflicting reports on the effects of adiponectin on bone formation and turnover. Many studies have shown a pro-osteogenic role for adiponectin in in vivo murine models and in vitro: with increased osteoblast differentiation and activity, alongside lower levels of osteoclastogenesis. However, human studies often demonstrate an inverse relationship between adiponectin concentration and bone activity. Moreover, the presence of multiple isoforms of adiponectin and multiple receptor subtypes has the potential to lead to more complex signalling and functional consequences. As such, we still do not fully understand the importance of the adiponectin signalling pathway in regulating bone homeostasis and repair in health, with age and in disease. In this review, we explore our current understanding of adiponectin bioactivity in the bone; the significance of its different isoforms; and how adiponectin biology is altered in disease. Ultimately, furthering our understanding of adiponectin regulation of bone biology is key to developing pharmacological and non-pharmacological (lifestyle) interventions that target adiponectin signalling to boost bone growth and repair in healthy ageing, following injury or in disease.

Electrophoretic deposition of silk fibroin coatings with pre-defined architecture to facilitate precise control over drug delivery

“…bm SF has recently attracted attention for biomacromolecule delivery due to its stabilizing effect on sensitive biological compounds (e.g. antibiotics) [ 24 ] and its hypoallergenicity [ 25 , 26 ]. However, bm SF molecules do not contain cell recognition motifs, such as arginylglycylaspartic acid (RGD), which facilitates cell adhesion and spreading.…”

Genome-Wide Association Study Identifies Candidate Genes Associated with Feet and Leg Conformation Traits in Chinese Holstein Cattle

“…Adiponectin receptor 2 (ADIPOR2) is a member of the adipocytokines gene family. Generally, adiponectin receptor genes play an important role in bone and whole-body energy homeostasis that could be induced by activation of the AMPK signaling pathway; ADIPOR1 and ADIPOR2 also play a crucial role in metabolic pathways, which lead to the regulation of lipid and glucose metabolism, oxidative stress and inflammation [49]. Ouyang et al [50] reported ADIPOR2 has a role in intramuscular fat content in the longissimus dorsi (LD) muscle of different pig breeds.…”

“…Ouyang et al [50] reported ADIPOR2 has a role in intramuscular fat content in the longissimus dorsi (LD) muscle of different pig breeds. Lewis et al [49] discussed in detail the role of adiponectin signaling in bone homeostasis and its effect on the lifestyle of human healthy aging and disease. Moreover, ADIPOR2 is considered to be one of the genes associated with conformation and reproductive performance traits (hip height, rump length, calving ease, height, ovulation, type and rump angle) in one of the South African cattle breeds [51].…”

Multifunctional and Self-Healable Intelligent Hydrogels for Cancer Drug Delivery and Promoting Tissue Regeneration In Vivo

“…Extracellular matrix (ECM) bone mainly comprises of 0–70% primarily inorganic hydroxyapatite (HAp), 20–40% organic constituents (primarily type I collagen), 5–10% water, and 3% lipid and proteins such as growth factors [ 25 ]. Conventional bone treatment methods, including autografts, allografts, and xenografts, are restricted due to their potential infection, risks of donor-site morbidity, high nonunion rate with host tissues, and adverse immune response [ 58 ].…”

“…The structure of intelligent hydrogels can be altered by different types of stimuli from internal (e.g., in-body) or external (i.e., out-body) sources. Internal and external sources are classified as biological, physical, and chemical [ 25 ].…”