Protective role of osteocalcin in diabetes pathogenesis
- PDF / 684,141 Bytes
- 7 Pages / 595.276 x 790.866 pts Page_size
- 18 Downloads / 203 Views
REVIEW ARTICLE
Protective role of osteocalcin in diabetes pathogenesis María Fernanda Desentis‑Desentis1,2 · Jorge David Rivas‑Carrillo1,2 · Sergio Sánchez‑Enríquez3 Received: 19 May 2020 / Accepted: 8 July 2020 © The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020
Abstract In diabetes, metabolic, inflammatory, and stress-associated alterations conduce to ß-cell failure and tissue damage. Osteocalcin is a bone protein with several endocrine functions in different tissues. In this review, we gathered scientific evidence of how osteocalcin could modulate functional disorders that are altered in diabetes in an integrative way. We include adipose tissue, pancreatic function, and oxidative stress aspects. In the first section, we focus on the role of inflammatory mediators and adiponectin in energy homeostasis and insulin sensitivity. In the following section, we discuss the effect of osteocalcin in metabolic and pancreatic function and its association in insulin signaling and in ß-cell proliferation. Finally, we focus on osteocalcin action in oxidative and endoplasmic reticulum stress, and in antioxidant regulation, since ß-cells are well known by its vulnerability to stress damage. These evidences support the notion that osteocalcin could have an important role in diabetes treatment. Keywords Diabetes · Bone metabolism · Osteocalcin · Oxidative stress
Introduction Diabetes is characterized for the lack of insulin secretion and/or the decrease in insulin sensitivity. In diabetes, genetic and environmental factors have a crucial role in the vulnerability of pancreatic cells to the loss of function and destruction of ß-cells, this condition develops as a consequence of multiple metabolic alterations, inflammatory, hormonal, and stress-related effects [1–3]. In obesity, the disturbed remodeling of adipose tissue triggers changes in its secretory and metabolic activity, these changes induce the release of metabolites and adipokines that perturbed the inflammatory balance and the integration of signals in the adipose tissue [4]. Macrophages recruited * Sergio Sánchez‑Enríquez [email protected]; [email protected] 1
Laboratory of Tissue Engineering and Transplant, Department of Physiology, University Center for Health Sciences, University de Guadalajara, 950 Sierra Mojada St., Col. Independencia, C.P. 44340 Guadalajara, Jalisco, Mexico
2
cGMP Cell Processing Facility, University Center for Health Sciences, University of Guadalajara, 950 Sierra Mojada St., Col. Independencia, C.P. 44340 Guadalajara, Jalisco, Mexico
3
Department of Clinics, University Center of Los Altos, University of Guadalajara, 1200 Rafael Casillas Ave, ZC47620 Tepatitlán de Morelos, Jalisco, Mexico
are an important source of pro-inflammatory cytokines, which in turn, are associated with adipokines (leptin and adiponectin) imbalance [5]. Adipose tissue cytokines act systemically to inhibit insulin secretion and sensibility, among these are: TNFα, IL1ß, IL6, and IL10 [6,7]. Ab
Data Loading...
