Role of estrogens in the control of skeletal muscle mass in a model of fetal programming of vitamin D deficiency.

• Grant number: 25/24374-4
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: December 01, 2025
• End date: November 30, 2026
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Luiz Carlos Carvalho Navegantes
• Grantee: Bianca Bozzi
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated research grant: 24/12709-9 - cAMP AS A THERAPEUTIC TARGET FOR MUSCLE ATROPHY, AP.TEM

Abstract

Calcitriol is the active form of vitamin D whose classic function is the control of osteomineral metabolism (Front Biosci 2024;29(8):281). A large part of the effects of this hormone are mediated by the activation of its nuclear receptor (VDR), a target of CREB, whose gene expression has already been identified in the skeletal muscle of rodents and humans (Endocrinology 2014;155(9):3227-37). Our group demonstrated that maternal vitamin D deficiency induces muscle atrophy in the offspring of male rats at weaning. In adulthood, these animals exhibit compensatory muscle hypertrophy associated with increased local synthesis of calcitriol in the muscle. These changes were not observed in female offspring, demonstrating a clear sexual dimorphism in fetal muscle programming induced by vitamin D deficiency (J Cachexia Sarcopenia Muscle. 2022;13(4):2175-2187). The mechanisms involved in the differences between males and females have not been elucidated, but it has been hypothesized that ovarian hormones attenuate the muscle changes induced by this nutritional deficiency in females. (AU)