Bones and Hormones: Interaction between Hormones of the Hypothalamus, Pituitary, Adipose Tissue and Bone

Abstract

The bony skeleton, as a structural foundation for the human body, is essential in providing mechanical function and movement. The human skeleton is a highly specialized and dynamic organ that undergoes continuous remodeling as it adapts to the demands of its environment. Advances in research over the last decade have shone light on the various hormones that influence this process, modulating the metabolism and structural integrity of bone. More recently, novel and non-traditional functions of hypothalamic, pituitary, and adipose hormones and their effects on bone homeostasis have been proposed. This review highlights recent work on physiological bone remodeling and discusses our knowledge, as it currently stands, on the systemic interplay of factors regulating this interaction. In this review, we provide a summary of the literature on the relationship between bone physiology and hormones including kisspeptin, neuropeptide Y, follicle-stimulating hormone (FSH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), growth hormone (GH), leptin, and adiponectin. The discovery and understanding of this new functionality unveils an entirely new layer of physiologic circuitry.

The Role of Aryl Hydrocarbon Receptor in Bone Biology

“…Bone remodeling is influenced by major systemic regulators, including parathyroid hormone (PTH), growth hormones, sex hormones, glucocorticoids, and notably calcitriol. 25 Various growth factors such as insulin-like growth factors (IGFs), tumor growth factor-beta (TGF-beta), and cytokines like interleukin-1 (IL-1) and interleukin-6 (IL-6), along with prostaglandins and bone morphogenic protein (BMP), intricately modulate the activity of osteoblasts. 26 Additionally, key proteins like type-1 collagen, osteocalcin, osteopontin, osteoprotegerin, and sialoprotein play crucial roles in regulating bone remodeling.…”

The Association between Obesity and Reduced Weight-Adjusted Bone Mineral Content in Older Adults: A New Paradigm That Contrasts with the Obesity Paradox

“…In our study, while we reported a decrease in w-BMC% across the BMI categories, we also observed increases in BF and BF% across normal-weight to overweight individuals and then individuals with obesity, as expected, and the negative impact of BF on w-BMC% may be due to some hormones secreted by the former. In this regard, advances in research over the last decade have highlighted various hormones involved in the interaction between bone and adipose tissue (i.e., body fat) [35]. For instance, adiponectin is a hormone secreted by adipose tissue that is able to suppress bone resorption through the inhibition of osteoclast differentiation and promotion of osteoblast mineralization activity [35].…”

“…In this regard, advances in research over the last decade have highlighted various hormones involved in the interaction between bone and adipose tissue (i.e., body fat) [35]. For instance, adiponectin is a hormone secreted by adipose tissue that is able to suppress bone resorption through the inhibition of osteoclast differentiation and promotion of osteoblast mineralization activity [35]. However, adiponectin may be negatively associated with body mass (i.e., body weight and BMI) [36], and recent papers have shown that individuals with obesity have lower levels [37,38], which therefore may explain its negative impact on bone in this population.…”

Higher Adiponectin Levels in Children and Adolescents with T1D Probably Contribute to the Osteopenic Phenotype through the RANKL/OPG System Activation

“…A crosstalk between bone and adipose tissue is well-established [4][5][6], with peptides such as the lipokines superfamily acting as mediators of this link, balancing between Endocrines 2023, 4 710 energy conservation and bone quality [4]. Leptin and adiponectin were the first pleiotropic adipokines that were studied regarding their bone morphogenic role.…”

“…A growing body of cell culture, animal and human studies has revealed conflicting results about the effect of leptin on the skeleton, leading to a theory of dual leptin action: one peripheral direct anabolic effect on osteoblasts and chondrocytes and one central indirect catabolic effect through sympathetic neural activity. The net action seems to be species specific and analogous to homeostatic body conditions [5,6,9]. Adiponectin is a 28 kDa protein, excreted mainly by adipose tissue.…”