Update on the Crosstalk Between Adipose Tissue and Mineral Balance in General Population and Chronic Kidney Disease

Abstract

Adipose tissue is nowadays considered as a major endocrine organ, which apart from controlling lipid metabolism, displays a significant role in energy expenditure, food intake and in the regulation of various systemic physiological processes. Adipose derived pro-inflammatory cytokines and adipokines, particularly leptin and adiponectin, provide inter-communication of adipose tissue with various metabolic pathways, ultimately resulting in a complex network of interconnected organ systems. Recent clinical and experimental research has been focused on exploring the direct interaction between adipokine profile and elements of mineral metabolism, including parathormone (PTH), fibroblast growth factor-23 (FGF23) and calcitriol. The emerging crosstalk between adipose tissue and calcium and phosphorus homeostasis suggests that metabolic disorders from one system may directly affect the other and vice versa. It is current knowledge that fat metabolism disturbance, commonly encountered in obese individuals, influences the expression of calciotriopic hormones in general population, while various clinical trials attempting to successfully achieve body fat loss by modulating mineral profile have been published. In chronic kidney disease (CKD) state, there is an increasing evidence suggesting that mineral disorders, influence adipose tissue and linked endocrine function. On the contrary, the impact of disturbed fat metabolism on CKD related mineral disorders has been also evocated in clinical studies. Recognizing the pathogenetic mechanisms of communication between adipose tissue and mineral balance is critical for understanding the effects of metabolic perturbations from the one system to the other and for identifying possible therapeutic targets in case of disrupted homeostasis in one of the two connected systems. To that end, this review aims to enlighten the recent advances regarding the interplay between mineral metabolism, fat mass and adipokine profile, based on in vitro, in vivo and clinical studies, in general population and in the course of CKD.

Circulating and Adipose Tissue Adiponectin Level and Outcomes in Incident Peritoneal Dialysis Patients

“… 15 , 37 In terms of its systemic effects, adiponectin directly improves endothelial dysfunction, at least in rat models, 39 , 40 and contributes to the pathogenesis of chronic kidney disease–mineral bone disease, mostly by downregulation of fibroblast growth factor 23 and kidney’s Klotho expression. 41 Increased adipose tissue results in a decrease in the secretion of adiponectin, which is an anti-inflammatory adipokine produced by adipocytes. 42 Plasma adiponectin level was associated with insulin resistance and serum triglyceride level in patients without diabetes 16 and was a powerful risk marker of incident prediabetes in patients with parental history of diabetes.…”

B. abortus Infection Promotes an Imbalance in the Adipocyte–Osteoblast Crosstalk Favoring Bone Resorption

“…Osteoblast mineralization comprises the deposition of phosphate and calcium with the concomitant deposition of organic matrix, thus contributing to bone architecture, strength, and rigidity [ 52 ]. Recent findings on the role of adipose tissue in calcium and phosphate homeostasis suggest that the unbalance in adipose tissue may affect bone tissue, and vice versa [ 53 ].…”

Chronic Low or High Nutrient Intake and Myokine Levels

“…Herein, we have demonstrated higher percentages of fat mass in runners with lower carbohydrate, phosphorus, and calcium intakes. There is crosstalk between adipose tissue, and calcium and phosphorus homeostasis, which involves some hormones such as leptin and parathormone [ 23 ].…”