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.
Highlights
It is current knowledge that white adipose tissue serves as a principal human energy repository in the form of triglycerides, and coordinates lipid metabolism in order to maintain whole body free fatty acid balance
We will focus on the reported impact of adipose tissue derived leptin and adiponectin on mineral metabolism
Effects of Leptin on Mineral Metabolism Tsuji et al were the first to demonstrate that leptin administration directly stimulates bone fibroblast growth factor-23 (FGF23) but not renal Klotho transcription in leptin-deficient mice [43], probably through activation of JAK-STAT pathway, leading to downregulation of type II sodium phosphate tubular cotransporter (NPT2a) and phosphaturia [43]
Summary
It is current knowledge that white adipose tissue serves as a principal human energy repository in the form of triglycerides, and coordinates lipid metabolism in order to maintain whole body free fatty acid balance. Among the adipocyte-derived secreted proteins, called adipokines, adiponectin boosts lipid storage and adipogenesis, while leptin blocks adipogenesis and enhances triglyceride hydrolysis [1] Both hormones stimulate fatty acid beta oxidation, inhibiting ectopic fat deposition [1]. Adipose tissue derived pro-inflammatory cytokines and adipokines are involved in the regulation of various physiological processes, such as local and systemic inflammation [3], cardiovascular function [4], glucose homeostasis [5], bone hematopoiesis [6], reninangiotensin system and sodium balance [7]. The purpose of this review paper is to enlighten the recent advances regarding the direct crosstalk between mineral metabolism, fat mass and adipokine profile, in general population and in CKD, based on in vitro, in vivo and clinical studies
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