Recently discovered adipokines and cardio-metabolic comorbidities in childhood obesity

Abstract

White adipose tissue (WAT) asset, in terms of cell number, fat storage capacity and endocrine function, is largely determined in early stages of life and is pivotal for shaping the WAT pro-inflammatory behavior. WAT derived adipokines have been shown to play a main role in several cardio-metabolic abnormalities of obesity. This review focuses on the most recently identified adipokines, namely adipocyte-fatty acid-binding protein, chemerin, fibroblast growth factor-21, lipocalin-2, omentin-1 and vaspin; their role in the pathogenesis of obesity and associated cardio-metabolic abnormalities; and on their adaptive response to body weight change. Evidence consistently suggests a pathogenic role for A-FABP, chemerin and FGF-21. Nevertheless, large population studies are needed to verify whether they can be useful to predict the risk of cardio-metabolic abnormalities in adulthood and/or monitor the clinical response to therapeutic interventions.

Figure 1

Permissive windows early in life. “Obesogenic” cues can enhance WAT hyperplasia. They encompass, for instance, hormonal stimuli (i.e., endocrine disruptors) and nutrient availability during the intrauterine life, maternal epigenome, gut microbiota soon after the birth, early feeding and weaning, physical activity and sedentary behaviors.

Figure 2

Metabolic functions of FGF-21. Abbreviations: glucose transporter-1 (GLUT-1); peroxisome proliferator-activated receptor gamma (PPARγ); protein kinase B (PKB or AKT); triacylglycerols (TAG); low density lipoprotein-cholesterol (LDL-c); high density lipoprotein-cholesterol (HDL-c); white adipose tissue (WAT); uncoupling protein 1 (UCP-1); carnitine palmitoyltransferase 1 (CPT1); type II iodothyronine deiodinase (DIO2); acetyl-CoA carboxylases 2 (ACC2); AMP-activated protein kinase—Sirtuin 1 (AMPK-SIRT1); peroxisome proliferator-activated receptor-γ coactivator-1 (PGC1α).