Abstract

Obesity favors the development of cardiometabolic alterations such as type 2 diabetes (T2D) and the metabolic syndrome (MS). Obesity and the MS are distinguished by an increase in circulating leptin concentrations, in parallel to a drop in the levels of adiponectin. Consequently, the Adpn/Lep ratio has been suggested as a maker of dysfunctional adipose tissue. We aimed to investigate in humans (n = 292) the reliability of the Adpn/Lep ratio as a biomarker of adipose tissue dysfunction. We considered that an Adpn/Lep ratio of ≥1.0 can be considered normal, a ratio of ≥0.5 <1.0 suggests moderate-medium increased risk, and a ratio of <0.5 indicates a severe increase in cardiometabolic risk. Using these cut-offs, 5%, 54% and 48% of the lean, normoglycemic and without-MS subjects, respectively, fall within the group with an Adpn/Lep ratio below 0.5; while 89%, 86% and 90% of the obese, with T2D and with MS patients fall within the same group (p < 0.001). A significant negative correlation (r = −0.21, p = 0.005) between the Adpn/Lep ratio and serum amyloid A (SAA) concentrations, a marker of adipose tissue dysfunction, was found. We concluded that the Adpn/Lep ratio is a good indicator of a dysfunctional adipose tissue that may be a useful estimator of obesity- and MS-associated cardiometabolic risk, allowing the identification of a higher number of subjects at risk.

Highlights

  • Obesity has become, over recent decades, the most prevalent metabolic alteration, constituting one of the main causes of death and disability [1]

  • Obesity increases the risk of developing cardiometabolic alterations such as type 2 diabetes (T2D), hypertension, dyslipidemia, and non-alcoholic fatty liver disease (NAFLD), endangering the health improvements achieved in recent decades and producing an increase in morbidity [3,4]

  • We considered that an Adpn/Lep ratio equal or higher to 1.0 can be considered normal, a ratio between 0.5 and 1.0 can indicate moderate-medium increased risk, and a ratio below 0.5 suggests a severe increase in cardiometabolic risk [22]

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Summary

Introduction

Over recent decades, the most prevalent metabolic alteration, constituting one of the main causes of death and disability [1]. Obesity increases the risk of developing cardiometabolic alterations such as type 2 diabetes (T2D), hypertension, dyslipidemia, and non-alcoholic fatty liver disease (NAFLD), endangering the health improvements achieved in recent decades and producing an increase in morbidity [3,4]. Obesity is defined medically as a condition of excessive accumulation of adipose tissue, of sufficient extent to produce adverse health consequences [5]. Nutrients 2019, 11, 454 involved in the development of obesity and the expansion of adipose tissue have not been fully clarified [6,7]. A couple of decades ago adipose tissue was considered a passive organ for excess energy storage as triglycerides [8]. In the last years adipose tissue has been shown to behave as a highly active endocrine organ, based on its ability to secrete a wide variety of biologically active adipokines, such as leptin, adiponectin, tumor necrosis factor-α (TNF-α), or interleukin-6

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