Abstract

Weight loss can reduce obesity-induced arterial stiffening that is attributed to decreased inflammation. Angiopoietin-like protein 2 (ANGPTL2) is a pro-inflammatory adipokine that is upregulated in obesity and is important in the progression of atherosclerosis and cardiovascular disease. The purpose of this study is to investigate the effects of dietary modification on circulating ANGPTL2 levels and arterial stiffness in overweight and obese men. Twenty-two overweight and obese men (with mean age of 56 ± 2 years and body mass index of 28.6 ± 2.6 kg/m2) completed a 12-week dietary modification program. We measured the arterial compliance and β-stiffness index (as the indices of arterial stiffness) and serum ANGPTL2 levels before and after the program. After the 12-week dietary modification, body mass and daily energy intake were significantly reduced. Arterial compliance was significantly increased and β-stiffness index was significantly decreased after the 12-week dietary modification program. Serum ANGPTL2 levels were significantly decreased. Also, the changes in arterial compliance were negatively correlated with the changes in serum ANGPTL2 levels, whereas the changes in β-stiffness index were positively correlated with the changes in serum ANGPTL2 levels. These results suggest that the decrease in circulating ANGPTL2 levels can be attributed to the dietary modification-induced reduction of arterial stiffness in overweight and obese men.

Highlights

  • Obesity has become a major health concern globally and is closely linked to increasing arterial stiffness[1,2] that is a primary risk factor for cardiovascular disease (CVD)

  • We investigated how 12 weeks of dietary modification affects circulating Angiopoietin-like protein 2 (ANGPTL2) levels and arterial stiffness in overweight and obese men

  • We observed that dietary modification reduced both circulating ANGPTL2 levels and arterial stiffness

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Summary

Introduction

Obesity has become a major health concern globally and is closely linked to increasing arterial stiffness[1,2] that is a primary risk factor for cardiovascular disease (CVD). Increasing evidence indicates that obesity is linked to chronic and systemic inflammation[3,4]. Arterial stiffness is associated with the production of pro-inflammatory adipokines in obese individuals[5,6]. It has been demonstrated that obese individuals are likely to exhibit increased arterial stiffness and pro-inflammatory biomolecules[2,3,5]. ANGPTL2 in adipose tissue is higher in diet-induced obese mice than in control mice[7] and circulating ANGPTL2 levels in obese individuals positively correlate with adiposity[10], indicating that ANGPTL2 is a pro-inflammatory adipokine. ANGPTL2 from perivascular adipose tissue and endothelial cell promotes local and vascular inflammation[8,11]. Since pro-inflammatory adipokines contribute to arterial stiffening[15], ANGPTL2 levels may be relevant for vascular function

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