Inflammatory and endothelial dysfunction indices among Egyptian females with obesity classes I–III

Abstract

Obesity is an alarming threat to health in Egypt. More than one in three Egyptians is obese, the highest rate in the world. We aimed to delineate the variability of inflammation and endothelial dysfunction markers among Egyptian females with different obesity classes. Out of 130 females, 70 were categorized into 3 obesity groups: Class I, BMI 30–34.9kg/m2; Class II, BMI 35–39.9 kg/m2 and Class III BMI ≥ 40kg/ m2, besides 60 control subjects. Anthropometric measurements were recorded and serum levels of tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), interleukin 6 (IL-6), IL-12, soluble intercellular adhesion molecule 1 (sICAM-1) and soluble vascular adhesion molecule 1(sVCAM-1) were assessed among participants. In all three classes of obesity, significant increase (P <0.05) in BMI, waist-hip ratio, fat mass and body fat mass % were noted. CRP and sVCAM-1 levels were increased among the 3 obesity groups. TNF-α levels were increased in class II and III obesity groups. IL-6 and IL-12 levels were elevated in class I and class III groups. While, ICAM-1 levels were increased in class III obesity group. Based on individuals’ BMI, serum levels of TNF-α, CRP, IL-6, IL-12, sVCAM-1 and sICAM-1 are differentially altered with the progression of obesity. We strongly support the hypothesis that, as the obesity rate is still mounting, a subclinical inflammatory reaction has a role in pathogenesis of obesity and emphasize the elevation of endothelial dysfunction in individuals with obesity.

Obesity: A Doorway to a Molecular Path Leading to Infertility

“…There is a similarity between the pattern of macrophage infiltration in chronic inflammatory disorders like rheumatoid arthritis and that in the case of chronic inflammation in obesity [ 56 , 126 ]. Obese female subjects also have raised circulating MCP-1, AGE, and markers of inflammation like TNF-α, CRP, and IL-6 [ 127 , 128 ].…”

Recent advances in polyphenols improving vascular endothelial dysfunction induced by endogenous toxicity

“…When the NO production is restricted or its degradation is promoted under some abnormal physiological conditions, endothelial dysfunction is probably to occur (Tesauro et al, 2017). The reduction in NO bioavailability can be induced by several endogenous or exogenous stimulates including reactive oxidative species (ROS) (Incalza et al, 2018), hyperglycemia (Gerardi, Cavia‐Saiz, Rivero‐Pérez, González‐SanJosé, & Muñiz, 2020), hyperlipidemia (Lee, Kim, & Bae, 2002), inflammatory cytokines (Mohamed et al, 2020), homocysteine (Lai & Kan, 2015), uric acid (Valle et al, 2015), and nicotine (Li et al, 2018). Endothelial dysfunction has been related to a variety of cardiovascular, renal, and metabolic diseases, including diabetes, atherosclerosis, hypercholesterolemia, uremia, nephrosclerosis, angiocarditis, and hypertension (Palomo et al, 2020; Ungvari et al, 2018; Vanhoutte, Shimokawa, Feletou, & Tang, 2017; Zhang et al, 2018).…”