Abstract
Background Frequently, ingestion of lipids exceeds our daily requirements and constantly exposes humans to circulating lipid overload which may lead to endothelial dysfunction (ED), the earliest marker of atherosclerosis. Nailfold videocapillaroscopy (NVC) technique can detect ED on microcirculation. Using NVC, we aimed to demonstrate if metabolic alterations evoked by high-fat meals can act differently on microvascular endothelial reactivity in lean and women with obesity. Methods Women, aged between 19 and 40 years, were allocated to control group (CG) and with obesity group (OBG) and were subjected to blood analysis for determination of glucose, total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) and NVC evaluation at fasting and 30, 60, 120, and 180-min after high-fat meal ingestion. NVC technique evaluated microvascular reactivity through the following variables: red blood cell velocity (RBCV) at rest and after 1-min ischemia (maximal red blood cell velocity, RBCVmax) and time taken to reach it (TRBCVmax). A P value ≤0.05 was considered significant. Results High-fat meal promoted a two-phase response in both groups: one until 60-min, associated with glucose and insulin levels, and the other after 120-min, associated with TG levels. Significant differences between groups were observed concerning insulin and HDL-c concentrations only at fasting and TC, TG, and LDL-c levels in all-time points. Regarding microvascular reactivity, RBCV, RBCVmax, and TRBCVmax were significantly different in OBG at 30-min compared to baseline. RBCVmax and TRBCVmax were significantly different in CG at 30-min and 60-min comparing to fasting. In all-time points, OBG presented RBCV, RBCVmax , and TRBCVmax significantly different in comparison to CG. ConclusionHigh-fat meal worsened ED on microcirculation in women with obesity and induced impairment of endothelial function in lean ones, reinforcing the association between high-fat meal and atherosclerosis.
Highlights
Cardiovascular diseases (CVD) are associated with atherosclerosis and are the main cause of death worldwide [1], and their incidence tends to rise as a consequence of world epidemic of obesity [2], which is known to be a risk factor for atherosclerosis [3]
obesity group (OBG) had significantly lower muscle mass when compared to control group (CG) (P
The OBG participants were age and gender-matched to CG, and according to exclusion criteria they were nondiabetic, nonhypertensive, and they were not diagnosed with metabolic syndrome, suggesting that obesity per se was the primary cause for microvascular dysfunction [26, 27]
Summary
Cardiovascular diseases (CVD) are associated with atherosclerosis and are the main cause of death worldwide [1], and their incidence tends to rise as a consequence of world epidemic of obesity [2], which is known to be a risk factor for atherosclerosis [3].Changes in plasma lipoprotein concentrations are a wellestablished cause of increased CVD risk [4,5,6]. Frequently the ingestion of lipids exceeds the real requirements of the organism, and as a consequence, we are regularly exposed to an overload of circulating lipids [8, 9]. Ingestion of lipids exceeds our daily requirements and constantly exposes humans to circulating lipid overload which may lead to endothelial dysfunction (ED), the earliest marker of atherosclerosis. Using NVC, we aimed to demonstrate if metabolic alterations evoked by high-fat meals can act differently on microvascular endothelial reactivity in lean and women with obesity. Women, aged between 19 and 40 years, were allocated to control group (CG) and with obesity group (OBG) and were subjected to blood analysis for determination of glucose, total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-c) and highdensity lipoprotein cholesterol (HDL-c) and NVC evaluation at fasting and 30, 60, 120, and 180-min after high-fat meal ingestion. High-fat meal worsened ED on microcirculation in women with obesity and induced impairment of endothelial function in lean ones, reinforcing the association between high-fat meal and atherosclerosis
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