RESUMEN
Background: a well balanced diet is important for normal function of endothelial cells. Diets high in fat and/or calories can lead to hypertriglyceridemia and postprandial lipidemia and thus are considered a risk factor for the development of atherosclerosis. Big meals may result in chronic elevations in the level of atherogenic lipoproteins as well as evoking chronic inflammatory response. Both may lead to pathological changes on the arterial vessel wall and myocardium
Objective[s]: to study the effect of the size of a well-balanced meal on the lipid profile in the post prandial state and its effect on the endothelial function, ventricular filling and diastolic function
Methods: one group pretest-posttest study was carried out on 40 young healthy lean volunteers aged 30 to 39 years who after overnight fast were invited to eat a big breakfast meal. Postprandial blood samples were then drawn after 3-4 hours to determine changes induced by the big meal in the blood. On the following day, the same procedure was adopted but with a breakfast meal which contains only one third of the size of the big meal [small meal]. The items of comparison between the two meals included: The changes induced by both types of meals on the lipid profile of the blood by assessing the postprandial levels of TG, TC, LDL-C, HDL-C and FFAs; assessment of the inflammatory response by assessing postprandial levels of CRP; The changes induced on endothelial cell functions by assessing the postprandial levels of ET1 and NO; and the changes induced by the two types of meals on the left ventricular function as determined by echo Doppler as well as tissue Doppler imaging [TDI]
Results: the big meal was associated with elevations in TG, TC, LDL-C, CRP, ET1 and NO [P=0.001, 0.021, 0.057, 0.110, 0.002, 0.001respectively]. The small meal showed significant increase in levels of HDL-C [P=0.001] and FFAs [P=0.048]. The diastolic function of the left ventricle showed significant reduction after the ingestion of the big meal versus the small meal
Conclusions: the study concluded that big meal size negatively impact lipid homeostasis and endothelial function and the recognition of this possible danger of big meals can lead to the possibility of prevention of atherosclerosis through controlling of the meal size
RESUMEN
The aim of the present work was to study insulin resistance [IR] in obesity and to detect any possible role of leptin in the mediation of such resistance, as well as its consequences. Subjects and The present study was conducted on twenty obese otherwise healthy women [mean body mass index [BMI], 32.58 +/- 2.09kg/m2] and twenty nonobese healthy control women [mean BMI, 23.13 +/- 1.62kg/m2] of matched age and menopausal status. All subjects were subjected to the following measures: 1] anthropometric measurements including BMI, waist circumference and waist/hip ratio [WHR] [The first parameter was used as a surrogate for overall obesity, while the latter 2 parameters were used as surrogates for abdominal obesity], 2] systolic and diastolic blood pressure [SBP and DBP, respectively] measurements, 3] fasting and 2-hour postoral glucose tolerance test, 4] fasting plasma insulin and fasting plasma glucose/insulin ratio [both are surrogates for IR], 5] fasting serum lipid profile including total cholesterol [TC], high density lipoprotein cholesterol [HDL-C], low density lipoprotein cholesterol [LDL-C], triglycerides [TG], free fatty acids [FFAs], and atherogenicity ratio [TC/HDL-C], and 6] plasma leptin. Compared to the nonobese healthy controls, obese women demonstrated statistically significant increase in the measures of abdominal obesity [waist circumference and WHR], both SBP and DBP, glycemic control measures [fasting and 2 hour postoral glucose tolerance test], fasting plasma insulin and leptin levels. Obese women also demonstrated statistically significant decrease in fasting plasma glucose/insulin ratio. They also showed statistically significant dyslipidemia [hyper-cholesterolemia, low HDL-C, high LDL-C, hypertriglyceridemia, and high FFAs] and high atherogenicity ratio. Conclusions: Obesity is frequently accompanied by both insulin resistance ana by leptin resistance that are parallel to each other. Obese subjects have a tendency for increased high blood pressure, increased blood glucose levels and atherosclerosis. They are also dyslipidemic. Hyperleptinemia of obesity may mediate such cardiovascular and metabolic abnormalities. The strong correlation of plasma leptin to the measures of abdominal [visceral] obesity [especially the waist circumference] and the measures of IR [e.g. fasting plasma insulin and fasting plasma glucose/insulin ratio] supports the possibility of the role of leptin in the link between abdominal visceral obesity and IR