Abstract
This study determined the effects of a high-fat meal on circulating endotoxin and cardiometabolic indices in adult Arab women. The cohort consisted of 92 consenting Saudi women (18 non-diabetic (ND)) control subjects; Age 24.4 ± 7.9 year; body mass index (BMI) 22.2 ± 2.2 Kg/m2), 24 overweight/obese (referred to as overweight-plus (overweight+)) subjects (Age 32.0 ± 7.8 year; BMI 28.5 ± 1.5 Kg/m2) and 50 type 2 diabetes mellitus (T2DM) patients (Age 41.5 ± 6.2 year; BMI 35.2 ± 7.7 Kg/m2). All were given a high-fat meal (standardized meal: 75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast of 12–14 h. Anthropometrics were obtained and fasting blood glucose, lipids, and endotoxin were serially measured for four consecutive postprandial hours. Endotoxin levels were significantly elevated prior to a high-fat meal in the overweight+ and T2DM than the controls (p < 0.05). Furthermore, the postprandial cardiometabolic changes led to a more detrimental risk profile in T2DM subjects than other groups, with serial changes most notable in glucose, triglycerides, high density lipoprotein-cholesterol (HDL-cholesterol), and insulin levels (p-values < 0.05). The same single meal given to subjects with different metabolic states had varying impacts on cardiometabolic health. Endotoxemia is exacerbated by a high-fat meal in Arab subjects with T2DM, accompanied by a parallel increase in cardiometabolic risk profile, suggesting disparity in disease pathogenesis of those with or without T2DM through the altered cardiometabolic risk profile rather than variance in metabolic endotoxinaemia with a high-fat meal.
Highlights
The nutritional transition and the rapid urbanization in the Middle East has introduced energy-dense refined carbohydrates and increased saturated fat intake [1]
Subjects with type 2 diabetes mellitus (T2DM) had a mean duration of diabetes of 2.04 years
The current study considered the impact of a high-fat meal on elevating glucose and cholesterol levels, both considered important in the development of coronary artery disease, coupled with obesity and T2DM
Summary
The nutritional transition and the rapid urbanization in the Middle East has introduced energy-dense refined carbohydrates and increased saturated fat intake [1]. Whilst obesity represents the single most influential risk factor for T2DM, weight gain itself is a result of a complex interaction between genetic, epigenetic, and environmental factors Amongst the latter, a carbohydrate-rich high-fat diet can quickly drive the increased obesity mediated T2DM [4]. Previous models of diet-induced and genetic obesity has shown that adipose tissue presents an important source of pro-inflammatory adipocytokines, such as tumor necrosis factor α (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) during weight gain [7,8] These adipocytokines can have a simultaneous dual impact leading to insulin resistance through activation of the pro-inflammatory mechanisms as well as a direct impact on insulin signaling capacity [9]. The development of the insulin resistance through a sustained energy dense diet promotes hyperinsulinaemic conditions, coupled with increased adipose tissue and ectopic fat accumulation [10]
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