Replacing carbohydrate with protein and fat in prediabetes or type-2 diabetes: greater effect on metabolites in PBMC than plasma

Abstract

BackgroundActive metabolism of peripheral blood mononuclear cells (PBMC) could suggest their suitability for metabolomics studies. This study examined whether reductions in PBMCs and plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) activities induced by dietary intervention affected the overall metabolic profiles of PBMC and plasma.MethodsEighty nonobese subjects aged 40–70 years (18.5 ≤ BMI < 30 kg/m2) with prediabetes or newly-diagnosed type-2 diabetes were assigned to consume either the usual refined-rice diet (control group, n = 40) or to replace refined rice with whole grains and legumes as carbohydrates (whole-grain group, n = 40) for three meals per day during the 12-week intervention. Fasting PBMC and plasma metabolomes were profiled using UPLC-LTQ-Orbitrap mass spectrometry.ResultsAfter 12 weeks, changes in fasting glucose, HbA1c, HOMA-IR, MDA, ox-LDL, LDL particle size, plasma Lp-PLA2 activity, and PBMC enzyme activity in the whole-grain group were significantly different from those in the control group before and after adjusting for baseline levels. The PBMC levels of L-leucine, oleamide, lysoPC (16:0), and lysoPC (18:0) in the whole-grain group showed greater reductions compared with those of the control group. Changes in plasma metabolites were not significantly different between the two groups. Changes in PBMC Lp-PLA2 activity positively correlated with changes in L-leucine, oleamide, lysoPC (16:0), lysoPC (18:0), glucose, and ox-LDL, and negatively correlated with changes in LDL particle size.ConclusionsThis study showed that dietary intervention in prediabetic or type-2 diabetic patients had a greater effect on PBMC Lp-PLA2 activity and metabolites compared with those of plasma metabolites.Trial registrationNCT02191644

Metabolomics Profiles of Hepatocellular Carcinoma in a Korean Prospective Cohort: The Korean Cancer Prevention Study-II

“…The detailed methods for sample preparation and analysis using ultraperformance liquid chromatography (UPLC)-linear-trap quadrupole (LTQ)-Orbitrap mass spectrometry (MS), data processing, and putative identification of serum metabolites were reported in a previous study (14).…”

Lipidomics Profile Changes of Type 2 Diabetes Mellitus with Acute Myocardial Infarction

“…LysoPC was involved in several possible pathways: (1) LCAT and oxidation of LDL production, (2) hepatocyte secretion, and (3) platelet activation and deletion of the LDL receptor [17]. Changed LysoPC concentrations have been found in cancers [18][19][20][21][22][23][24], inflammatory disorders [25], mitochondrial disease [26], Alzheimer's disease [27], diabetes [28][29][30][31], and acute coronary syndrome [17]. Nowadays, many researches showed that LysoPC18:0 concentration was associated with cancer risk [20][21][22][23]32] and mitochondrial disease [26]; meanwhile, studies on the association between LysoPC18:0 and diabetes [29][30][31] or CVD/AMI/acute coronary syndrome [17] are still insufficient.…”

Apolipoprotein A5 gene variants are associated with decreased adiponectin levels and increased arterial stiffness in subjects with low high‐density lipoprotein‐cholesterol levels

“…Blood samples were collected following an overnight fast of at least 12 hours. The levels of fasting triglycerides, total cholesterol, HDL‐cholesterol, LDL‐cholesterol, glucose, and insulin and the LDL particle size were measured using previously described methods . Insulin resistance (IR) was calculated as follows: the homeostasis model assessment (HOMA)‐IR = (fasting glucose [mmol/L] × fasting insulin [μIU/mL])/22.5.…”

“…The levels of fasting triglycerides, total cholesterol, HDL-cholesterol, LDL-cholesterol, glucose, and insulin and the LDL particle size were measured using previously described methods. 10 Insulin resistance (IR) was calculated as follows: the homeostasis model assessment (HOMA)-IR = (fasting glucose [mmol/L] × fasting insulin [μIU/mL])/22.5. The apoA-I concentrations in serum were measured using a specific antiserum (Roche, Basel, Switzerland), and the apoA-V concentrations in plasma were assessed via a Human Apolipoprotein A5 ELISA Kit (Cusabio, Zhejiang, China).…”