1.
[Biomarkers of vitamin status in obese school children].
Beketova, NA, Pavlovskaya, EV, Kodentsova, VM, Vrzhesinskaya, OA, Kosheleva, OA, Sokolnikov, AA, Strokova, TV
Voprosy pitaniia. 2019;(4):66-74
Abstract
Inadequate intake of vitamins, noted in children with obesity, reduces the immune system activity, contributes to the metabolic disorders aggravation and may result in comorbidity. The aim of the work was to study sufficiency with vitamins and carotenoids of children with obesity. Material and methods. Examination of vitamin D, B2, C, A, E and β-carotene status in 50 children (male 36.0%) aged 11-17 years [median (Me) - 14 years] with obesity [Z-score body mass index (BMI) >=2.0, Ме=2.86] by determining serum biomarkers has been conducted. Results and discussion. All of the children had an adequate supply with vitamin C (ascorbic acid level >0.4 mg/dL). Low vitamin A status (retinol <30 μg/dl) was revealed in 8% children. Deficiency of vitamin D [25(OH)D<20 ng/ml], vitamin B2 (riboflavin <5 ng/ml) and β-carotene (<10 μg/dl) was detected in 62.0, 38.8 and 74.0% of obese children. The percentage of persons with reduced vitamin E serum level (<0.8 mg/dl) was amounted 54.0%. A severe vitamin D deficit (<10 ng/ml) has been detected in 24.0% of children with Z-score BMI >=2.86 (median value) and has not been observed in children with lower body weight, whose serum β-carotene median was 1.5 fold higher (p<0.05). No one was adequately supplied with all 5 studied vitamins and β-carotene. The combined deficiency of 3 or more vitamins took place in 54.0% of obese children. Synchronously suboptimal serum level of ascorbic acid (<50 μmol/l), β-carotene (<0.4 μmol/l) and α-tocopherol/cholesterol ratio (<5.0 μmol/mmol) which is a cardiovascular disease risk factor, has been found in 28.0% of children. BMI was inversely associated with 25(OH)D serum concentration (ρ=-0.313, р=0.027). There was a pronounced negative correlation between serum level of β-carotene and atherogenic LDL cholesterol (ρ=-0.514, p<0.001). Conclusion. The prevalence of combined vitamin D, tocopherol and carotenoids' inadequacy in obese children indicates the importance of vitamin status correction to reduce the risk of metabolic syndrome.
2.
Twelve Weeks of Medium-Intensity Exercise Therapy Affects the Lipoprotein Profile of Multiple Sclerosis Patients.
Jorissen, W, Vanmierlo, T, Wens, I, Somers, V, Van Wijmeersch, B, Bogie, JF, Remaley, AT, Eijnde, BO, Hendriks, JJA
International journal of molecular sciences. 2018;(1)
Abstract
Multiple sclerosis (MS) is an inflammatory auto-immune disease of the central nervous system (CNS). Serum glucose alterations and impaired glucose tolerance (IGT) are reported in MS patients, and are commonly associated with the development of cardio-metabolic co-morbidities. We previously found that a subgroup of MS patients shows alterations in their lipoprotein profile that are similar to a pre-cardiovascular risk profile. In addition, we showed that a high-intensity exercise training has a positive effect on IGT in MS patients. In this study, we hypothesize that exercise training positively influences the lipoprotein profile of MS patients. To this end, we performed a pilot study and determined the lipoprotein profile before (controls, n = 40; MS patients, n = 41) and after (n = 41 MS only) 12 weeks of medium-intensity continuous training (MIT, n = 21, ~60% of VO2max) or high-intensity interval training (HIT, n = 20, ~100-200% of VO2max) using nuclear magnetic resonance spectroscopy (NMR). Twelve weeks of MIT reduced intermediate-density lipoprotein particle count ((nmol/L); -43.4%; p < 0.01), low-density lipoprotein cholesterol (LDL-c (mg/dL); -7.6%; p < 0.05) and VLDL size ((nm); -6.6%; p < 0.05), whereas HIT did not influence the lipoprotein profile. These results show that MIT partially normalizes lipoprotein alterations in MS patients. Future studies including larger patient and control groups should determine whether MIT can reverse other lipoprotein levels and function and if these alterations are related to MS disease progression and the development of co-morbidities.
3.
Effects of atorvastatin on biomarkers of immune activation, inflammation, and lipids in virologically suppressed, human immunodeficiency virus-1-infected individuals with low-density lipoprotein cholesterol <130 mg/dL (AIDS Clinical Trials Group Study A5275).
Nixon, DE, Bosch, RJ, Chan, ES, Funderburg, NT, Hodder, S, Lake, JE, Lederman, MM, Klingman, KL, Aberg, JA, ,
Journal of clinical lipidology. 2017;(1):61-69
-
-
Free full text
-
Abstract
BACKGROUND Persistent immune activation and inflammation in virologically suppressed human immunodeficiency virus (HIV) infection are linked to excess cardiovascular risk. OBJECTIVE To evaluate atorvastatin as a strategy to reduce cardiovascular risk. METHODS A5275 was a multicenter, prospective, randomized, double-blind, placebo-controlled, cross-over pilot study of atorvastatin (10 mg/day for 4 weeks then 20 mg/day for 16 weeks) with a planned enrollment of 97 HIV-infected participants ≥18 years old, receiving boosted protease inhibitor-based antiretroviral therapy for ≥6 months, with plasma HIV-1 RNAs below limits of quantification ≥180 days, and fasting low-density lipoprotein (LDL) cholesterol ≥70 and <130 mg/dL. Primary endpoints were differences of changes ([week 44-week 24]-[week 20-baseline]) in CD4+ and CD8+ T-lymphocyte activation (% CD38+/DR+) and plasma levels of IL-6 and D-dimer. Arms were compared using the Wilcoxon rank-sum tests and also summarized changes pre-to-post atorvastatin treatment. Analyses were as-treated. RESULTS Ninety-eight participants were enrolled at 31 U S sites and 73 completed study treatment. Atorvastatin treatment did not decrease T-lymphocyte or monocyte activation, circulating biomarker levels (interleukin-6, D-dimer, soluble CD14, soluble CD163, monocyte chemoattractant protein-1, interferon-gamma-induced protein-10, high-sensitivity C-reactive protein, CD40L, and P-selectin) or white blood cell Krüppel-like Factor 2/4 messenger RNA levels. Pre-to-post atorvastatin reductions in calculated LDL (-38%), oxidized-LDL (-33%), and lipoprotein-associated phospholipase A2 (-31%) were significant (P < .01). CONCLUSION In virologically suppressed individuals with HIV infection, atorvastatin did not significantly decrease levels of soluble or cellular biomarkers of immune activation and inflammation but resulted in robust reductions in LDL cholesterol, oxLDL, and lipoprotein-associated phospholipase A2, biomarkers associated with cardiovascular risk.