scholarly journals Antioxidant Complexes and Lipoprotein Metabolism – Experience of Grape Extracts Application Under Metabolic Syndrome and Neurogenic Stress

Author(s):  
Andriy L. ◽  
Anna B. ◽  
Mykhaylo V. ◽  
Oxana A.
Lipids ◽  
2014 ◽  
Vol 49 (7) ◽  
pp. 677-684 ◽  
Author(s):  
Vanessa M. Silva ◽  
Carmen G. C. Vinagre ◽  
Luis A. O. Dallan ◽  
Ana P. M. Chacra ◽  
Raul C. Maranhão

2018 ◽  
Vol 46 (11) ◽  
pp. 4447-4454 ◽  
Author(s):  
Ajit Ramakant Mahale ◽  
Sonali Dattatray Prabhu ◽  
Muthiah Nachiappan ◽  
Merwyn Fernandes ◽  
Sonali Ullal

Objective Ultrasonography is an efficient technique for detecting fatty liver. Its sensitivity and specificity in detecting moderate to severe fatty liver are comparable to those of histology. Fatty liver is associated with abnormal lipid and lipoprotein metabolism and insulin resistance, metabolic syndrome, cardiovascular/renal disease, type 2 diabetes, and other conditions. This study was performed to compare the serum lipid profiles and serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), and glycosylated hemoglobin (HbA1c) levels in patients diagnosed with fatty liver on ultrasonography versus controls without fatty liver and evaluate the clinical relevance of an ultrasound diagnosis of fatty liver in routine health checkups. Methods This hospital-based cross-sectional study included 390 patients who underwent health checkups; 226 were diagnosed with fatty liver (cases) and 164 were not (controls). The lipid profile, serum GOT and GPT levels, and HbA1c level were compared between the cases and controls. Results The cases had considerably higher levels of lipids, liver enzymes (serum GOT and GPT), and HbA1c than controls. Conclusion Ultrasonography is a noninvasive simple tool for early detection of fatty liver in asymptomatic patients and can help clinicians achieve early detection of metabolic syndrome.


2004 ◽  
Vol 107 (3) ◽  
pp. 221-232 ◽  
Author(s):  
Dick C. CHAN ◽  
P. Hugh R. BARRETT ◽  
Gerald F. WATTS

The metabolic syndrome encapsulates visceral obesity, insulin resistance, diabetes, hypertension and dyslipidaemia. Dyslipidaemia is a cardinal feature of the metabolic syndrome that accelerates the risk of cardiovascular disease. It is usually characterized by high plasma concentrations of triacylglycerol (triglyceride)-rich and apoB (apolipoprotein B)-containing lipoproteins, with depressed concentrations of HDL (high-density lipoprotein). However, lipoprotein metabolism is complex and abnormal plasma concentrations can result from alterations in the rates of production and/or catabolism of these lipoprotein particles. Our in vivo understanding of kinetic defects in lipoprotein metabolism in the metabolic syndrome has been achieved chiefly by ongoing developments in the use of stable isotope tracers and mathematical modelling. This review deals with the methodological aspects of stable isotope kinetic studies. The design of in vivo turnover studies requires considerations related to stable isotope tracer administration, duration of sampling protocol and interpretation of tracer data, all of which are critically dependent on the kinetic properties of the lipoproteins under investigation. Such models provide novel insight that further understanding of metabolic disorders and effects of treatments. Future investigations of the pathophysiology and therapy of the dyslipoproteinaemia of the metabolic syndrome will require the development of novel kinetic methodologies. Specifically, new stable isotope techniques are required for investigating in vivo the turnover of the HDL subpopulation of particles, as well as the cellular efflux of cholesterol into the extracellular space and its subsequent transport in plasma and metabolic fate in the liver.


2014 ◽  
Vol 307 (9) ◽  
pp. E729-E737 ◽  
Author(s):  
Patricia Christian ◽  
Qiaozhu Su

The development of metabolic syndrome is closely associated with the deregulation of lipid metabolism. Emerging evidence has demonstrated that microRNAs (miRNAs) are intensively engaged in lipid and lipoprotein metabolism by regulating genes involved in control of intracellular lipid synthesis, mitochondrial fatty acid oxidation, and lipoprotein assembly. Mitochondrial dysfunction induced by altered miRNA expression has been proposed to be a contributing factor in the onset of metabolic diseases, while at the same time, aberrant expression of certain miRNAs is associated with the induction of endoplasmic reticulum (ER) stress induced by nutrient-surplus. These studies position miRNAs as a link between oxidative stress and ER stress, two cellular stress pathways that are deregulated in metabolic disease and are associated with very-low-density lipoprotein (VLDL) overproduction. Dyslipoproteinemia frequently accompanied with metabolic syndrome is initiated largely by the overproduction of VLDL and altered biogenesis of high-density lipoprotein (HDL). In this review, we highlight recent findings on the regulatory impact of miRNAs on the metabolic homeostasis of mitochondria and ER as well as their contribution to the aberrant biogenesis of both VLDL and HDL in the context of metabolic disorders, in an attempt to gain further insights into the molecular mechanisms of dyslipidemia in the metabolic syndrome.


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