scholarly journals SERPINE1, PAI-1 protein coding gene, methylation levels and epigenetic relationships with adiposity changes in obese subjects with metabolic syndrome features under dietary restriction

2013 ◽  
Vol 53 (3) ◽  
pp. 139-144 ◽  
Author(s):  
Patricia Lopez-Legarrea ◽  
Maria Luisa Mansego ◽  
Marian Angeles Zulet ◽  
Jose Alfredo Martinez
2014 ◽  
Vol 47 ◽  
pp. 98-106 ◽  
Author(s):  
Aurora Perez-Cornago ◽  
María J. Ramírez ◽  
M. Ángeles Zulet ◽  
J. Alfredo Martinez

2019 ◽  
Vol 1 (4) ◽  
pp. 21-26 ◽  
Author(s):  
O. V. Bobko ◽  
O. V. Tikhomirova ◽  
N. N. Zybina ◽  
O. A. Klitsenko

The objective of the study is to show significance of desynchronosis laboratory markers in risk assessment of metabolic syndrome (MS) development. Materials and Methods. There were examined 98 men, aged 43-88, diagnosed with dyscirculatory encephalopathy showing one and more risk factors for development of cardiovascular diseases. They were divided into 2 groups according to the international guidelines of 2009: with MS (n = 61) and without MS (n = 37). Parameters of fats, glucose metabolism, inflammatory mediators, fat tissue metabolism markers, melatonin metabolite excretion (6-sulfatoxymelatonin) were defined in blood serum and urine. Results. The article presents data on changes in leptin, adiponectin, PAI-1, testosterone production and 6-sulfatoxymela-tonin excretion in patients with MS. There are calculated threshold values of these markers definitely increasing MS risk and logistic regression equation which allows assessing MS risk for an individual patient. Conclusion. Detected disorders of melatonin synthesis diurnal dynamics in patients with MS and interconnection between melatonin production and adiponectin, leptin, PAI-1, testosterone synthesis allow considering these parameters as desynchronosis markers significant for MS development.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jin-Shuen Chen ◽  
Chung-Ze Wu ◽  
Nain-Feng Chu ◽  
Li-Chien Chang ◽  
Dee Pei ◽  
...  

We investigated the role of urokinase plasminogen activator (uPA) and its soluble receptors (suPAR) and plasminogen activator inhibitor-1 (PAI-1) in metabolic syndrome (MetS) components, insulin secretion, and resistance in schoolchildren. We enrolled 387 children, aged 10.3 ± 1.5 years, in Taipei. Anthropometry, fibrinolytic proteins, MetS components, insulin secretion, and resistance were measured. Subjects were divided into normal, overweight, and obese groups. Finally, the relationship between fibrinolytic proteins and metabolic syndrome in boys and girls was analyzed. In boys, PAI-1 was positively associated with body mass index (BMI) percentile, hypertriglyceride, insulin secretion, and resistance. In girls, PAI-1 was positively associated with obesity, hypertriglyceridemia, and insulin secretion. In girls, uPA was positively associated with insulin secretion. suPAR was positively associated with high-sensitivity C-reactive protein in both boys and girls, and with BMI percentile and body fat in girls. The obese boys had higher suPAR and PAI-1 levels than the normal group. The obese girls had higher uPA, suPAR, and PAI-1 than the normal group. Boys and girls with MetS had higher PAI-1. Fibrinolytic proteins, especially PAI-1, are associated with MetS components and insulin secretion in children. Fibrinolytic proteins changes were more likely to occur in girls than in boys.


2011 ◽  
Vol 9 (4) ◽  
pp. 429-435
Author(s):  
Ary Serpa Neto ◽  
Felipe Martin Bianco Rossi ◽  
Rodrigo Dal Moro Amarante ◽  
Marçal Rossi

ABSTRACT Objectives: To evaluate the relations between liver markers (GGT, ALT and AST) and the metabolic syndrome (and its components) in morbidly obese subjects, and to determine the response of these metabolic factors and hepatic enzymes after weight loss induced by Roux-en-Y gastric bypass. Methods: This study was carried out at a university hospital, in Santo André (SP), Brazil. We evaluated 140 morbidly obese subjects aged from 18 to 60 years submitted to a Roux-en-Y gastric bypass, who were followed for a mean period of 8 months. Patients with a history of heavy drinking, type 1 diabetes, and/or liver disease were excluded. Results: Liver markers, most notably GGT, were strongly associated with metabolic abnormalities, mainly hyperglycemia. The prevalence of type 2 diabetes significantly increased with increasing levels of GGT (highest versus lowest quartile GGT: odds ratio 3.89 [95%CI: 1.07-14.17]). Liver markers significantly decreased 8 months after the Roux-en-Y gastric bypass and the reduction of GGT levels were associated with the reduction of glucose levels (Pearson r = 0.286; p = 0.001). Conclusions: Elevated levels of liver markers, principally GGT, in morbidly obese subjects are associated with metabolic abnormalities. In addition to the well-known benefits of bariatric surgery, Roux-en-Y gastric bypass, reduced the levels of liver markers to the normal range.


Molecules ◽  
2022 ◽  
Vol 27 (2) ◽  
pp. 334
Author(s):  
Ji-Eun Kim ◽  
Jin-Sun Kim ◽  
Min-Jee Jo ◽  
Eunjung Cho ◽  
Shin-Young Ahn ◽  
...  

Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered adipose tissue, adipokines, play critical roles in the development of metabolic syndrome. Although the adipokines leptin and adiponectin improve insulin sensitivity, others contribute to the development of glucose intolerance, including visfatin, fetuin-A, resistin, and plasminogen activator inhibitor-1 (PAI-1). Leptin and adiponectin increase fatty acid oxidation, prevent foam cell formation, and improve lipid metabolism, while visfatin, fetuin-A, PAI-1, and resistin have pro-atherogenic properties. In this review, we briefly summarize the role of various adipokines in the development of metabolic syndrome, focusing on glucose homeostasis and lipid metabolism.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jawed Fareed ◽  
Vinod Bansal ◽  
Debra Hoppensteadt ◽  
Daneyal Syed ◽  
Syed Ahmad

Introduction: Metabolic syndrome (MS) represents a cluster of cardiovascular risk factors which contribute to myocardial infarction and stroke in end stage renal disease (ESRD) patients. Several metabolic biomarkers have been identified and their circulating levels provide a better understanding of the pathogenesis of MS/ESRD. The purpose of this investigation is to profile biomarkers of MS in ESRD patients. Materials and Methods: Plasma samples from 87 patients with ESRD undergoing maintenance hemodialysis and 50 normals were collected prior to a routine session. These samples were profiled for metabolic biomarkers using protein chip bioarray technology. The protein chip array was comprised of several biomarkers of MS. All results were compiled in terms of group means +/- 1 SD (SEM) and statistically analyzed. Results: In comparison to the normal samples, the ESRD group showed marked increase in circulating levels of all biomarkers. TNFa (47.4 +/- 18.3 vs 4.1 +/- 1.1 ng/mL) and IL-6 (7.8 +/- 9.1 vs 0.8 +/- 0.4 ng/mL) showed the most pronounced increase. C-peptide (14.5 +/- 4.1 vs 2.8 +/- 1.6 ng/mL), leptin (29.7 +/- 29.2 vs 5.2 +/- 7.9 ng/mL), resistan (16.1 +/- 6.0 vs 2.3 +/- 0.7 ng/mL) and ferritin (274 +/- 57 vs 57 +/- 63 ng/mL) showed a 5-fold increase in the ESRD group compared to normal. PAI-1 (5.4 +/- 5.2 vs 2.9 +/- 2.5 ng/mL), IL-1a (1.3 +/- 1.7 vs 0.35 +/- 0.07 ng/mL) and insulin (32.1 +/- 17.3 vs 17.1 +/- 1.7 ng/mL) showed modest increase in the ESRD patients. The increase in all of the MS biomarkers in the ESRD patients were highly significantly elevated, p <0.05. Conclusion: The specific biochip array for MS allows the selective determination of various biomarkers associated with this syndrome in the ESRD patients and normals. Parallel increase in resistan, insulin, C-peptide, and leptin points to the derangement of glucose metabolism in these patients. Increase IL-1a, TNFa, and ferritin suggests the upregulation of an inflammatory process. PAI-1 increase suggests a fibrinolytic deficit. The parallel derangement of the inflammatory process and metabolic syndrome contributes to the cardiovascular and cerebrovascular complications in these patients.


2007 ◽  
Vol 97 (01) ◽  
pp. 62-66 ◽  
Author(s):  
Alenka Mavri ◽  
Delphine Bastelica ◽  
Marjorie Poggi ◽  
Pierre Morange ◽  
Franck Peiretti ◽  
...  

SummaryThe tumor necrosis factor (TNF) pathway may be implicated in etiopathogenesis of PAI-1 overexpression during obesity. The aim of this study was to investigate the influence of polymorphismA36G of the TNF receptor 1 (TNFRSF1A +36A/G) on plasma concentrations of PAI-1 in 163 obese (31 with the metabolic syndrome, MetS) and 150 lean, healthy women. Genotypic and allele frequencies did not significantly differ between obese and lean subjects. TNFRSF1A genotypes were significantly associated with sTNFR1 plasma levels in obese women only (p<0.01); TNFRSF1A +36G/G obese carriers exhibited higher sTNFR1 and PAI-1 levels than A carriers (p<0.01 and p<0.05, respectively). In obese women, the presence of the MetS significantly potentiated the elevation of sTNFR1 and PAI-1 levels observed in the TNFRSF1A+36G/G carriers. Our results suggest that association between TNFRSF1A +36G/G genotype and the MetS renders obese women more prone to activation of the TNF pathway reflected by high circulating sTNFR1 and PAI-1 levels.


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