scholarly journals Genetic Variability at the Six Transmembrane Protein of Prostate 2 Locus and the Metabolic Syndrome: The Data from an Epidemiological Study on the Insulin Resistance Syndrome (DESIR) Study

2010 ◽  
Vol 95 (6) ◽  
pp. 2942-2947 ◽  
Author(s):  
Aurélie Miot ◽  
Suliya Maimaitiming ◽  
Nathalie Emery ◽  
Naima Bellili ◽  
Ronan Roussel ◽  
...  
2021 ◽  
Vol 17 ◽  
Author(s):  
Basheer Marzoog

: Undeniably, lipid plays an extremely important role in the homeostasis balance, since lipid contributes to the regulation of the metabolic processes. The metabolic syndrome pathogenesis is multi-pathway that composes neurohormonal disorders, endothelial cell dysfunction, metabolic disturbance, genetic predisposition, in addition to gut commensal microbiota. The heterogenicity of the possible mechanisms gives the metabolic syndrome its complexity and limitation of therapeutic accesses. The main pathological link that lipid contributes to the emergence of metabolic syndrome via central obesity and visceral obesity that consequently lead to oxidative stress and chronic inflammatory response promotion. Physiologically, a balance is kept between the adiponectin and adipokines level to maintain the lipid level in the organism. Clinically, extremely important to define the borders of the lipid level in which the pathogenesis of the metabolic syndrome is reversible, otherwise will be accompanied by irreversible complications and sequelae of the metabolic syndrome (cardiovascular, insulin resistance). The present paper is dedicated to providing novel insights into the role of lipid in the development of metabolic syndrome hence dyslipidemia is the initiator of insulin resistance syndrome (metabolic syndrome).


2019 ◽  
Vol 9 (5) ◽  
pp. 327-347
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin

Hypertension is one of the key risk factors for cardiovascular morbidity and mortality. Metabolic syndrome (synonyms: syndrome X, insulin resistance syndrome) is characterized by increased visceral fat mass, decreased sensitivity of peripheral tissues to insulin (insulin resistance) and hyperinsulinemia, which cause disorders of carbohydrate, lipid, and purine metabolism. Hypertension is an integral component of the metabolic syndrome. The severity of hypertension in patients with metabolic syndrome is higher in comparison with patients without metabolic disorders. In patients with metabolic syndrome, the probability of cardiac and brain damage increases fivefold, kidney damage threefold, and the vessels twofold. The presence of diabetes reduces the likelihood of achieving effective control of blood pressure by 1.4 times, hypercholesterolemia — by 1.5 times, obesity — by 1.7 times. In the presence of any three factors, the effectiveness of treatment is reduced twofold. In this article, approaches to the management of patients with hypertension and metabolic syndrome, aspects of non-drug therapy, target blood pressure levels, and the choice of drugs are presented in accordance with evidence-based medicine and current recommendations.


2007 ◽  
Vol 64 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Aleksandra Nikolic ◽  
Dejan Nikolic ◽  
Violeta Stanimirovic

2000 ◽  
Vol 83 (S1) ◽  
pp. S39-S48 ◽  
Author(s):  
Leif Groop

The clustering of cardiovascular risk factors such as abdominal obesity, hypertension, dyslipidaemia and glucose intolerance in the same persons has been called the metabolic or insulin-resistance syndrome. In 1998 WHO proposed a unifying definition for the syndrome and chose to call it the metabolic syndrome rather than the insulin-resistance syndrome. Although insulin resistance has been considered as a common denominator for the different components of the syndrome, there is still debate as to whether it is pathogenically involved in all of the different components of the syndrome. Clustering of the syndrome in families suggests a genetic component. It is plausible that so-called thrifty genes, which have ensured optimal storage of energy during periods of fasting, could contribute to the phenotype of the metabolic syndrome. Common variants in a number of candidate genes influencing fat and glucose metabolism can probably, together with environmental triggers, increase susceptibility to the syndrome. Among these, the genes for β3-adrenergic receptor, hormone-sensitive lipase, lipoprotein lipase, IRS-1, PC-1, skeletal muscle glycogen synthase, etc. appear to increase the risk of the metabolic syndrome. In addition, novel genes may be identified by genome-wide searches.


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