The metabolic syndrome or the insulin resistance syndrome? Different names, different concepts, and different goals

2004 ◽  
Vol 33 (2) ◽  
pp. 283-303 ◽  
Author(s):  
Gerald Reaven
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Resistance Syndrome ◽  
The Metabolic Syndrome

Lipid behavior in metabolic syndrome pathophysiology

2021 ◽  
Vol 17 ◽  
Author(s):  
Basheer Marzoog
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Lipid Level ◽  
Visceral Obesity ◽  
Insulin Resistance Syndrome ◽  
Chronic Inflammatory Response ◽  
Cell Dysfunction ◽  
Commensal Microbiota ◽  
The Metabolic Syndrome

: 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).

scholarly journals HYPERTENSION MANAGEMENT IN METABOLIC SYNDROME

2019 ◽  
Vol 9 (5) ◽  
pp. 327-347
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Insulin Resistance Syndrome ◽  
Effective Control ◽  
Peripheral Tissues ◽  
The Metabolic Syndrome ◽  
Cardiovascular Morbidity And Mortality ◽  
Therapy Target ◽  
Based Medicine

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.

scholarly journals The metabolic syndrome X or insulin resistance syndrome

2007 ◽  
Vol 64 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Aleksandra Nikolic ◽  
Dejan Nikolic ◽  
Violeta Stanimirovic
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Resistance Syndrome ◽  
Metabolic Syndrome X ◽  
Syndrome X ◽  
The Metabolic Syndrome

scholarly journals Genetics of the metabolic syndrome

2000 ◽  
Vol 83 (S1) ◽  
pp. S39-S48 ◽  
Author(s):  
Leif Groop
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glycogen Synthase ◽  
Insulin Resistance Syndrome ◽  
Hormone Sensitive Lipase ◽  
Common Denominator ◽  
The Metabolic Syndrome ◽  
Genome Wide ◽  
Hormone Sensitive ◽  
Obesity Hypertension

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.

Metabolic Syndrome During Menopause

2019 ◽  
Vol 17 (6) ◽  
pp. 595-603 ◽  
Author(s):  
Sezcan Mumusoglu ◽  
Bulent Okan Yildiz
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Central Obesity ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Natural Menopause ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Aging Women

The metabolic syndrome (MetS) comprises individual components including central obesity, insulin resistance, dyslipidaemia and hypertension and it is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The menopause per se increases the incidence of MetS in aging women. The effect(s) of menopause on individual components of MetS include: i) increasing central obesity with changes in the fat tissue distribution, ii) potential increase in insulin resistance, iii) changes in serum lipid concentrations, which seem to be associated with increasing weight rather than menopause itself, and, iv) an association between menopause and hypertension, although available data are inconclusive. With regard to the consequences of MetS during menopause, there is no consistent data supporting a causal relationship between menopause and CVD. However, concomitant MetS during menopause appears to increase the risk of CVD. Furthermore, despite the data supporting the association between early menopause and increased risk of T2DM, the association between natural menopause itself and risk of T2DM is not evident. However, the presence and the severity of MetS appears to be associated with an increased risk of T2DM. Although the mechanism is not clear, surgical menopause is strongly linked with a higher incidence of MetS. Interestingly, women with polycystic ovary syndrome (PCOS) have an increased risk of MetS during their reproductive years; however, with menopausal transition, the risk of MetS becomes similar to that of non-PCOS women.

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