Growth hormone and IGFBP-3 but not IGF-1 are independent predictors of insulin sensitivity in healthy subjects: on the role of hGH in the metabolic syndrome

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
MA Arafat ◽  
F Perschel ◽  
C Schöfl ◽  
M Weickert ◽  
J Purschwitz ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Growth Hormone ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
The Metabolic Syndrome ◽  
Igfbp 3

Adiponectin, type 2 diabetes and the metabolic syndrome: lessons from human genetic studies

2006 ◽  
Vol 8 (27) ◽  
pp. 1-12 ◽  
Author(s):  
Francis Vasseur ◽  
David Meyre ◽  
Philippe Froguel
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Vascular Complications ◽  
Physiological Role ◽  
Nucleotide Polymorphisms ◽  
The Metabolic Syndrome ◽  
And Function

Adiponectin, a protein exclusively secreted by adipose tissue but present at low levels in obesity, is now widely recognised as a key determinant of insulin sensitivity and of protection against obesity-associated metabolic syndrome. In this review we explain how genetic findings have contributed to a better understanding of the physiological role of adiponectin in humans. The adiponectin-encoding gene, ADIPOQ (ACDC), is very polymorphic: many frequent exonic synonymous, intronic and promoter single-nucleotide polymorphisms (SNPs) have been identified, as well as a few rare exonic amino acid substitutions. Several of these variations additively contribute to the modulation of adiponectin level and function, and associate with insulin sensitivity, type 2 diabetes and vascular complications of obesity.

Role of genetic factors in the development of hypertension in young patients with metabolic syndrome

2020 ◽  
pp. 23-32
Author(s):  
Elena Korneeva ◽  
Mikhail Voevoda ◽  
Sergey Semaev ◽  
Vladimir Maksimov
Keyword(s):  
Metabolic Syndrome ◽  
High Risk ◽  
Arterial Hypertension ◽  
Genetic Factors ◽  
Young Patients ◽  
Integrin Αiibβ3 ◽  
Ace Gene ◽  
The Metabolic Syndrome

Results of the study related to polymorphism of ACE gene (rs1799752)‎, integrin αIIbβ3, and CSK gene (rs1378942) influencing development of arterial hypertension in young patients with metabolic syndrome are presented. Hypertension as a component of the metabolic syndrome was detected in 15.0% of young patients. Prevalence of mutant alleles of the studied genes among the examined patients was quite high, so homozygous DD genotype was found in 21.6%, and mutant D allele of the ACE gene in 47.4%. A high risk of hypertension in patients with MS was detected in carriers of the T allele of the CSK (rs1378942) gene – 54.8%, which was most often observed in a combination of polymorphic ACE and CSK gene loci (p = 0.0053).

The Role of Quinapril in the Presence of a Weight Loss Regimen: Endothelial Function and Markers of Obesity in Patients With the Metabolic Syndrome

2007 ◽  
Vol 10 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Sameer Nagamia ◽  
Anbu Pandian ◽  
Faiz Cheema ◽  
Rama Natarajan ◽  
Qamar A. Khan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Endothelial Function ◽  
The Metabolic Syndrome

scholarly journals The Metabolic Syndrome in Overweight Hispanic Youth and the Role of Insulin Sensitivity

2004 ◽  
Vol 89 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Martha L. Cruz ◽  
Marc J. Weigensberg ◽  
Terry T.-K. Huang ◽  
Geoff Ball ◽  
Gabriel Q. Shaibi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Family History ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Hdl Cholesterol ◽  
Hispanic Youth ◽  
The Metabolic Syndrome

The prevalence of the metabolic syndrome is highest among Hispanic adults. However, studies exploring the metabolic syndrome in overweight Hispanic youth are lacking. Subjects were 126 overweight children (8–13 yr of age) with a family history for type 2 diabetes. The metabolic syndrome was defined as having at least three of the following: abdominal obesity, low high-density lipoprotein (HDL) cholesterol, hypertriglyceridemia, hypertension, and/or impaired glucose tolerance. Insulin sensitivity was determined by the frequently sampled iv glucose tolerance test and minimal modeling. The prevalence of abdominal obesity, low HDL cholesterol, hypertriglyceridemia, systolic and diastolic hypertension, and impaired glucose tolerance was 62, 67, 26, 22, 4, and 27%, respectively. The presence of zero, one, two, or three or more features of the metabolic syndrome was 9, 22, 38, and 30%, respectively. After controlling for body composition, insulin sensitivity was positively related to HDL cholesterol (P < 0.01) and negatively related to triglycerides (P < 0.001) and systolic (P < 0.01) and diastolic blood pressure (P < 0.05). Insulin sensitivity significantly decreased (P < 0.001) as the number of features of the metabolic syndrome increased. In conclusion, overweight Hispanic youth with a family history for type 2 diabetes are at increased risk for cardiovascular disease and type 2 diabetes, and this appears to be due to decreased insulin sensitivity. Improving insulin resistance may be crucial for the prevention of chronic disease in this at-risk population.

The Role of Endocannabinoid System Blockade in the Treatment of the Metabolic Syndrome

2007 ◽  
Vol 47 (5) ◽  
pp. 642-652 ◽  
Author(s):  
Anna I. Kakafika ◽  
Dimitri P. Mikhailidis ◽  
Asterios Karagiannis ◽  
Vasilios G. Athyros
Keyword(s):  
Metabolic Syndrome ◽  
Endocannabinoid System ◽  
The Metabolic Syndrome

scholarly journals Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin

2012 ◽  
Vol 123 (11) ◽  
pp. 635-647 ◽  
Author(s):  
Radko Komers ◽  
Shaunessy Rogers ◽  
Terry T. Oyama ◽  
Bei Xu ◽  
Chao-Ling Yang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Time Course ◽  
Kinase Inhibitor ◽  
Endogenous Expression ◽  
The Metabolic Syndrome ◽  
Mammalian Cell Lines ◽  
Phosphoinositide 3 Kinase

In the present study, we investigated the activity of the thiazide-sensitive NCC (Na+–Cl− co-transporter) in experimental metabolic syndrome and the role of insulin in NCC activation. Renal responses to the NCC inhibitor HCTZ (hydrochlorothiazide), as a measure of NCC activity in vivo, were studied in 12-week-old ZO (Zucker obese) rats, a model of the metabolic syndrome, and in ZL (Zucker lean) control animals, together with renal NCC expression and molecular markers of NCC activity, such as localization and phosphorylation. Effects of insulin were studied further in mammalian cell lines with inducible and endogenous expression of this molecule. ZO rats displayed marked hyperinsulinaemia, but no differences in plasma aldosterone, compared with ZL rats. In ZO rats, natriuretic and diuretic responses to NCC inhibition with HCTZ were enhanced compared with ZL rats, and were associated with a decrease in BP (blood pressure). ZO rats displayed enhanced Thr53 NCC phosphorylation and predominant membrane localization of both total and phosphorylated NCC, together with a different profile in expression of SPAK (Ste20-related proline/alanine-rich kinase) isoforms, and lower expression of WNK4. In vitro, insulin induced NCC phosphorylation, which was blocked by a PI3K (phosphoinositide 3-kinase) inhibitor. Insulin-induced reduction in WNK4 expression was also observed, but delayed compared with the time course of NCC phosphorylation. In summary, we report increased NCC activity in hyperinsulinaemic rodents in conjunction with the SPAK expression profile consistent with NCC activation and reduced WNK4, as well as an ability of insulin to induce NCC stimulatory phosphorylation in vitro. Together, these findings indicate that hyperinsulinaemia is an important driving force of NCC activity in the metabolic syndrome with possible consequences for BP regulation.

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