W09.220 Endothelial dysfunction in subjects with early stages of the metabolic syndrome. Association with visceral adiposity and insulin resistance

2004 ◽  
Vol 5 (1) ◽  
pp. 51
Author(s):  
R GILABERT
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Visceral Adiposity ◽  
Early Stages ◽  
The Metabolic Syndrome ◽  
Syndrome Association

scholarly journals Visceral obesity, metabolic syndrome, insulin resistance and cancer

2011 ◽  
Vol 71 (1) ◽  
pp. 181-189 ◽  
Author(s):  
Suzanne L. Doyle ◽  
Claire L. Donohoe ◽  
Joanne Lysaght ◽  
John V. Reynolds
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Visceral Adipose Tissue ◽  
Tumour Progression ◽  
Visceral Adiposity ◽  
Oesophageal Adenocarcinoma ◽  
The Metabolic Syndrome ◽  
Visceral Adipose

This paper presents emerging evidence linking visceral adiposity and the metabolic syndrome (MetSyn) with carcinogenesis. The link between obesity and cancer has been clearly identified in a multitude of robust epidemiological studies. Research is now focusing on the role of visceral adipose tissue in carcinogenesis; as it is recognised as an important metabolic tissue that secretes factors that systemically alter the immunological, metabolic and endocrine milieu. Excess visceral adipose tissue gives rise to a state of chronic systemic inflammation with associated insulin resistance and dysmetabolism, collectively known as the MetSyn. Prospective cohort studies have shown associations between visceral adiposity, the MetSyn and increased risk of breast cancer, colorectal cancer and oesophageal adenocarcinoma. Furthermore, visceral adiposity and the MetSyn have been associated with increased tumour progression and reduced survival. The mechanisms by which visceral adiposity and the MetSyn are thought to promote tumorigenesis are manifold. These include alterations in adipokine secretion and cell signalling pathways. In addition, hyperinsulinaemia, subsequent insulin resistance and stimulation of the insulin-like growth factor-1 axis have all been linked with visceral adiposity and promote tumour progression. Furthermore, the abundance of inflammatory cells in visceral adipose tissue, including macrophages and T-cells, create systemic inflammation and a pro-tumorigenic environment. It is clear from current research that excess visceral adiposity and associated dysmetabolism play a central role in the pathogenesis of certain cancer types. Further research is required to elucidate the exact mechanisms at play and identify potential targets for intervention.

scholarly journals Mediterranean diet, endothelial function and vascular inflammatory markers

2006 ◽  
Vol 9 (8A) ◽  
pp. 1073-1076 ◽  
Author(s):  
Katherine Esposito ◽  
Miryam Ciotola ◽  
Dario Giugliano
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Low Grade ◽  
The Metabolic Syndrome ◽  
Inflammatory State ◽  
Triggering Factor ◽  
Inflammatory Milieu ◽  
Visceral Adipose

AbstractObjectivesTo discuss present knowledge about the relation between adipose tissue, inflammation and the Mediterranean-style diet.DesignReview of the literature and personal perspectives.Setting and resultsRecent studies indicate that adipose tissue is an endocrine organ producing numerous proteins, collectively referred to as adipokines, with broad biological activity, which play an important autocrine role in obesity-associated complications. Adipose tissue in general and visceral fat in particular are thought to be key regulators of inflammation which is heavily involved in the onset and development of atherothrombotic disease. Moreover, chronic inflammation may also represent a triggering factor in the origin of the metabolic syndrome and type 2 diabetes mellitus. An increased release of proinflammatory adipokines from the visceral adipose tissue, associated with a reduced secretion of anti-inflammatory adipokines and cytokines, could determine a low-grade chronic inflammatory state which might play a role in the future development of the metabolic syndrome, diabetes and atherosclerosis through both insulin resistance and endothelial dysfunction. Interventions aimed at decreasing weight loss and improving adherence to a Mediterranean-style diet in people with obesity or metabolic syndrome decrease the inflammatory milieu and ameliorate both insulin resistance and endothelial dysfunction.ConclusionsAppropriate dietary patterns, as those associated with the eating model of Mediterranean-type diets, represent therapeutic strategies to reduce inflammation and the associated metabolic and cardiovascular risk.

scholarly journals Peak Growth Hormone-Releasing Hormone-Arginine-Stimulated Growth Hormone Is Inversely Associated with Intramyocellular and Intrahepatic Lipid Content in Premenopausal Women with Obesity

2009 ◽  
Vol 94 (10) ◽  
pp. 3995-4002 ◽  
Author(s):  
Miriam A. Bredella ◽  
Martin Torriani ◽  
Bijoy J. Thomas ◽  
Reza Hosseini Ghomi ◽  
Danielle J. Brick ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Growth Hormone ◽  
Premenopausal Women ◽  
Normal Weight ◽  
Visceral Adiposity ◽  
Gh Secretion ◽  
The Metabolic Syndrome ◽  
Intrahepatic Lipids ◽  
Peak Growth Hormone

Context: Visceral adiposity is a strong determinant of GH secretion, and low endogenous GH secretion is associated with increased insulin resistance, a key component of the metabolic syndrome. Increased fat accumulation in skeletal muscle and liver may play an etiological role in the development of insulin resistance and other complications of the metabolic syndrome. Little is known about the role of decreased endogenous GH secretion in the pathogenesis of insulin resistance in obesity. Objective: To investigate the relationship between intramyocellular lipids (IMCL), intrahepatic lipids, and peak-stimulated GH in premenopausal women with obesity. Design and Setting: We conducted a cross-sectional study at a clinical translational research center. Patients: Patients included 21 premenopausal women with obesity (mean body mass index, 34.0 ± 4.5 kg/m2) and 17 normal-weight controls (mean body mass index, 21.9 ± 2.0 kg/m2) of comparable mean age. Main Outcomes Measures: IMCL and intrahepatic lipids were measured with proton magnetic resonance spectroscopy (1H-MRS). Body composition was measured with magnetic resonance imaging. Peak GH was measured after stimulation with GHRH-arginine. Results: Obese subjects had higher IMCL, intrahepatic lipids, abdominal and thigh fat, and thigh muscle mass compared with normal-weight controls. There were strong inverse associations between peak GH and both IMCL and intrahepatic lipids independent of age and visceral adiposity. There were positive associations between IMCL and intrahepatic lipids with measures of insulin resistance and serum triglycerides. Conclusion: In premenopausal women with obesity, peak GH is inversely associated with IMCL and intrahepatic lipids independent of age and visceral adiposity. This suggests that low GH may contribute to insulin resistance in obesity through effects on muscle and intrahepatic lipids. Peak growth hormone after GHRH-arginine stimulation is inversely associated with intramyocellular and intrahepatic lipids in premenopausal women with obesity.

scholarly journals Parameters of endothelial function and insulin resistance in patients with metabolic syndrome before and after weight loss

2008 ◽  
Vol 5 (1) ◽  
pp. 18-22 ◽  
Author(s):  
A M Mkrtumyan ◽  
E V Biryukova ◽  
N V Markina ◽  
M A Garbuzova
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Coronary Heart Disease ◽  
Weight Loss ◽  
Heart Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Main Role ◽  
Pathophysiological Mechanism ◽  
The Metabolic Syndrome

In clinical practice, physicians of different specialties often faced with the metabolic syndrome (MS) is a set of hormonal and metabolic disorders that share a common pathophysiological mechanism - insulin resistance (IR) [1, 5, 11]. MS is important for the clinician not only how widespread pathology, but primarily as a life-threatening condition. Of course, this syndrome plays an important role in accelerating the development and progression of diseases associated with atherosclerosis, which, according to experts WHO, ranks first among the causes of mortality in industrialized countries [12, 16, 19]. This situation is particularly important for Russia due to the relatively high spread of the syndrome, component, according to several authors, about 20% of the population, and high rates of death from coronary heart disease and stroke in the Russian population [2, 4, 5]. It is known that the risk of coronary heart disease (CHD), stroke, and total coronary mortality increases with the number of components of metabolic syndrome [14, 15, 20]. The study J.H. Park et al., Which included 478 patients with ischemic stroke, MS was diagnosed in 53.4% of patients (criteria NCEP ATP III), the thickness of the complex value of the index "intima-media" of the carotid arteries was increased in direct proportion to an increase in the number of available components of MS [20] . Link between R D and cardiovascular disease, apparently, is endothelial dysfunction, which is the study at various metabolic diseases received much attention [9, 10, 22]. Endothelial dysfunction, which is typical for many patients with MS, is a marker of metabolic and vascular disorders [15, 22]. In the initial period of development of the atherosclerotic process, even when there are no obvious clinical manifestations and visible morphological changes of blood vessels, the main role is played by endothelial dysfunction [9, 21]. Endothelial dysfunction is also discussed as one of the reasons for the rapid development, progression of atherosclerosis and its complications in patients with MS [11,18]. For example, recent studies have shown that tears plaques leading to myocardial infarction, do not always occur in the zone of maximum stenosis of the coronary arteries [13]. Rather, they tend to occur in places restrictions of small - less than 50% by angiography. The study of endothelial function in patients with MS is at the initial stages of the study [8, 15, 18]. In addition, of particular interest is the study of the effect of weight loss on the state of the endothelium in the syndrome of insulin resistance.

scholarly journals Adipose tissue at the crossroads in the development of the metabolic syndrome, inflammation and atherosclerosis

2009 ◽  
Vol 53 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Bernardo Léo Wajchenberg ◽  
Marcia Nery ◽  
Maria Rosaria Cunha ◽  
Maria Elizabeth Rossi da Silva
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Low Grade ◽  
Inflammatory Signaling ◽  
The Metabolic Syndrome ◽  
Inflammatory State ◽  
Low Grade Inflammation ◽  
Adipose Tissue Depot

The authors analyze insulin resistance, the metabolic syndrome and endothelial dysfunction as consequence of a common antecedent, a low grade inflammation, indicating that in obesity there is a chronically activated inflammatory state of the adipose tissue. Furthermore, the inflammatory signaling is discussed according to the adipose tissue depot, visceral or subcutaneous.

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