The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

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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Association of homeostasis model assessment of insulin resistance, adiponectin, and low-grade inflammation with the course of the metabolic syndrome

Clinical Biochemistry ◽

10.1016/j.clinbiochem.2015.02.005 ◽

2015 ◽

Vol 48 (7-8) ◽

pp. 503-507 ◽

Cited By ~ 13

Author(s):

YuSong Ding ◽

ShuGang Li ◽

Ru-Lin Ma ◽

Heng Guo ◽

JingYu Zhang ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Low Grade ◽

Model Assessment ◽

Homeostasis Model Assessment ◽

The Metabolic Syndrome ◽

Low Grade Inflammation

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04.02 THE METABOLIC SYNDROME IS ASSOCIATED WITH CENTRAL AND PERIPHERAL ARTERIAL STIFFNESS IN YOUNG WOMEN BUT NOT IN MEN: THE MEDIATING ROLE OF INSULIN RESISTANCE AND LOW-GRADE INFLAMMATION. THE NORTHERN IRELAND YOUNG HEARTS PROJECT (NIYHP)

Artery Research ◽

10.1016/s1872-9312(07)70009-1 ◽

2007 ◽

Vol 1 (S1) ◽

pp. S24

Author(s):

I. Ferreira* ◽

C.A. Boreham ◽

J.W.R. Twisk ◽

A.M. Gallagher ◽

I.S. Young ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Northern Ireland ◽

Young Women ◽

Low Grade ◽

Mediating Role ◽

The Metabolic Syndrome ◽

Peripheral Arterial ◽

Low Grade Inflammation

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Mediterranean diet, endothelial function and vascular inflammatory markers

Public Health Nutrition ◽

10.1017/s1368980007668529 ◽

2006 ◽

Vol 9 (8A) ◽

pp. 1073-1076 ◽

Cited By ~ 58

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.

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Regulation of adipokine secretion byn-3 fatty acids

Proceedings of The Nutrition Society ◽

10.1017/s0029665110001801 ◽

2010 ◽

Vol 69 (3) ◽

pp. 324-332 ◽

Cited By ~ 60

Author(s):

María J. Moreno-Aliaga ◽

Silvia Lorente-Cebrián ◽

J. Alfredo Martínez

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Fatty Acids ◽

Adipose Tissue ◽

Physiological Role ◽

Low Grade ◽

Protective Effects ◽

Metabolic Disturbances ◽

The Metabolic Syndrome ◽

Low Grade Inflammation

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. Then-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact,n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability ofn-3 PUFA to regulate adipokine gene expression and secretion has been observed bothin vitroandin vivoin rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions ofn-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability ofn-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.

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Adipose Tissue Dysfunction in Nascent Metabolic Syndrome

Journal of Obesity ◽

10.1155/2013/393192 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 75

Author(s):

Andrew A. Bremer ◽

Ishwarlal Jialal

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

Subcutaneous Adipose Tissue ◽

Low Grade ◽

The Metabolic Syndrome ◽

Adipose Tissue Dysfunction ◽

Increased Risk ◽

Subcutaneous Adipose ◽

Low Grade Inflammation

The metabolic syndrome (MetS) confers an increased risk for both type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Moreover, studies on adipose tissue biology in nascent MetS uncomplicated by T2DM and/or CVD are scanty. Recently, we demonstrated that adipose tissue dysregulation and aberrant adipokine secretion contribute towards the syndrome’s low-grade chronic proinflammatory state and insulin resistance. Specifically, we have made the novel observation that subcutaneous adipose tissue (SAT) in subjects with nascent MetS has increased macrophage recruitment with cardinal crown-like structures. We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1. The majority of these abnormalities persisted following correction for increased adiposity. Our data, as well as data from other investigators, thus, highlight the importance of subcutaneous adipose tissue dysfunction in subjects with MetS and its contribution to the proinflammatory state and insulin resistance. This adipokine profile may contribute to increased insulin resistance and low-grade inflammation, promoting the increased risk of T2DM and CVD.

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