scholarly journals Pericytopathy: Oxidative Stress and Impaired Cellular Longevity in the Pancreas and Skeletal Muscle in Metabolic Syndrome and Type 2 Diabetes

2010 ◽  
Vol 3 (5) ◽  
pp. 290-303 ◽  
Author(s):  
Melvin R. Hayden ◽  
Ying Yang ◽  
Javad Habibi ◽  
Sarika V. Bagree ◽  
James R. Sowers
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Screening Method ◽  
Lifestyle Changes ◽  
Pancreatic Stellate Cells ◽  
Rodent Models ◽  
The Metabolic Syndrome

The pericyte's role has been extensively studied in retinal tissues of diabetic retinopathy; however, little is known regarding its role in such tissues as the pancreas and skeletal muscle. This supportive microvascular mural cell plays an important and novel role in cellular and extracellular matrix remodeling in the pancreas and skeletal muscle of young rodent models representing the metabolic syndrome and type 2 diabetes mellitus (T2DM). Transmission electron microscopy can be used to evaluate these tissues from young rodent models of insulin resistance and T2DM, including the transgenic Ren2 rat, db/db obese insulin resistantߞT2DM mouse, and human islet amyloid polypeptide (HIP) rat model of T2DM. With this method, the earliest pancreatic remodeling change was widening of the islet exocrine interface and pericyte hypercellularity, followed by pericyte differentiation into islet and pancreatic stellate cells with early fibrosis involving the islet exocrine interface and interlobular interstitium. In skeletal muscle there was a unique endothelial capillary connectivity via elongated longitudinal pericyte processes in addition to pericyte to pericyte and pericyte to myocyte cellcell connections allowing for paracrine communication. Initial pericyte activation due to moderate oxidative stress signaling may be followed by hyperplasia, migration and differentiation into adult mesenchymal cells. Continued robust oxidative stress may induce pericyte apoptosis and impaired cellular longevity. Circulating antipericyte autoantibodies have recently been characterized, and may provide a screening method to detect those patients who are developing pericyte loss and are at greater risk for the development of complications of T2DM due to pericytopathy and rarefaction. Once detected, these patients may be offered more aggressive treatment strategies such as early pharmacotherapy in addition to lifestyle changes targeted to maintaining pericyte integrity. In conclusion, we have provided a review of current knowledge regarding the pericyte and novel ultrastructural findings regarding its role in metabolic syndrome and T2DM.

The metabolic syndrome: linking oxidative stress and inflammation to obesity, type 2 diabetes, and the syndrome

2006 ◽  
Vol 67 (7) ◽  
pp. 619-626 ◽  
Author(s):  
Paresh Dandona ◽  
Husam Ghanim ◽  
Priya Mohanty ◽  
Ajay Chaudhuri
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
The Metabolic Syndrome

scholarly journals Treating Arterial Stiffness in Metabolic Syndrome and Type 2 Diabetes Mellitus

2013 ◽  
Vol 5 (1) ◽  
pp. 102-106
Author(s):  
Niki Katsiki ◽  
Eugenia Gkaliagkousi ◽  
Asterios Karagiannis ◽  
Dimitri P. Mikhailidis
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Type 2 Diabetes Mellitus ◽  
Arterial Stiffness ◽  
Antiplatelet Agents ◽  
Lifestyle Changes ◽  
The Metabolic Syndrome ◽  
Lifestyle Measures

Arterial stiffening characterizes ageing and several diseases related to increased cardiovascular (CV) risk such as the metabolic syndrome (MetS), type 2 diabetes mellitus (T2DM), hypertension, obesity and smoking. Several studies have shown that arterial stiffness is a strong, independent predictor of CV morbidity and mortality risk in such patient populations. Lifestyle measures and drugs frequently prescribed in MetS and T2DM patients such as hypolipidaemic, antihypertensive, hypoglycaemic and antiplatelet agents, may improve arterial stiffness, thus further reducing vascular risk. The current review considers the effects of these drugs and lifestyle changes on arterial stiffness in MetS and T2DM patients. The potential clinical implications of such effects on treatment decisions in clinical practice remain to be established. Multifactorial interventions may be even more beneficial in terms of CV risk reduction and thus their impact on arterial stiffness should also be evaluated.

Thrombosis in central obesity and metabolic syndrome: Mechanisms and epidemiology

2013 ◽  
Vol 110 (10) ◽  
pp. 669-680 ◽  
Author(s):  
Pierre-Emmanuel Morange ◽  
Marie-Christine Alessi
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Central Obesity ◽  
Subsequent Development ◽  
Ectopic Fat ◽  
Metabolic Alterations ◽  
The Metabolic Syndrome

summaryCentral obesity is a key feature of the metabolic syndrome (metS), a multiplex risk factor for subsequent development of type 2 diabetes and cardiovascular disease. Many metabolic alterations closely related to this condition exert effects on platelets and vascular cells. A procoagulant and hypofibrinolytic state has been identified, mainly underlain by inflammation, oxidative stress, dyslipidaemia, and ectopic fat that accompany central obesity. In support of these data, central obesity independently predisposes not only to atherothrombosis but also to venous thrombosis.

scholarly journals Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-21 ◽  
Author(s):  
Nobuko Hagiwara
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Model Organisms ◽  
Human Populations ◽  
Peripheral Tissues ◽  
The Metabolic Syndrome ◽  
Muscle Remodeling

The primary deficiency underlying metabolic syndrome is insulin resistance, in which insulin-responsive peripheral tissues fail to maintain glucose homeostasis. Because skeletal muscle is the major site for insulin-induced glucose uptake, impairments in skeletal muscle’s insulin responsiveness play a major role in the development of insulin resistance and type 2 diabetes. For example, skeletal muscle of type 2 diabetes patients and their offspring exhibit reduced ratios of slow oxidative muscle. These observations suggest the possibility of applying muscle remodeling to recover insulin sensitivity in metabolic syndrome. Skeletal muscle is highly adaptive to external stimulations such as exercise; however, in practice it is often not practical or possible to enforce the necessary intensity to obtain measurable benefits to the metabolic syndrome patient population. Therefore, identifying molecular targets for inducing muscle remodeling would provide new approaches to treat metabolic syndrome. In this review, the physiological properties of skeletal muscle, genetic analysis of metabolic syndrome in human populations and model organisms, and genetically engineered mouse models will be discussed in regard to the prospect of applying skeletal muscle remodeling as possible therapy for metabolic syndrome.

scholarly journals Telomere Length and Oxidative Stress and Its Relation with Metabolic Syndrome Components in the Aging

Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 253
Author(s):  
Graciela Gavia-García ◽  
Juana Rosado-Pérez ◽  
Taide Laurita Arista-Ugalde ◽  
Itzen Aguiñiga-Sánchez ◽  
Edelmiro Santiago-Osorio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Telomere Length ◽  
Scientific Evidence ◽  
Telomeric Dna ◽  
Biochemical Alterations ◽  
The Metabolic Syndrome ◽  
Age Related ◽  
And Function

A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations such as obesity, dyslipidaemia, arterial hypertension, hyperglycaemia, and insulin resistance, all of which are considered as risk factors for type 2 diabetes mellitus (T2DM) and cardiovascular diseases, which are associated in turn with an increase of OxS. In this sense, we review scientific evidence that supports the association between OxS with telomere length (TL) dynamics and the relationship with MetS components in aging. It was analysed whether each MetS component affects the telomere length separately or if they all affect it together. Likewise, this review provides a summary of the structure and function of telomeres and telomerase, the mechanisms of telomeric DNA repair, how telomere length may influence the fate of cells or be linked to inflammation and the development of age-related diseases, and finally, how the lifestyles can affect telomere length.

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