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.

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.

Redox-inflammatory synergy in the metabolic syndrome

2013 ◽  
Vol 91 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Sean Bryan ◽  
Boran Baregzay ◽  
Drew Spicer ◽  
Pawan K. Singal ◽  
Neelam Khaper
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Atherogenic Dyslipidemia ◽  
Disease States ◽  
The Metabolic Syndrome ◽  
Anthropometric Features ◽  
Inflammatory Processes ◽  
Inflammatory Milieu

Metabolic syndrome (MetS) comprises interrelated disease states including obesity, insulin resistance and type 2 diabetes (T2DM), dyslipidemia, and hypertension. Essential to normal physiological function, and yet massively damaging in excess, oxidative stress and inflammation are pivotal common threads among the pathologies of MetS. Increasing evidence indicates that redox and inflammatory dysregulation parallels the syndrome's physiological, biochemical, and anthropometric features, leading many to consider the pro-oxidative, pro-inflammatory milieu an unofficial criterion in itself. Left unchecked, cross-promotion of oxidative stress and inflammation creates a feed-forward cycle that can initiate and advance disease progression. Such redox-inflammatory integration is evident in the pathogenesis of obesity, insulin resistance and T2DM, atherogenic dyslipidemia, and hypertension, and is thus hypothesized to be the “common soil” from which they develop. The present review highlights the synergistic contributions of redox-inflammatory processes to each of the components of the MetS.

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 Gone with the Wnts: β-Catenin, T-Cell Factor, Forkhead Box O, and Oxidative Stress in Age-Dependent Diseases of Bone, Lipid, and Glucose Metabolism

2007 ◽  
Vol 21 (11) ◽  
pp. 2605-2614 ◽  
Author(s):  
Stavros C. Manolagas ◽  
Maria Almeida
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Stem Cell ◽  
Wnt Signaling ◽  
Cell Fate ◽  
Stem Cell Fate ◽  
T Cell Factor ◽  
The Metabolic Syndrome ◽  
Forkhead Box ◽  
Age Related

Abstract The Wnt/β-catenin signaling pathway affects several biological processes ranging from embryonic development, patterning, and postembryonic stem cell fate, to bone formation and insulin secretion in adulthood. β-Catenin mediates canonical Wnt signaling by binding to and activating members of the T-cell factor (TCF) transcription factor family. Similar to the Wnt/β-catenin pathway, oxidative stress influences fundamental cellular processes including stem cell fate and has been linked to aging and the development of age-related diseases. However, the molecular details of the pathogenetic effects of oxidative stress on the homeostasis of many different tissues remain unclear. β-Catenin has been recently implicated as a pivotal molecule in defense against oxidative stress by serving as a cofactor of the forkhead box O (FOXO) transcription factors. In addition, it has been shown that oxidative stress is a pivotal pathogenetic factor of age-related bone loss and strength in mice, leading to, among other changes, a decrease in osteoblast number and bone formation. These particular cellular changes evidently result from diversion of the limited pool of β-catenin from TCF- to FOXO-mediated transcription in osteoblastic cells. Fascinatingly, attenuation of Wnt-mediated transcription, resulting from an autosomal-dominant missense mutation in LRP6, a coreceptor for the Wnt-signaling pathway, has been linked recently genetically not only to premature osteoporosis, but also to coronary artery disease as well as several features of the metabolic syndrome including hyperlipidemia, hypertension, and diabetes, but not obesity. In this minireview, we highlight evidence linking the age-associated oxidative stress with FOXOs, Wnt/β-catenin signaling, osteoblastogenesis, adipogenesis, osteoporosis, and several features of the metabolic syndrome. We hypothesize that antagonism of Wnt signaling by oxidative stress with increasing age may be a common molecular mechanism contributing to the development not only of involutional osteoporosis, but several pathologies such as atherosclerosis, insulin resistance, and hyperlipidemia, all of which become more prevalent with advancing age.

Impact of the metabolic syndrome on peripheral nerve structure and function in type 2 diabetes

2021 ◽  
Author(s):  
Tushar Issar ◽  
Shyam S. Tummanapalli ◽  
Adeniyi A. Borire ◽  
Natalie C. G. Kwai ◽  
Ann M. Poynten ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Peripheral Nerve ◽  
Structure And Function ◽  
Nerve Structure ◽  
The Metabolic Syndrome ◽  
And Function

scholarly journals Comparison of purple carrot juice and β-carotene in a high-carbohydrate, high-fat diet-fed rat model of the metabolic syndrome

2010 ◽  
Vol 104 (9) ◽  
pp. 1322-1332 ◽  
Author(s):  
Hemant Poudyal ◽  
Sunil Panchal ◽  
Lindsay Brown
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Structure And Function ◽  
Carrot Juice ◽  
High Fat ◽  
High Carbohydrate ◽  
The Metabolic Syndrome ◽  
And Function ◽  
Β Carotene

Anthocyanins, phenolic acids and carotenoids are the predominant phytochemicals present in purple carrots. These phytochemicals could be useful in treatment of the metabolic syndrome since anthocyanins improve dyslipidaemia, glucose tolerance, hypertension and insulin resistance; the phenolic acids may also protect against CVD and β-carotene may protect against oxidative processes. In the present study, we have compared the ability of purple carrot juice and β-carotene to reverse the structural and functional changes in rats fed a high-carbohydrate, high-fat diet as a model of the metabolic syndrome induced by diet. Cardiac structure and function were defined by histology, echocardiography and in isolated hearts and blood vessels; liver structure and function, oxidative stress and inflammation were defined by histology and plasma markers. High-carbohydrate, high-fat diet-fed rats developed hypertension, cardiac fibrosis, increased cardiac stiffness, endothelial dysfunction, impaired glucose tolerance, increased abdominal fat deposition, altered plasma lipid profile, liver fibrosis and increased plasma liver enzymes together with increased plasma markers of oxidative stress and inflammation as well as increased inflammatory cell infiltration. Purple carrot juice attenuated or reversed all changes while β-carotene did not reduce oxidative stress, cardiac stiffness or hepatic fat deposition. As the juice itself contained low concentrations of carotenoids, it is likely that the anthocyanins are responsible for the antioxidant and anti-inflammatory properties of purple carrot juice to improve glucose tolerance as well as cardiovascular and hepatic structure and function.

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.

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 “Obesity and Insulin Resistance” Is the Component of the Metabolic Syndrome Most Strongly Associated with Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 79
Author(s):  
Grzegorz K. Jakubiak ◽  
Kamila Osadnik ◽  
Mateusz Lejawa ◽  
Tadeusz Osadnik ◽  
Marcin Goławski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Young Adults ◽  
Anthropometric Parameters ◽  
The Metabolic Syndrome ◽  
Total Antioxidant ◽  
History Of

Metabolic syndrome (MS) is not a homogeneous entity, but this term refers to the coexistence of factors that increase the risk for the development of type 2 diabetes and cardiovascular disease. There are different versions of the criteria for the diagnosis of MS, which makes the population of patients diagnosed with MS heterogeneous. Research to date shows that MS is associated with oxidative stress (OS), but it is unclear which MS component is most strongly associated with OS. The purpose of the study was to investigate the relationship between the parameters of OS and the presence of individual elements of MS in young adults, as well as to identify the components of MS by means of principal components analysis (PCA) and to investigate how the parameters of OS correlate with the presence of individual components. The study included 724 young adults with or without a family history of coronary heart disease (population of the MAGNETIC study). Blood samples were taken from the participants of the study to determine peripheral blood counts, biochemical parameters, and selected parameters of OS. In addition, blood pressure and anthropometric parameters were measured. In subjects with MS, significantly lower activity of superoxide dismutase (SOD), copper- and zinc-containing SOD (CuZnSOD), and manganese-containing SOD (MnSOD) were found, along with significantly higher total antioxidant capacity (TAC) and significantly lower concentration of thiol groups per gram of protein (PSH). We identified three components of MS by means of PCA: “Obesity and insulin resistance”, “Dyslipidemia”, and “Blood pressure”, and showed the component “Obesity and insulin resistance” to have the strongest relationship with OS. In conclusion, we documented significant differences in some parameters of OS between young adults with and without MS. We showed that “Obesity and insulin resistance” is the most important component of MS in terms of relationship with OS.

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