Metaflammatory responses during obesity: Pathomechanism and treatment

Debnath, Monalisa; Agrawal, Shailesh; Agrawal, Aruna; Dubey, Govind Prasad

doi:10.1016/j.orcp.2015.10.012

Cited by 38 publications

(34 citation statements)

References 145 publications

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“…Systemic inflammation can increase during obesity, resulting in increased proinflammatory cytokines such as IL-1 β and TNF- α [54], which induce muscle wasting [55]. Therefore, it is possible that the presently obtained results are due to decreased TNF- α plasma levels, which, in turn, could decrease the atrophic effect on skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

High Fat Diet‐Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

Ábrigo

Rivera

Aravena

et al. 2016

Oxidative Medicine and Cellular Longevity

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Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.

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Section: Discussionmentioning

confidence: 99%

High Fat Diet‐Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

Ábrigo

Rivera

Aravena

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…Obesity, T2DM, and MDD share increased peripheral levels of cytokines like IL-6, TNF-α, and IL-1β [1,121,122] . Type 2 diabetes and obesity are also marked by higher concentrations of acute-phase proteins such as CRP, plasminogen activator inhibitor, and serum amyloid A [123][124][125][126] .…”

Section: Obesity and Type 2 Diabetesmentioning

confidence: 99%

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Slyepchenko

Maes

Jacka

et al. 2016

Psychother Psychosom

211

136

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Background: Persistent low-grade immune-inflammatory processes, oxidative and nitrosative stress (O&NS), and hypothalamic-pituitary-adrenal axis activation are integral to the pathophysiology of major depressive disorder (MDD). The microbiome, intestinal compositional changes, and resultant bacterial translocation add a new element to the bidirectional interactions of the gut-brain axis; new evidence implicates these pathways in the patho-aetiology of MDD. In addition, abnormalities in the gut-brain axis are associated with several chronic non-communicable disorders, which frequently co-occur in individuals with MDD, including but not limited to irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS), obesity, and type 2 diabetes mellitus (T2DM). Methods: We searched the PubMed/MEDLINE database up until May 1, 2016 for studies which investigated intestinal dysbiosis and bacterial translocation (the ‘leaky gut') in the pathophysiology of MDD and co-occurring somatic comorbidities with an emphasis on IBS, CFS, obesity, and T2DM. Results: The composition of the gut microbiota is influenced by several genetic and environmental factors (e.g. diet). Several lines of evidence indicate that gut-microbiota-diet interactions play a significant pathophysiological role in MDD and related medical comorbidities. Gut dysbiosis and the leaky gut may influence several pathways implicated in the biology of MDD, including but not limited to immune activation, O&NS, and neuroplasticity cascades. However, methodological inconsistencies and limitations limit comparisons across studies. Conclusions: Intestinal dysbiosis and the leaky gut may constitute a key pathophysiological link between MDD and its medical comorbidities. This emerging literature opens relevant preventative and therapeutic perspectives.

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“…Human mast cells may be also a direct target of adipokine activity (27,28). Systemic inflammation generated during obesity is characterized by an oversecretion of inflammatory markers such as CRP, IL-6, IL-1beta, TNF-alpha, leptin and visfatin, with a simultaneous hyposecretion of anti-inflammatory and anti-atherogenic substances (12,15,29). Trinh et al recently described an imbalance in pro-and anti-inflammatory adipokines in CU.…”

Section: Metabolic Syndromementioning

confidence: 99%

The link between chronic spontaneous urticaria and metabolic syndrome

Veña¹,

Cassano²

2017

Eur Ann Allergy Clin Immunol

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Summary Metabolic syndrome (MS) is a cluster of risk factors for cardiovascular disease and is considered a chronic low-level systemic inflammatory condition. Recent preliminary findings have shown an increased prevalence of MS among patients with chronic urticaria (CU) as compared to controls, with a particularly higher prevalence detected in patients with uncontrolled CU. Chronic spontaneous urticaria (CSU) appears to share some pathomechanisms with MS, including a pro-inflammatory state, increased oxidative stress, alterations in adipokine profile

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Metaflammatory responses during obesity: Pathomechanism and treatment

Cited by 38 publications

References 145 publications

High Fat Diet‐Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

High Fat Diet‐Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

The link between chronic spontaneous urticaria and metabolic syndrome

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