scholarly journals Exercise-induced increases in insulin sensitivity after bariatric surgery are mediated by muscle extracellular matrix remodeling

2021 ◽  
Author(s):  
Wagner S. Dantas ◽  
Hamilton Roschel ◽  
Igor H. Murai ◽  
Saulo Gil ◽  
Gangarao Davuluri ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bariatric Surgery ◽  
Extracellular Matrix ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Transforming Growth Factor ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Exercise Induced

Exercise seems to enhance the beneficial effect of bariatric surgery (RYGB) on insulin resistance. We hypothesized that skeletal muscle extracellular matrix (ECM) remodeling may underly these benefits. Women were randomized to either a combined aerobic and resistance exercise training program following RYGB or standard of care (RYGB). Insulin sensitivity was assessed by OGTT. Muscle biopsies were obtained at baseline, and 3 and 9 months after surgery and subjected to comprehensive phenotyping, transcriptome profiling, molecular pathway identification and validation <i>in vitro</i>. Exercise training improved insulin sensitivity beyond surgery alone (<i>e.g</i>., Matsuda index - RYGB: +123% vs. RYGB + ET: +325%; <i>P </i>≤ 0.0001). ECM remodeling was reduced by surgery alone, with an additive benefit of surgery and exercise training (<i>e.g.,</i> collagen I - RYGB: -41% vs. RYGB + ET: -76%; <i>P </i>≤ 0.0001). Exercise and RYGB had an additive effect on enhancing insulin sensitivity, but surgery alone did not resolve insulin resistance and ECM remodeling. We identified candidates modulated by exercise training that may become therapeutic targets for treating insulin resistance, in particular, the transforming growth factor-beta 1/SMAD 2/3 pathway and its antagonist follistatin. Exercise-induced increases in insulin sensitivity after bariatric surgery are at least partially mediated by muscle extracellular matrix remodeling.

scholarly journals Exercise-induced increases in insulin sensitivity after bariatric surgery are mediated by muscle extracellular matrix remodeling

2020 ◽  
Author(s):  
Ada Admin ◽  
Wagner S. Dantas ◽  
Hamilton Roschel ◽  
Igor H. Murai ◽  
Saulo Gil ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bariatric Surgery ◽  
Extracellular Matrix ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Transforming Growth Factor ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Exercise Induced

Exercise seems to enhance the beneficial effect of bariatric surgery (RYGB) on insulin resistance. We hypothesized that skeletal muscle extracellular matrix (ECM) remodeling may underly these benefits. Women were randomized to either a combined aerobic and resistance exercise training program following RYGB or standard of care (RYGB). Insulin sensitivity was assessed by OGTT. Muscle biopsies were obtained at baseline, and 3 and 9 months after surgery and subjected to comprehensive phenotyping, transcriptome profiling, molecular pathway identification and validation <i>in vitro</i>. Exercise training improved insulin sensitivity beyond surgery alone (<i>e.g</i>., Matsuda index - RYGB: +123% vs. RYGB + ET: +325%; <i>P </i>≤ 0.0001). ECM remodeling was reduced by surgery alone, with an additive benefit of surgery and exercise training (<i>e.g.,</i> collagen I - RYGB: -41% vs. RYGB + ET: -76%; <i>P </i>≤ 0.0001). Exercise and RYGB had an additive effect on enhancing insulin sensitivity, but surgery alone did not resolve insulin resistance and ECM remodeling. We identified candidates modulated by exercise training that may become therapeutic targets for treating insulin resistance, in particular, the transforming growth factor-beta 1/SMAD 2/3 pathway and its antagonist follistatin. Exercise-induced increases in insulin sensitivity after bariatric surgery are at least partially mediated by muscle extracellular matrix remodeling.

scholarly journals Exercise-induced increases in insulin sensitivity after bariatric surgery are mediated by muscle extracellular matrix remodeling

2020 ◽  
Author(s):  
Ada Admin ◽  
Wagner S. Dantas ◽  
Hamilton Roschel ◽  
Igor H. Murai ◽  
Saulo Gil ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bariatric Surgery ◽  
Extracellular Matrix ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Transforming Growth Factor ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Exercise Induced

Exercise seems to enhance the beneficial effect of bariatric surgery (RYGB) on insulin resistance. We hypothesized that skeletal muscle extracellular matrix (ECM) remodeling may underly these benefits. Women were randomized to either a combined aerobic and resistance exercise training program following RYGB or standard of care (RYGB). Insulin sensitivity was assessed by OGTT. Muscle biopsies were obtained at baseline, and 3 and 9 months after surgery and subjected to comprehensive phenotyping, transcriptome profiling, molecular pathway identification and validation <i>in vitro</i>. Exercise training improved insulin sensitivity beyond surgery alone (<i>e.g</i>., Matsuda index - RYGB: +123% vs. RYGB + ET: +325%; <i>P </i>≤ 0.0001). ECM remodeling was reduced by surgery alone, with an additive benefit of surgery and exercise training (<i>e.g.,</i> collagen I - RYGB: -41% vs. RYGB + ET: -76%; <i>P </i>≤ 0.0001). Exercise and RYGB had an additive effect on enhancing insulin sensitivity, but surgery alone did not resolve insulin resistance and ECM remodeling. We identified candidates modulated by exercise training that may become therapeutic targets for treating insulin resistance, in particular, the transforming growth factor-beta 1/SMAD 2/3 pathway and its antagonist follistatin. Exercise-induced increases in insulin sensitivity after bariatric surgery are at least partially mediated by muscle extracellular matrix remodeling.

scholarly journals Exercise-Induced Increases in Insulin Sensitivity After Bariatric Surgery Are Mediated By Muscle Extracellular Matrix Remodeling

Diabetes ◽  
2020 ◽  
Vol 69 (8) ◽  
pp. 1675-1691
Author(s):  
Wagner S. Dantas ◽  
Hamilton Roschel ◽  
Igor H. Murai ◽  
Saulo Gil ◽  
Gangarao Davuluri ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Extracellular Matrix ◽  
Insulin Sensitivity ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Exercise Induced

scholarly journals AMPK Activation by Metformin Suppresses Abnormal Extracellular Matrix Remodeling in Adipose Tissue and Ameliorates Insulin Resistance in Obesity

Diabetes ◽  
2016 ◽  
Vol 65 (8) ◽  
pp. 2295-2310 ◽  
Author(s):  
Ting Luo ◽  
Allison Nocon ◽  
Jessica Fry ◽  
Alex Sherban ◽  
Xianliang Rui ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ampk Activation

scholarly journals Meta-fibrosis links positive energy balance and mitochondrial metabolism to insulin resistance

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 1758 ◽  
Author(s):  
Daniel S. Lark ◽  
David H. Wasserman
Keyword(s):  
Insulin Resistance ◽  
Extracellular Matrix ◽  
Energy Balance ◽  
Positive Energy ◽  
Extracellular Matrix Remodeling ◽  
Low Grade ◽  
Matrix Remodeling ◽  
Matrix Expansion ◽  
Positive Energy Balance ◽  
Low Grade Inflammation

Obesity and insulin resistance often emerge from positive energy balance and generally are linked to low-grade inflammation. This low-grade inflammation has been called “meta-inflammation” because it is a consequence of the metabolic dysregulation that can accompany overnutrition. One means by which meta-inflammation is linked to insulin resistance is extracellular matrix expansion secondary to meta-inflammation, which we define here as “meta-fibrosis”. The significance of meta-fibrosis is that it reflects a situation in which the extracellular matrix functions as a multi-level integrator of local (for example, mitochondrial reactive oxygen species production) and systemic (for example, inflammation) inputs that couple to cellular processes creating insulin resistance. While adipose tissue extracellular matrix remodeling has received considerable attention, it is becoming increasingly apparent that liver and skeletal muscle extracellular matrix remodeling also contributes to insulin resistance. In this review, we address recent advances in our understanding of energy balance, mitochondrial energetics, meta-inflammation, and meta-fibrosis in the development of insulin resistance.

scholarly journals Extracellular matrix remodeling through endocytosis and resurfacing of Tenascin-R

2020 ◽  
Author(s):  
Tal M. Dankovich ◽  
Rahul Kaushik ◽  
Gabriel Cassinelli Petersen ◽  
Philipp Emanuel Giro ◽  
Hannah Abdul Hadi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Protein Synthesis ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Activity Dependent ◽  
The Brain ◽  
Brain Extracellular Matrix

SummaryThe brain extracellular matrix (ECM) assembles around neurons and synapses, and is thought to change only rarely, through proteolysis and renewed protein synthesis. We report here an alternative ECM remodeling mechanism, based on the recycling of ECM molecules. We found that a key ECM protein, Tenascin-R, is frequently endocytosed, and later resurfaces, preferentially near synapses. The TNR molecules complete this cycle within ∼3 days, in an activity-dependent fashion.

scholarly journals Tumor Extracellular Matrix Remodeling: New Perspectives as a Circulating Tool in the Diagnosis and Prognosis of Solid Tumors

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 81 ◽  
Author(s):  
Marta Giussani ◽  
Tiziana Triulzi ◽  
Gabriella Sozzi ◽  
Elda Tagliabue
Keyword(s):  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Tumor Tissue ◽  
Prognostic Markers ◽  
Complex Mixture ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Diagnosis And Prognosis ◽  
Novel Concept

: In recent years, it has become increasingly evident that cancer cells and the local microenvironment are crucial in the development and progression of tumors. One of the major components of the tumor microenvironment is the extracellular matrix (ECM), which comprises a complex mixture of components, including proteins, glycoproteins, proteoglycans, and polysaccharides. In addition to providing structural and biochemical support to tumor tissue, the ECM undergoes remodeling that alters the biochemical and mechanical properties of the tumor microenvironment and contributes to tumor progression and resistance to therapy. A novel concept has emerged, in which tumor-driven ECM remodeling affects the release of ECM components into peripheral blood, the levels of which are potential diagnostic or prognostic markers for tumors. This review discusses the most recent evidence on ECM remodeling-derived signals that are detectable in the bloodstream, as new early diagnostic and risk prediction tools for the most frequent solid cancers.

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