scholarly journals Diet-Induced Muscle Insulin Resistance Is Associated With Extracellular Matrix Remodeling and Interaction With Integrin  2 1 in Mice

Diabetes ◽  
2011 ◽  
Vol 60 (2) ◽  
pp. 416-426 ◽  
Author(s):  
L. Kang ◽  
J. E. Ayala ◽  
R. S. Lee-Young ◽  
Z. Zhang ◽  
F. D. James ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Extracellular Matrix ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Muscle Insulin Resistance

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 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.

Adipose Extracellular Matrix Remodeling in Obesity and Insulin Resistance

2021 ◽  
pp. 215-229
Author(s):  
Francisco Javier Ruiz-Ojeda ◽  
Julio Plaza-Díaz ◽  
Augusto Anguita-Ruiz ◽  
Andrea Méndez-Gutiérrez ◽  
Concepción María Aguilera
Keyword(s):  
Insulin Resistance ◽  
Extracellular Matrix ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

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 The Dynamic Interaction between Extracellular Matrix Remodeling and Breast Tumor Progression

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1046
Author(s):  
Jorge Martinez ◽  
Patricio C. Smith
Keyword(s):  
Extracellular Matrix ◽  
Type I Collagen ◽  
Cell Metabolism ◽  
Breast Tumors ◽  
Extracellular Matrix Remodeling ◽  
Type I ◽  
Matrix Remodeling ◽  
Desmoplastic Reaction ◽  
The Impact

Desmoplastic tumors correspond to a unique tissue structure characterized by the abnormal deposition of extracellular matrix. Breast tumors are a typical example of this type of lesion, a property that allows its palpation and early detection. Fibrillar type I collagen is a major component of tumor desmoplasia and its accumulation is causally linked to tumor cell survival and metastasis. For many years, the desmoplastic phenomenon was considered to be a reaction and response of the host tissue against tumor cells and, accordingly, designated as “desmoplastic reaction”. This notion has been challenged in the last decades when desmoplastic tissue was detected in breast tissue in the absence of tumor. This finding suggests that desmoplasia is a preexisting condition that stimulates the development of a malignant phenotype. With this perspective, in the present review, we analyze the role of extracellular matrix remodeling in the development of the desmoplastic response. Importantly, during the discussion, we also analyze the impact of obesity and cell metabolism as critical drivers of tissue remodeling during the development of desmoplasia. New knowledge derived from the dynamic remodeling of the extracellular matrix may lead to novel targets of interest for early diagnosis or therapy in the context of breast tumors.

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