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 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 Increased Interleukin-32 Levels in Obesity Promote Adipose Tissue Inflammation and Extracellular Matrix Remodeling: Effect of Weight Loss

Diabetes ◽  
2016 ◽  
Vol 65 (12) ◽  
pp. 3636-3648 ◽  
Author(s):  
Victoria Catalán ◽  
Javier Gómez-Ambrosi ◽  
Amaia Rodríguez ◽  
Beatriz Ramírez ◽  
Víctor Valentí ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

scholarly journals Extracellular Matrix Remodeling of Adipose Tissue in Obesity and Metabolic Diseases

2019 ◽  
Vol 20 (19) ◽  
pp. 4888 ◽  
Author(s):  
Ruiz-Ojeda ◽  
Méndez-Gutiérrez ◽  
Aguilera ◽  
Plaza-Díaz
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Tissue Expansion ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Survival And Development ◽  
Tissue Receptors

The extracellular matrix (ECM) is a network of different proteins and proteoglycans that controls differentiation, migration, repair, survival, and development, and it seems that its remodeling is required for healthy adipose tissue expansion. Obesity drives an excessive lipid accumulation in adipocytes, which provokes immune cells infiltration, fibrosis (an excess of deposition of ECM components such as collagens, elastin, and fibronectin) and inflammation, considered a consequence of local hypoxia, and ultimately insulin resistance. To understand the mechanism of this process is a challenge to treat the metabolic diseases. This review is focused at identifying the putative role of ECM in adipose tissue, describing its structure and components, its main tissue receptors, and how it is affected in obesity, and subsequently the importance of an appropriate ECM remodeling in adipose tissue expansion to prevent metabolic diseases.

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.

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