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 Adipokine inflammation and insulin resistance: the role of glucose, lipids and endotoxin

2012 ◽  
Vol 216 (1) ◽  
pp. T1-T15 ◽  
Author(s):  
M K Piya ◽  
P G McTernan ◽  
S Kumar
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Dietary Factors ◽  
Positive Energy ◽  
Low Grade ◽  
Positive Energy Balance ◽  
Secretory Tissue ◽  
The Impact ◽  
Low Grade Inflammation

Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multifunctional secretory organ with the capacity to control energy homoeostasis through peripheral and central regulation of energy homoeostasis. It also plays an important role in innate immunity. However, the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low-grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or LPS. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, how nutrients such as these can influence adipokine inflammation and consequently insulin resistance directly through their effects on secretion of adipocytokines (TNFα, IL6 and resistin) as well as indirectly through increases in endotoxin is discussed.

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 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 Seafood intake and the development of obesity, insulin resistance and type 2 diabetes

2019 ◽  
Vol 32 (1) ◽  
pp. 146-167 ◽  
Author(s):  
Bjørn Liaset ◽  
Jannike Øyen ◽  
Hélène Jacques ◽  
Karsten Kristiansen ◽  
Lise Madsen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Trace Elements ◽  
Energy Balance ◽  
Energy Intake ◽  
Overweight And Obesity ◽  
Positive Energy ◽  
High Intake ◽  
Positive Energy Balance

AbstractWe provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent intake of lean seafood, as compared with intake of terrestrial meats, reduces energy intake by 4–9 %, sufficient to prevent a positive energy balance and obesity. At equal energy intake, lean seafood reduces fasting and postprandial risk markers of insulin resistance, and improves insulin sensitivity in insulin-resistant adults. Energy restriction combined with intake of lean and fatty seafood seems to increase weight loss. Marinen-3 PUFA are probably of importance throughn-3 PUFA-derived lipid mediators such as endocannabinoids and oxylipins, but other constituents of seafood such as the fish proteinper se, trace elements or vitamins also seem to play a largely neglected role. A high intake of fatty seafood increases circulating levels of the insulin-sensitising hormone adiponectin. As compared with a high meat intake, high intake of seafood has been reported to reduce plasma levels of the hepatic acute-phase protein C-reactive protein level in some, but not all studies. More studies are needed to confirm the dietary effects on energy intake, obesity and insulin resistance. Future studies should be designed to elucidate the potential contribution of trace elements, vitamins and undesirables present in seafood, and we argue that stratification into responders and non-responders in randomised controlled trials may improve the understanding of health effects from intake of seafood.

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.

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