scholarly journals Obesity-induced insulin resistance and macrophage infiltration of the adipose tissue: A vicious cycle

2018 ◽  
Vol 10 (1) ◽  
pp. 29-31 ◽  
Author(s):  
Chi Ho Lee ◽  
Karen SL Lam
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Vicious Cycle

scholarly journals Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

2007 ◽  
Vol 117 (10) ◽  
pp. 2877-2888 ◽  
Author(s):  
Takashi Nomiyama ◽  
Diego Perez-Tilve ◽  
Daisuke Ogawa ◽  
Florence Gizard ◽  
Yue Zhao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

scholarly journals Irisin and Myonectin Regulation in the Insulin Resistant Muscle: Implications to Adipose Tissue: Muscle Crosstalk

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Luis Gamas ◽  
Paulo Matafome ◽  
Raquel Seiça
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Current Knowledge ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Vicious Cycle ◽  
Muscle Insulin Resistance ◽  
Insulin Resistant ◽  
Skeletal Muscle Insulin Resistance

Myokines are peptides produced and secreted by the skeletal muscle, with autocrine, paracrine, and endocrine actions. Many of them are overexpressed during physical exercise and appear to contribute to the benefits of exercise to metabolic homeostasis. Irisin, resulting from the cleavage of the membrane protein FNDC5, was shown to induce adipocyte browning, with increased lipid oxidation and thermogenesis. Myonectin was only recently discovered and initial studies revealed a role in fatty acid uptake and oxidation in adipose tissue and liver. However, the mechanisms of their regulation by exercise are not entirely established. Impaired secretion and action of myokines, such as irisin and myonectin, may have a role in the establishment of insulin resistance. On the other hand, several studies have shown that insulin resistance in the skeletal muscle may change myokines expression and secretion. This may have consequences on lipid and glucose metabolism in adipose tissue and lead to a vicious cycle between impaired myokines production and insulin resistance. This review summarizes the current knowledge about the influence of skeletal muscle insulin resistance on the secretion of irisin and myonectin, as well as its impact on adipose tissue metabolism.

Chronic Ethanol-Induced Insulin Resistance Is Associated With Macrophage Infiltration Into Adipose Tissue and Altered Expression of Adipocytokines

2007 ◽  
Vol 31 (9) ◽  
pp. 1581-1588 ◽  
Author(s):  
Li Kang ◽  
Becky M. Sebastian ◽  
Michele T. Pritchard ◽  
Brian T. Pratt ◽  
Stephen F. Previs ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Chronic Ethanol ◽  
Macrophage Infiltration ◽  
Altered Expression

scholarly journals An Increase in the Circulating Concentration of Monocyte Chemoattractant Protein-1 Elicits Systemic Insulin Resistance Irrespective of Adipose Tissue Inflammation in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 971-979 ◽  
Author(s):  
Sanshiro Tateya ◽  
Yoshikazu Tamori ◽  
Takayuki Kawaguchi ◽  
Hajime Kanda ◽  
Masato Kasuga
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Whole Body ◽  
Adipose Tissue Inflammation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tissue Inflammation ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Systemic Insulin Resistance

Chronic inflammation in adipose tissue is thought to be important for the development of insulin resistance in obesity. Furthermore, the level of monocyte chemoattractant protein-1 (MCP-1) is increased not only in adipose tissue but also in the circulation in association with obesity. However, it has remained unclear to what extent the increased circulating level of MCP-1 contributes to insulin resistance. We have now examined the relevance of circulating MCP-1 to the development of insulin resistance in mice. The plasma concentration of MCP-1 was increased chronically or acutely in mice to the level observed in obese animals by chronic subcutaneous infusion of recombinant MCP-1 with an osmotic pump or by acute intravenous infusion of MCP-1 with an infusion pump, respectively. Whole-body metabolic parameters as well as inflammatory changes in adipose tissue were examined. A chronic increase in the circulating level of MCP-1 induced insulin resistance, macrophage infiltration into adipose tissue, and an increase in hepatic triacylglycerol content. An acute increase in the circulating MCP-1 concentration also induced insulin resistance but not macrophage infiltration into adipose tissue. In addition, inhibition of signaling by MCP-1 and its receptor CCR2 by administration of a novel CCR2 antagonist ameliorated insulin resistance in mice fed a high-fat diet without affecting macrophage infiltration into adipose tissue. These data indicate that an increase in the concentration of MCP-1 in the circulation is sufficient to induce systemic insulin resistance irrespective of adipose tissue inflammation.

Do adipose tissue macrophages promote insulin resistance or adipose tissue remodelling in humans?

2014 ◽  
Vol 20 (1) ◽  
Author(s):  
Leonie K. Heilbronn ◽  
Bo Liu
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expansion ◽  
Macrophage Infiltration ◽  
Low Grade ◽  
Tissue Remodelling ◽  
Inflammatory Phenotype ◽  
Inflammatory State ◽  
Caloric Excess

AbstractIn diet induced and genetically obese rodent models, adipose tissue is associated with macrophage infiltration, which promotes a low grade inflammatory state and the development of insulin resistance. In humans, obesity is also closely linked with macrophage infiltration in adipose tissue, a pro-inflammatory phenotype and insulin resistance. However, whether macrophage infiltration is a direct contributor to the development of insulin resistance that occurs in response to weight gain, or is a later consequence of the obese state is unclear. There are a number of concomitant changes that occur during adipose tissue expansion, including the number and size of adipocytes, the vasculature and the extracellular matrix. In this review, we will examine evidence for and against the role of macrophage recruitment into adipose tissue in promoting the development of insulin resistance in rodents and humans, as well as discuss the emerging role of macrophages in mediating healthy adipose tissue expansion during periods of caloric excess.

scholarly journals Inhibition of Thrombin Action Ameliorates Insulin Resistance in Type 2 Diabetic db/db Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 513-519 ◽  
Author(s):  
Masatomo Mihara ◽  
Ken-ichi Aihara ◽  
Yasumasa Ikeda ◽  
Sumiko Yoshida ◽  
Mizuho Kinouchi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Receptor ◽  
Coagulation Factor ◽  
Macrophage Infiltration ◽  
Factor Vii ◽  
Thrombin Inhibitor ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Inhibition Of Thrombin

The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr−/−:db/db) mice. The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. It also reduced adipocyte size and macrophage infiltration into adipose tissue. The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation.

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