![]() Obesity is associated with the accumulation of pro-inflammatory cells in visceral adipose tissue (VAT), which is an important underlying cause of insulin resistance and progression to diabetes mellitus type 2 (DM2). Wensveen, Felix M Valentić, Sonja Å estan, Marko Turk Wensveen, Tamara Polić, Bojan The "Big Bang" in obese fat: Events initiating obesity-induced adipose tissue inflammation. Conclusions In conclusion, IL-33 may play a protective role in the development of adipose tissue inflammation during obesity. Furthermore, mice lacking endogenous ST2 fed HFD had increased body weight and fat mass, impaired insulin secretion and glucose regulation compared to WT controls fed HFD. IL-33 also induced accumulation of Th2 cells in adipose tissue and polarization of adipose tissue macrophages towards an M2 alternatively activated phenotype (CD206+), a lineage associated with protection against obesity-related metabolic events. Administration of recombinant IL-33 to genetically obese diabetic (ob/ob) mice led to reduced adiposity, reduced fasting glucose and improved glucose and insulin tolerance. Methods and Results We demonstrate that treatment of adipose tissue cultures in vitro with IL-33 induced production of Th2 cytokines (IL-5, IL-13, IL-10), and reduced expression of adipogenic and metabolic genes. Objective To examine the functional role of IL-33 in adipose tissues, and investigate the effects on adipose tissue inflammation and obesity in vivo. The cytokine IL-33 and its receptor ST2 are expressed in adipose tissue but their role in adipose tissue inflammation during obesity is unclear. Rationale Chronic low-grade inflammation involving adipose tissue likely contributes to the metabolic consequences of obesity. ![]() IL-33 induces protective effects in adipose tissue inflammation during obesity in mice Selective regulation of PPARγ activity is a Siah2-mediated mechanism contributing to obesity-induced adipose tissue inflammation. Siah2 links adipocyte hypertrophy with adipocyte dysfunction and recruitment of proinflammatory immune cells to adipose tissue. Loss of Siah2 increased expression of PPARγ target genes involved in lipid metabolism and decreased expression of proinflammatory adipokines regulated by PPARγ. Proinflammatory gene expression, stress kinase signaling, fibrosis, and crown-like structures were reduced in the Siah2KO adipose tissue, and Siah2KO adipocytes were more responsive to insulin-dependent inhibition of lipolysis. Enlarged adipocytes in obese Siah2KO mice were not associated with obesity-induced insulin resistance. Gene and protein expression, immunohistochemistry, adipocyte size distribution, and lipolysis were also analyzed. Indirect calorimetry, body composition, and glucose and insulin tolerance were assayed along with glucose and insulin levels. Wild-type and Siah2KO mice were fed a low- or high-fat diet for 16 weeks. Herein, the effect of the ubiquitin ligase Siah2 on obesity-related adipose tissue inflammation was examined. Although ubiquitin ligases regulate inflammatory processes, the role of these enzymes in metabolically driven adipose tissue inflammation is relatively unexplored. ![]() Kilroy, Gail Carter, Lauren E Newman, Susan Burk, David H Manuel, Justin Möller, Andreas Bowtell, David D Mynatt, Randall L Ghosh, Sujoy Floyd, Z ElizabethĬhronic, low-grade adipose tissue inflammation associated with adipocyte hypertrophy is an important link in the relationship between obesity and insulin resistance. The ubiquitin ligase Siah2 regulates obesity-induced adipose tissue inflammation. These results indicate that ER stress plays important pathophysiological roles in obesity-induced adipose tissue dysfunction. ![]() Oral administration to obese mice of chemical chaperons, which alleviate ER stress, improved chronic inflammation in adipose tissue, followed by the suppression of increased body weight and improved insulin signaling. MIANA KASSIS FREEWe found that ER stress is induced by free fatty acid (FFA)-mediated reactive oxygen species (ROS) generation and up-regulated gene expression of inflammatory cytokines in 3T3-L1 adipocytes. After 16 weeks of feeding, ER stress markers increased and chronic inflammation occurred in adipose tissue. In this study, we observed that endoplasmic reticulum (ER) stress and the inflammatory response occurred in adipose tissue of mice fed a high-fat diet for a period of 16 weeks. Metabolic diseases such as obesity and type 2 diabetes are often accompanied by chronic inflammation and adipose tissue dysfunction. Kawasaki, Noritaka Asada, Rie Saito, Atsushi Kanemoto, Soshi Imaizumi, KazunoriĪdipose tissue plays a central role in maintaining metabolic homeostasis under normal conditions. Obesity-induced endoplasmic reticulum stress causes chronic inflammation in adipose tissue. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |