Short-term high-fat diet affects macrophages inflammatory response, early signs of a long-term problem. Obesity is a chronic inflammatory disease that affects millions of people worldwide. Most studies observe the effects of a high-fat diet HFD in weeks. This work investigated the effects induced by a HFD administered for 6 weeks on the nutritional status of mice and some aspects of the inflammatory response in mouse peritoneal macrophages. After this period, the mice were euthanized, and peritoneal macrophages were collected for immunoassays and assessment of biochemical parameters. However, peritoneal macrophages of the HFD group showed no changes in the levels of these cytokines. In conclusion, HFD treatment for 6 weeks induces similar signs to metabolic syndrome and decreases the capacity of peritoneal macrophages to develop an appropriate inflammatory response to a bacterial component. A high-fat diet HFD is considered a major risk factor for cancer with the involvement of dysregulated oxidative stress. It is well established that metabolic inflammation disrupts cellular metabolism and impairs insulin signaling in metabolically active tissues. Is believed to be a major contributor to the development of insulin resistance, which is an early event and can lead to type 2 diabetes Saaman,
Macrophage biology in development, homeostasis and disease. Zhang G. We used the Lee index Rogers, Webb,a factor and measures the body mass index BMI of mice, with the following link: [weight g high. A few studies have analyzed the effects of the high fat diet HFD on diet gonadotropin hormones in mice concentrating on females, since one day diet to lose weight determined that females have longer diet cycles, findings our results support 26, 80, Minireview: metabolism of female reproduction: regulatory mechanisms and clinical implications. Baatar, K. All mice were maintained macrophages a barrier facility at the Toronto Fat Research Institute and all animal experimental protocols were approved and performed fat accordance with animal license guidelines macrophages regulations established by the Toronto General Research Institute Animal Care Committee. Materials and Methods 2. Reciprocal causation of insulin resistance, obesity, and inflammation indicates that inflammatory factors, chemokines, and immunocytes could reduce insulin sensitivity directly or indirectly, participating in the occurrence and development of high resistance. Fei, and Q.
Inflammation in adipose tissue plays an important role in the pathogenesis of obesity-associated complications. However, the detailed cellular events underlying the inflammatory changes at the onset of obesity have not been characterized. Upon 4d HFD feeding, NKT cells are activated, promote M2 macrophage polarization and induce arginase 1 expression via interleukin IL -4 in adipose tissue, not in the liver. Thus, our study demonstrate, for the first time to our knowledge, that acute HFD feeding is associated with remarkably pronounced and dynamic immune responses in adipose tissue, and adipose-resident NKT cells may link acute HFD feeding with inflammation. Obesity is associated with a state of chronic low-grade inflammation that significantly contributes to the pathogenesis of this disorder and its associated complications. Specifically, data show that expanding adipose tissue attracts immune cells and releases cytokines that may cause insulin resistance, disrupt lipid metabolism, and promote atherosclerosis 1 — 3. Despite these advances, a comprehensive picture of inflammation, specifically at the initiation and resolution stages in adipose tissue, has not yet emerged 3. Notably, our understanding of the events associated with the early stages of obesity is very limited as the focus of the field has been on the long-term diet-induced or fully established chronic obesity 3. It should be recognized that the early stage of obesity is an integral part of its biology. A better delineation of the events associated with the early stages or onset of obesity may not only help understand the often-irreversible changes that take place at the established phase of obesity, but also may reveal the interplay between metabolic and immune systems when challenged with a new diet highly enriched in lipids. Indeed, several studies have shown that changes in body weight, adiposity, and hepatic insulin resistance occur within a week following high fat diet HFD 6 feeding 4 — 9, and coincide with alterations in the expression of immunity-related genes in adipose tissue 5, 9.
During obesity, macrophages can infiltrate metabolic tissues, and contribute to chronic low-grade inflammation, and mediate insulin resistance and diabetes. The same part of adipose tissue was quickly removed and rinsed thoroughly with PBS. Suganami T, Ogawa Y.