Macrophage function in obesity-induced inflammation and insulin resistance.

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Insulin 1 endocrinologydiseasesdrugs
cortisol 1 endocrinologydiseasesdrugs
hyperglycemia 2 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 41 endocrinologydiseases

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Insulin 1194 instance, obesity alters whole body metabolism that frequently results in insulin resistance [[5]]. Insulin is produced by the pancreatic beta cells in response to rising blood glucose levels, thereby leading
cortisol 43685 gluconeogenesis in the liver and muscle during sepsis. Central mediators include glucagon, epinephrine, and cortisol , which are released as a consequence of the inflammatory cascade [[32]]. From an evolutionary point
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hyperglycemia 2437 frequent in obese patients. In obesity, the compromised glucose uptake into metabolic organs induces hyperglycemia in turn accelerating insulin production in beta cells. The excessive insulin production can partly compensate
hyperglycemia 28771 metabolic as well as immunoregulatory functions. On the one hand, under high energy conditions and hyperglycemia , hepatocytes in the liver import excessive glucose that is converted to glycogen. During fasting periods,
metabolic syndrome 28297 insulin sensitivity that would prevent fatal diseases associated with obesity such as development of metabolic syndrome and the progression to cancer. In line with this evidence, nematode infection or vaccination with nematode
obesity 45 Title: Pflugers ArchivMacrophage function in obesity -induced inflammation and insulin resistanceMario A. R. LauterbachF. Thomas WunderlichPublication date
obesity 269 2/2017Publication date (pmc-release): 2/2017Publication date (ppub): /2017AbstractThe steadily increasing obesity epidemic affects currently 30% of western populations and is causative for numerous disorders. It has
obesity 730 insulin resistance. Here, we report on data that specifically address macrophage biology/physiology in obesity -induced inflammation and insulin resistance.IntroductionThe steadily rising prevalence of obesity incorporates
obesity 828 in obesity-induced inflammation and insulin resistance.IntroductionThe steadily rising prevalence of obesity incorporates a major health issue because it is attended by fatal obesity-associated disorders including
obesity 902 steadily rising prevalence of obesity incorporates a major health issue because it is attended by fatal obesity -associated disorders including not only the development of type 2 diabetes and fatty liver diseases
obesity 1104 diseases but also the rising incidence for certain cancer entities [[7], [54]]. In the first instance, obesity alters whole body metabolism that frequently results in insulin resistance [[5]]. Insulin is produced
obesity 2367 type 2 diabetes develops as a consequence of insulin resistance that is frequent in obese patients. In obesity , the compromised glucose uptake into metabolic organs induces hyperglycemia in turn accelerating insulin
obesity 2677 insulin sensitivity but progresses to increased beta cell mass and ultimately to beta cell death. How obesity facilitates the development of insulin resistance has been discovered over the last decade. Obesity
obesity 21318 crucial functions of the liver resident Kupffer cells (KC) and adipose tissue macrophages (ATM). In obesity , insulin resistance develops as a consequence of metaflammation in which elevated circulating levels
obesity 21588 negatively affect the insulin signaling cascade [[37]]. The main source for these inflammatory mediators in obesity is hepatic and WAT macrophages [[122]]. Macrophages adapt in their residing tissue to local circumstances
obesity 22136 affected tissue. We will refer here on the impact of ATM and liver-derived KC in the development of obesity -associated insulin resistance.Adipose tissue macrophagesAdipose tissue is one of the major metabolic
obesity 23624 Spiegelman identified adipocytes as source of TNFα in the WAT that ultimately impaired insulin signaling in obesity [[39]]. However, findings by Xu et al. demonstrated that mainly the stromal vascular fraction of the
obesity 25778 IL-13, and IL-33 in the lean WAT to keep ATMs in an Manti like state [[49], [117]]. In the course of obesity , monocyte recruitment as well as local proliferation gives rise to novel ATMs that polarize towards
obesity 28266 strategy to resume whole body insulin sensitivity that would prevent fatal diseases associated with obesity such as development of metabolic syndrome and the progression to cancer. In line with this evidence,
obesity 29650 [[88]]. Gut-derived LPS for example can be detected in portal vein but less in circulation [[45]]. In obesity , impaired storage of excessive lipids in the WAT leads to liver fat accumulation resulting in steatosis
obesity 29940 results in lipotoxicity which in turn leads to liver damage and inflammation [[74], [118]]. Thus, in obesity , lipotoxicity and elevated microbial load from the microbiota result in excessive inflammation mediated
obesity 30304 inflammation, and the development of insulin resistance thereby identifying hepatic macrophages as mediators of obesity -associated pathologies [[58]]. Hepatic macrophages crosstalk to liver non-parenchymal cells and adapt
obesity 30695 IL-1β that further boosts and deteriorates liver functions [[46], [53]]. The inflammatory boost in obesity does not alter KC numbers but dramatically increases infiltration of CCR2-positive monocytes [[52],
obesity 31329 insulin resistanceObesity contributes to the development of insulin resistance through the so-called obesity -associated low-grade inflammation or metaflammation. Over the course of this process, immune cells infiltrate
obesity 31640 act locally but also systemically after being released into circulation [[82]].The cytokine levels in obesity do not reach levels upon infection, but instead are elevated 2–3-fold compared to homeostatic conditions.
obesity 31889 pro-inflammatory cytokines increase acutely and stagnate with the elimination of the pathogen, the obesity -associated low-grade inflammation exhibits chronic character suggesting that dynamic modes of action
obesity 32070 that dynamic modes of action have to be taken into account. The best-studied inflammatory players in obesity are TNFα and IL-6, but also include IL-17, CCL-2, and many others. In this paragraph, we will delineate
obesity 32782 molecules, but also the IR. While at that time, adipocytes were believed to be the source of TNFα in obesity , Xu et al. demonstrated that the stromal vascular fraction of WAT secretes pro-inflammatory cytokines
obesity 33768 models provided novel insight into how TNFα-induced signaling interferes with insulin signaling in obesity . On the one hand, TNFα knockout mice exhibit normal glucose tolerance when exposed to normal food,
obesity 33918 exhibit normal glucose tolerance when exposed to normal food, but are protected from the development of obesity -induced insulin resistance in the absence of body weight gain alterations on the other [[106]]. While
obesity 34584 as revealed by knockout studies. Muscle-specific IKK-2 inactivation showed no effect on diet-induced obesity and alterations in glucose homeostasis [[89]]. However, while hepatic IKK-2 inactivation conferred insulin
obesity 35669 embryonic lethal [[57]]. It has been shown that JNK-1 but not JNK-2 knockout mice are protected against obesity -induced impairments of glucose homeostasis suggesting an essential role for JNK-1 in serine phosphorylation
obesity 35957 unraveling the cell type-specific as well as redundant functions of the JNK genes in the development of obesity -associated insulin resistance. Opposite to what was expected, hepatic inactivation of JNK-1 revealed
obesity 36383 deficiency revealed a minor role in glucose metabolism [[84]], whereas WAT-specific JNK-1 deletion decreased obesity -induced IL-6 levels and thus ameliorated diet-induced insulin resistance [[92]]. However, neuronal-specific
obesity 36871 inflammatory cytokines, and thus, mice with macrophage-specific deletion of JNK-1 and 2 are protected against obesity -induced disorders [[30], [31]]. Collectively, deciphering organ-specific downstream actions of TNFα
obesity 36983 obesity-induced disorders [[30], [31]]. Collectively, deciphering organ-specific downstream actions of TNFα in obesity -induced insulin resistance revealed redundant as well as non-redundant kinase functions on inhibitory
obesity 38785 and subsequent proteasomal degradation of IRS1 [[104], [105]]. Consistently, clinical studies link obesity -induced insulin resistance with increased IL-6 levels. Importantly, weight loss reduces circulating
obesity 39577 Wallenius and colleagues demonstrated that IL-6 inactivation favors the development of mature onset obesity and diabetes implicating that IL-6 action on metabolism might be even more complex than hitherto assumed
obesity 39805 potential aspect that may explain these differences might be the chronic/constant presence of IL-6 under obesity conditions. We have demonstrated that in diet-induced obesity, the chronically high IL-6 levels lead
obesity 39867 chronic/constant presence of IL-6 under obesity conditions. We have demonstrated that in diet-induced obesity , the chronically high IL-6 levels lead to the development of hepatic IL-6 resistance [[29]]. IL-6 resistance
obesity 40566 hepatocytes improves hepatic insulin action and steatosis in young mice, but at older age, these mice develop obesity and insulin resistance due to the activation of acute phase response and overt inflammation [[103]].
obesity 41473 disorders. Given that IL-6 not only impacts on metabolism but also on the development of cancer and that obesity increases the incidence of cancer entities with an inflammatory microenvironment, the context-specific
obesity 41711 cascades will be necessary for the development of novel therapeutic interventions to combat such fatal obesity -associated diseases [[68]].Conclusion/outlookInflammation triggered by macrophages constitutes a turning
obesity 41852 [[68]].Conclusion/outlookInflammation triggered by macrophages constitutes a turning point in the development of obesity -related insulin resistance. It is not only that mediators secreted by macrophages trigger insulin resistance,
obesity 42792 strategy to recover whole body insulin sensitivity that would prevent fatal diseases associated with obesity . Indeed, thiazolidinediones and omega 3 fatty acids are such exemplary drugs or dietary factors that
obesity 44142 to fuel their inflammatory response to fight infection [[83]]. In the context of type 2 diabetes and obesity , increased glucose availability to immune cells might initiate a feed forward loop that fosters inflammation

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