Only the abstract is available publicly. Toll-like receptors, particularly TLR-4 has been shown to be associated with insulin resistance. These TLRs have specific pathogen recognition sites. TLRs are stimulated by fatty acids (FA) and endotoxemia from bacteria. Thus, dietary intake of high trans fats, inflammation originating from the gut can be the source of insulin receptor dysfunction through TLRs.
Activation of the innate immune system controls macronutrient metabolism
the innate immune response is the first line of defense against invading pathogens, wherein highly conserved pathogen-associated molecular patterns (PAMPs) are recognized by cognate pattern recognition receptors (PRRs
many studies have supported the idea that cytokine signaling directly promotes insulin resistance
innate immune system may be causally linked to obesity
adipose tissue contains a substantial population of macrophages, and macrophage-driven adipose inflammation contributes significantly to the pathogenesis of obesity
Collectively, activation of the innate immune system is strongly associated with ASCVD, insulin resistance, and obesity, and recent evidence suggests that much of this association can be traced to a unique family of PRRs known as TLRs
TLRs are a family of type I transmembrane receptors, currently thought to comprise at least 13 members in mammals, that specifically recognize a variety of microbial PAMPs and trigger host cellular responses
Free SFAs have indeed been demonstrated to elicit TLR4-dependent and TLR2-dependent responses in several cell types.
Endogenous SFAs released from adipocytes activate cocultured macrophages via TLR4 [18], indicating the potential for cellular crosstalk in adipose tissue. Collectively, there is a growing body of evidence that SFAs promote, whereas long chain PUFA antagonize, TLR4-dependent and TLR2-dependent signaling in multiple cell models
In an elegant study, Shi et al. [16] demonstrated that SFAs activate TLR4-dependent signaling in both macrophages and adipocytes, and mice lacking TLR4 are protected against insulin resistance driven by intravenous lipid infusion
In addition to effects in macrophages and adipocytes, SFAs can activate TLR4 in the hypothalamus, which triggers a central inflammatory response that results in resistance to anorexigenic signals
endogenous SFAs can indeed promote innate immunity and inflammatory disease
This finding strongly supports the work of Hwang and coworkers [19–22] demonstrating that ω-3 PUFAs can effectively counteract SFA-induced TLR4 activation in cultured macrophages and dendritic cells.
OMega-3 inhibits inflammation via decreased phosphorylation of lkappaBalpha and resultant decreased disassociation of NF-kappaB and decreased cytokine production. This occurs through TLR-4.
If your Pc hassle from one of these problem just call us our Windows technical support toll free number 1-800-261-4071 we will help you. We are providing for windows like windows installation, windows update, windows upgrade, security setting, data recovery from the disk. Dial our Windows tech support number 1-800-261-4071 for an instant help, for more details you can also visit our websites as http://technicalsupportnumberforwindows.com
Stimulation of TLRs initiates intracellular signaling cascades resulting in downstream NF-B and mitogen-activated protein kinase activation and production of proinflammatory chemokines associated with mechanisms of metabolic dysfunction and cardiovascular disease progression.
Elevated fatty acids levels associated with obesity activate TLR4 signaling in fat cells and macrophages, and induce insulin resistance in murine models