Fatty acids do not pay the toll: effect of SFA and PUFA on human adipose tissue and mature adipocytes inflammation

Murumalla, Ravi Kumar; Gunasekaran, Manoj Kumar; Padhan, Jibesh Kumar; Bencharif, Karima; Gence, Lydie; Festy, Franck; Césari, Maya; Roche, Régis; Hoareau, Laurence

doi:10.1186/1476-511x-11-175

Cited by 72 publications

(63 citation statements)

References 52 publications

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“…Oleic acid down-regulated TNF-α and IL-6 in human adipose tissue and adipocyte cultures [32]. However, in another study, oleic acid had no effect on the TNF-α and IL-10 mRNA expression [17].…”

Section: Discussionmentioning

confidence: 98%

The pro-/anti-inflammatory effects of different fatty acids on visceral adipocytes are partially mediated by GPR120

et al. 2016

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Section: Discussionmentioning

confidence: 98%

The pro-/anti-inflammatory effects of different fatty acids on visceral adipocytes are partially mediated by GPR120

et al. 2016

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“…Furthermore, the absence of TLR2 was shown to attenuate local inflammatory cytokine expression and enhance insulin action in the liver 54 . Although TLR2 is implicated in the inflammatory response in high-fat diet (HFD)-induced obesity in rodents and in human gene expression studies 55 , saturated and polyunsaturated fatty acids did not elicit proinflammatory effects in human adipose tissue and primary adipocyte culture 56 . Conversely, administration of a HFD for 1 week to healthy males reduced the expression of TLR2 57 .…”

Section: [H3] Tlr2 and Tlr4mentioning

confidence: 99%

Innate immunity in diabetes and diabetic nephropathy

2015

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Abstract:The innate immune system consists of several classes of pattern recognition receptors (PRRs), including membrane-bound Toll-like receptors (TLRs) and nucleotide-binding domain leucine-rich oligomerization domain (NOD)-like receptors (NLRs).These receptors detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the extracellular and intracellular space. Intracellular NLRs constitute inflammasomes, which activate and release caspase-1, IL1β, and IL18 and thus initiate an inflammatory response. Systemic and local low-grade inflammation and release of proinflammatory cytokines are implicated in the development and progression of diabetes mellitus and diabetic nephropathy. TLR2, TLR4, and the NLRP3 inflammasome are critically involved in the inflammatory responses in pancreatic islets, adipose, liver and kidney tissues. This Review discusses how innate immune system-driven inflammatory processes can lead to apoptosis, tissue fibrosis, and organ dysfunction to cause insulin resistance, impaired insulin secretion, and renal failure. We propose that careful targeting of TLR2, TLR4, and NLRP3 signalling pathways may be beneficial for the treatment of diabetes mellitus and diabetic nephropathy. 2 Key points The innate immune system consists of several classes of pattern recognition receptors, including TLRs and NLRs, which detect pathogen-associated and danger-associated molecular patterns and initiate an inflammatory response  TLR2 and TLR4 are the predominant toll-like receptors expressed on pancreatic β cells that trigger an inflammatory response in insulitis during type 1 diabetes mellitus  TLR2 and TLR4 signaling, and activation of NLRP3 inflammasomes results in production of various proinflammatory cytokines that can induce insulin resistance in type 2 diabetes mellitus (T2DM) and obesity  Innate immune responses in T2DM and obesity are modulated by the status of the gut microbiota, autophagy, and adipokines  TLR2, TLR4, NOD2, and NLRP3 inflammasome-mediated inflammation are involved in the perpetuation of inflammation in diabetic nephropathy  The activation of TLRs and NLRs stimulates the expression of MCP-1, which is associated with the progression of diabetic nephropathy [H1] IntroductionThe prevalence of diabetes mellitus is estimated to be 8.3%, affecting ~387 million people as of 2014. The number of patients living with diabetes mellitus is expected to increase to ~592 million by 2035, as reported by the International Diabetes Federation 1 . The incidence of end-stage renal disease (ESRD) is also rapidly increasing worldwide but varies up to 15-fold by country. In 2012, the number of new diagnoses of ESRD worldwide ranged from 25 to 467 patients per million. The proportion of new cases of ESRD with diabetes mellitus as the primary cause also differs by country, with 66% cases reported in Singapore and 12-16% cases reported in Ukraine, Romania, and the Netherlands 2 . Although intensified multifactorial intervention in patients with type 2 diabete...

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“…Moreover, Vandanmagsar et al [100] showed that macrophage inflammation was also mediated by an excess of fatty acids (FAs) via TLR or NOD-like receptor family, one of which is the NOD-like receptor family, the pyrin domain containing 3 (NLRP3) dependent pathway. However, there was one study showing that endotoxin-free, free fatty acids did not have the ability to activate TLR4 and thereby cause inflammation [101]. More importantly, they showed that some polyunsaturated fatty acids exerted an anti-inflammatory action in human adipose tissue and adipocytes.…”

Section: Role Of Hmgb1 In Type 2 Diabetesmentioning

confidence: 99%

The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes

Wang

Zhong

Zhang

et al. 2016

Journal of Diabetes Research

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Significance. With an alarming increase in recent years, diabetes mellitus has become a global challenge. Despite advances in treatment of diabetes mellitus, currently, medications available are unable to control the progression of diabetes and its complications. Growing evidence suggests that inflammation is an important pathogenic mediator in the development of diabetes mellitus. The perspectives including suggestions for new therapies involving the shift from metabolic stress to inflammation should be taken into account. Critical Issues. High-mobility group box 1 (HMGB1), a nonhistone nuclear protein regulating gene expression, was rediscovered as an endogenous danger signal molecule to trigger inflammatory responses when released into extracellular milieu in the late 1990s. Given the similarities of inflammatory response in the development of T2D, we will discuss the potential implication of HMGB1 in the pathogenesis of T2D. Importantly, we will summarize and renovate the role of HMGB1 and HMGB1-mediated inflammatory pathways in adipose tissue inflammation, insulin resistance, and islet dysfunction. Future Directions. HMGB1 and its downstream receptors RAGE and TLRs may serve as potential antidiabetic targets. Current and forthcoming projects in this territory will pave the way for prospective approaches targeting the center of HMGB1-mediated inflammation to improve T2D and its complications.

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Fatty acids do not pay the toll: effect of SFA and PUFA on human adipose tissue and mature adipocytes inflammation

Cited by 72 publications

References 52 publications

The pro-/anti-inflammatory effects of different fatty acids on visceral adipocytes are partially mediated by GPR120

The pro-/anti-inflammatory effects of different fatty acids on visceral adipocytes are partially mediated by GPR120

Innate immunity in diabetes and diabetic nephropathy

The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes

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