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The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
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Journal Article
The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
2011
Overview
Obesity is generally considered an inflammatory state. Vishwa Dixit and his colleagues have now shown that excess dietary lipids leads to the activation of the Nlrp3 inflammasome, a sensor of the innate immune system, and that its genetic deficiency results in decreased inflammation and improved insulin sensitivity. These results suggest a possible new therapeutic avenue to treat the effects of obesity.
The emergence of chronic inflammation during obesity in the absence of overt infection or well-defined autoimmune processes is a puzzling phenomenon. The Nod-like receptor (NLR) family of innate immune cell sensors, such as the nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (Nlrp3, but also known as Nalp3 or cryopyrin) inflammasome are implicated in recognizing certain nonmicrobial originated 'danger signals' leading to caspase-1 activation and subsequent interleukin-1β (IL-1β) and IL-18 secretion. We show that calorie restriction and exercise-mediated weight loss in obese individuals with type 2 diabetes is associated with a reduction in adipose tissue expression of Nlrp3 as well as with decreased inflammation and improved insulin sensitivity. We further found that the Nlrp3 inflammasome senses lipotoxicity-associated increases in intracellular ceramide to induce caspase-1 cleavage in macrophages and adipose tissue. Ablation of Nlrp3 in mice prevents obesity-induced inflammasome activation in fat depots and liver as well as enhances insulin signaling. Furthermore, elimination of Nlrp3 in obese mice reduces IL-18 and adipose tissue interferon-γ (IFN-γ) expression, increases naive T cell numbers and reduces effector T cell numbers in adipose tissue. Collectively, these data establish that the Nlrp3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflammation and insulin resistance.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Adipose Tissue - physiopathology
/ Animals
/ Biomedical and Life Sciences
/ Carrier Proteins - physiology
/ Complications and side effects
/ Female
/ Humans
/ Inflammation - physiopathology
/ Insulin Resistance - physiology
/ Interleukin-1beta - physiology
/ Male
/ Mice
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Obesity
/ Proteins
/ Reverse Transcriptase Polymerase Chain Reaction
/ Sensors
