IL-33 is negatively associated with the BMI and confers a protective lipid/metabolic profile in non-diabetic but not diabetic subjects

Hasan, Amal; Al-Ghimlas, Fahad; Warsame, Samia; Alhubail, Asma; Ahmad, Rasheed; Bennakhi, Abdullah; Alarouj, Monira; Behbehani, Kazem; Dehbi, Mohammed; Dermime, Said

doi:10.1186/1471-2172-15-19

Cited by 54 publications

(34 citation statements)

References 28 publications

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“…In our research, we found IL-33 levels were associated with HbA1c and insulin in the control group, but there no association of this marker with (14,15).…”

Section: Discussioncontrasting

confidence: 57%

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WITHDRAWN: Relationship between circulating irisin, retinol binding protein-4, adiponectin and inflammatory mediators in patients with metabolic syndrome

Tabak

Sözer

Erdenen³

et al. 2016

Diabetes & Metabolic Syndrome: Clinical Research & Revi

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“…In our research, we found IL-33 levels were associated with HbA1c and insulin in the control group, but there no association of this marker with (14,15).…”

Section: Discussioncontrasting

confidence: 57%

“…Its receptor, soluble ST-2, has been shown to be protective in certain conditions such as obesity and atherosclerosis. IL-33 exerts protective metabolic effects by decreasing IR, leading to the accumulation of protective Th2 cells and cytokines and consequently reducing adipogenesis (14,15).…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Relationship between circulating irisin, retinol binding protein-4, adiponectin and inflammatory mediators in patients with metabolic syndrome

Tabak

Sözer

Erdenen³

et al. 2016

Diabetes & Metabolic Syndrome: Clinical Research & Revi

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“…Conflicting data exist with regard to the role of the IL-33/Il1rl1/ ST2 axis in metabolism. On one hand, IL-33 has been considered to prevent adipose tissue inflammation and thus reduce metabolic complications (38,41). However, other studies have linked increased Il-33 levels to morbid obesity and the development of diabetes (40,41).…”

Section: Discussionmentioning

confidence: 99%

Regulation of De Novo Adipocyte Differentiation Through Cross Talk Between Adipocytes and Preadipocytes

et al. 2015

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There are many known adipokines differentially secreted from the different adipose depots; however, their paracrine and autocrine effects on de novo adipocyte formation are not fully understood. By developing a coculture method of preadipocytes with primary subcutaneous and visceral adipocytes or tissue explants, we could show that the total secretome inhibited preadipocyte differentiation. Using a proteomics approach with fractionated secretome samples, we were able to identify a spectrum of factors that either positively or negatively affected adipocyte formation. Among the secreted factors, Slc27a1, Vim, Cp, and Ecm1 promoted adipocyte differentiation, whereas Got2, Cpq, interleukin-1 receptor-like 1/ST2-IL-33, Sparc, and Lgals3bp decreased adipocyte differentiation. In human subcutaneous adipocytes of lean subjects, obese subjects, and obese subjects with type 2 diabetes, Vim and Slc27a1 expression was negatively correlated with adipocyte size and BMI and positively correlated with insulin sensitivity, while Sparc and Got2 showed the opposite trend. Furthermore, we demonstrate that Slc27a1 was increased upon weight loss in morbidly obese patients, while Sparc expression was reduced. Taken together, our findings identify adipokines that regulate adipocyte differentiation through positive or negative paracrine and autocrine feedback loop mechanisms, which could potentially affect whole-body energy metabolism.

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“…Several studies provide evidence for a protective or beneficial role of IL‐33 in cardiovascular biology 9, 10. Of note, the administration of recombinant IL‐33 exerted a protective effect in the apolipoprotein E‐deficient (ApoE ‐/‐ ) mouse model of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Martin

Palmer

Rodriguez

et al. 2015

Immunity Inflam & Disease

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Interleukin (IL)‐33 is a cytokine of the IL‐1 family, which signals through the ST2 receptor. Previous work demonstrated that the systemic administration of recombinant IL‐33 reduces the development of atherosclerosis in apolipoprotein E‐deficient (ApoE−/−) mice by inducing a Th1‐to‐Th2 shift. The objective of our study was to examine the role of endogenous IL‐33 and ST2 in atherosclerosis. ApoE−/−, IL‐33−/−ApoE−/−, and ST2−/−ApoE−/− mice were fed with a cholesterol‐rich diet for 10 weeks. Additionally, a group of ApoE−/− mice was injected with a neutralizing anti‐ST2 or an isotype control antibody during the period of the cholesterol‐rich diet. Atherosclerotic lesion development was measured by Oil Red O staining in the thoracic‐abdominal aorta and the aortic sinus. There were no significant differences in the lipid‐staining area of IL‐33−/−ApoE−/−, ST2−/−ApoE−/−, or anti‐ST2 antibody‐treated ApoE−/− mice, compared to ApoE−/− controls. The absence of IL‐33 signaling had no major and consistent impact on the Th1/Th2 cytokine responses in the supernatant of in vitro‐stimulated lymph node cells. In summary, deficiency of the endogenously produced IL‐33 and its receptor ST2 does not impact the development of atherosclerosis in ApoE‐deficient mice.

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IL-33 is negatively associated with the BMI and confers a protective lipid/metabolic profile in non-diabetic but not diabetic subjects

Cited by 54 publications

References 28 publications

WITHDRAWN: Relationship between circulating irisin, retinol binding protein-4, adiponectin and inflammatory mediators in patients with metabolic syndrome

WITHDRAWN: Relationship between circulating irisin, retinol binding protein-4, adiponectin and inflammatory mediators in patients with metabolic syndrome

Regulation of De Novo Adipocyte Differentiation Through Cross Talk Between Adipocytes and Preadipocytes

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

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