Treatment of type 2 diabetes by targeting interleukin-1: a meta-analysis of 2921 patients

Kataria, Yachana; Ellervik, Christina; Mandrup‐Poulsen, Thomas

doi:10.1007/s00281-019-00743-6

Cited by 33 publications

(23 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As canakinumab treatment substantially reduces the recurrence of cardiovascular events, these results suggest that anti-inflammatory therapy can provide beneficial effects for individuals with obesity and/or T2DM. A meta-analysis performed in 2019 of 2,921 individuals from eight phase I-IV studies found a statistically significant overall HbA 1c -lowering effect of IL-1 antagonism, achieved through either anti-IL-1 antibodies or IL-1R antagonists 123 . In this meta-analysis, a statistically significant correlation between baseline C-reactive protein and C-peptide, and HbA 1c outcomes was also revealed.…”

Section: Nature Reviews | Endocrinologymentioning

confidence: 99%

The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities

et al. 2019

View full text Add to dashboard Cite

Section: Nature Reviews | Endocrinologymentioning

confidence: 99%

The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities

et al. 2019

View full text Add to dashboard Cite

“…In rodents, it contributes to β-cell glucotoxicity and lipotoxicity, which lead to β-cell destruction and dedifferentiation [28][29][30] . In clinical trials, IL-1Ra improved glycaemia and insulin secretion in patients with T2DM 31,32 . Moreover, the CANTOS trial involving 10'061 patients showed that IL-1β antagonism with canakinumab, a neutralizing anti-IL-1β antibody, is effective in reducing the glycated hemoglobin (HbA1c) during the first 6 months of treatment in patients with a history of myocardial infarction 33,34 .…”

mentioning

confidence: 99%

Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes

Schulze

Wehner

Kratschmar

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Gestational diabetes mellitus (GDM) is one of the most common diseases associated with pregnancy, however, the underlying mechanisms remain unclear. Based on the well documented role of inflammation in type 2 diabetes, the aim was to investigate the role of inflammation in GDM. We established a mouse model for GDM on the basis of its two major risk factors, obesity and aging. In these GDM mice, we observed increased Interleukin-1β (IL-1β) expression in the uterus and the placenta along with elevated circulating IL-1β concentrations compared to normoglycemic pregnant mice. Treatment with an anti-IL-1β antibody improved glucose-tolerance of GDM mice without apparent deleterious effects for the fetus. Finally, IL-1β antagonism showed a tendency for reduced plasma corticosterone concentrations, possibly explaining the metabolic improvement. We conclude that IL-1β is a causal driver of impaired glucose tolerance in GDM.

show abstract

“…Therefore, it remains controversial whether or not pancreatic β-cells can produce IL-1β, though one cannot exclude the possibility that the T2DM environment with a uniquely composed mixture of various proinflammatory and nutrient factors may induce cytokine production or maturation within β-cells in vivo. Though the anti-IL-1β targeted therapeutic approaches for T2DM resulted in incons is tent outcomes in terms of pancreatic β-cell function protection [261][262][263], they were shown to reduce serum CRP levels and to promote cardioprotection [257]. Other anti-inflammatory interventions resulted in rather modest protection as discussed in detail in [250].…”

Section: Pancreasmentioning

confidence: 99%

Immunometabolism in type 2 diabetes mellitus: tissue-specific interactions

2020

View full text Add to dashboard Cite

The immune system is frequently described in the context of its protective function against infections and its role in the development of autoimmunity. For more than a decade, the interactions between the immune system and metabolic processes have been reported, in effect creating a new research field, termed immunometabolism. Accumulating evidence supports the hypo thesis that the development of metabolic diseases may be linked to inflammation, and reflects, in some cases, the activation of immune responses. As such, immunometabolism is defined by 1) inflammation as a driver of disease development and/or 2) metabolic processes stimulating cellular differentiation of the immune components. In this review, the main factors capable of altering the immuno-metabolic communication leading to the development and establishment of obesity and diabetes are comprehensively presented. Tissue-specific immune responses suggested to impair metabolic processes are described, with an emphasis on the adipose tissue, gut, muscle, liver, and pancreas.

show abstract

Treatment of type 2 diabetes by targeting interleukin-1: a meta-analysis of 2921 patients

Cited by 33 publications

References 43 publications

The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities

The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities

Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes

Immunometabolism in type 2 diabetes mellitus: tissue-specific interactions

Contact Info

Product

Resources

About