What is the clinical evidence from this study?

Study design: Other. Population: Type 2 diabetes and microvascular disease. Intervention: Ibrutinib vs. Vehicle. Primary outcome: Blood glucose (mmol).

What does this research mean for the field?

Inhibition of Bruton's tyrosine kinase with ibrutinib reduces NF-kB and NLRP3 inflammasome activity, thereby protecting against insulin resistance and diabetic nephropathy in high-fat diet-fed mice. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.ESTABLISHES_NEW_DIRECTION.

August 28, 2019Open Access

Inhibition of Bruton’s tyrosine kinase reduces NF-kB and NLRP3 inflammasome activity preventing insulin resistance and microvascular disease

View Full Paper

Ask AI

Bookmark

Key result

Ibrutinib lowers blood glucose ~37% in mice, protecting against insulin resistance and diabetic nephropathy.

Why the study?

There are currently no therapies available that target inflammation in type-2 diabetes or microvascular disease.

Population

High fat diet-fed mice and human monocyte derived macrophages

Comparison

Ibrutinib treatment vs no treatment

Design

Preclinical experimental study

Authors

GPGareth S. D. Purvis MCMassimo Collino HTHaidee M. A. Tavio

Discussion

Member takes

Overview

BTK inhibition merits further metabolic research; does not support ibrutinib use in T2D or microvascular disease.

PICO

Population

C57BL/6J mice fed a high fat diet to induce insulin resistance and microvascular disease, treated with ibrutinib for 6 weeks.

Intervention / Comparator

Ibrutinib vs Vehicle (3 or 30 mg/kg; p.o.; 5 times per week)

Primary Outcome

Blood glucose (mmol)

Main Result

Absolute Event Rate: 8.04% vs 12.82%

Cite This Study

Purvis et al. (2019) studied Type 2 diabetes and microvascular disease. Ibrutinib vs. Vehicle was evaluated on Blood glucose (mmol). Ibrutinib treatment significantly lowered blood glucose from 12.82 mmol to 8.04-7.71 mmol in high fat diet-fed mice, protecting them from insulin resistance and diabetic nephropathy.

synapsesocial.com/papers/6aaca7e561b2bb69fb3a626c https://doi.org/10.1101/745943

View Full Paper

Ask AI

Bookmark

August 28, 2019Open Access

Inhibition of Bruton’s tyrosine kinase reduces NF-kB and NLRP3 inflammasome activity preventing insulin resistance and microvascular disease

View Full Paper

Ask AI

Bookmark

Key result

Ibrutinib lowers blood glucose ~37% in mice, protecting against insulin resistance and diabetic nephropathy.

Why the study?

There are currently no therapies available that target inflammation in type-2 diabetes or microvascular disease.

Population

High fat diet-fed mice and human monocyte derived macrophages

Comparison

Ibrutinib treatment vs no treatment

Design

Preclinical experimental study

Authors

GPGareth S. D. Purvis MCMassimo Collino HTHaidee M. A. Tavio

Discussion

Member takes

Overview

BTK inhibition merits further metabolic research; does not support ibrutinib use in T2D or microvascular disease.

PICO

Population

C57BL/6J mice fed a high fat diet to induce insulin resistance and microvascular disease, treated with ibrutinib for 6 weeks.

Intervention / Comparator

Ibrutinib vs Vehicle (3 or 30 mg/kg; p.o.; 5 times per week)

Primary Outcome

Blood glucose (mmol)

Main Result

Absolute Event Rate: 8.04% vs 12.82%

Cite This Study

synapsesocial.com/papers/6aaca7e561b2bb69fb3a626c https://doi.org/10.1101/745943

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark