Key result
Overnutrition exacerbates pro-inflammatory signaling in vascular and adipose tissues, contributing to the risk of insulin resistance, type 2 diabetes, and cardiovascular diseases.
Why the study?
The molecular and cellular mechanisms underlying the increased risk of cardiovascular diseases in obesity and diabetes remain poorly characterised.
Answers are grounded in this paper and cite their sources.
This review highlights the molecular mechanisms linking overnutrition to pro-inflammatory signaling in adipose and vascular tissues, offering potential therapeutic targets for obesity and vascular disease.
Despite obesity and diabetes markedly increasing the risk of developing cardiovascular diseases, the molecular and cellular mechanisms that underlie this association remain poorly characterised. In the last 20 years it has become apparent that chronic, low-grade inflammation in obese adipose tissue may contribute to the risk of developing insulin resistance and type 2 diabetes. Furthermore, increased vascular pro-inflammatory signalling is a key event in the development of cardiovascular diseases. Overnutrition exacerbates pro-inflammatory signalling in vascular and adipose tissues, with several mechanisms proposed to mediate this. In this article, we review the molecular and cellular mechanisms by which nutrients are proposed to regulate pro-inflammatory signalling in adipose and vascular tissues. In addition, we examine the potential therapeutic opportunities that these mechanisms provide for suppression of inappropriate inflammation in obesity and vascular disease.
No takes yet. Share an insight, caveat, or question.
Palmer et al. (2021) conducted a review in Obesity and vascular disease. Overnutrition was evaluated. Overnutrition exacerbates pro-inflammatory signaling in vascular and adipose tissues, contributing to the risk of insulin resistance, type 2 diabetes, and cardiovascular diseases.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: