Hormonal
In humans, adipose tissue is the predominant source of serum amyloid A (A-SAA), and elevated A-SAA levels in obesity drive systemic inflammation and insulin resistance through the stimulation of proinflammatory cytokines and increased lipolysis.
This research highlights that obesity is not just about excess fat mass but involves active hormonal signaling from fat cells that drives inflammation and insulin resistance. Specifically, fat cells in obese individuals produce high levels of Serum Amyloid A (A-SAA), which triggers inflammatory responses and increases fat breakdown (lipolysis), contributing to metabolic issues. Weight loss significantly reduces these A-SAA levels, which correlates with improved insulin sensitivity. This suggests that treating obesity involves resolving this specific inflammatory signaling pathway, not just reducing energy storage.
We demonstrate that A-SAA was highly and selectively expressed in human adipocytes... A-SAA is a proinflammatory and lipolytic adipokine in humans... The increased expression of A-SAA by adipocytes in obesity suggests that it may play a critical role in local and systemic inflammation and free fatty acid production and could be a direct link between obesity and its comorbidities, such as insulin resistance and atherosclerosis.
Why this rating
Strong human clinical data (correlations, intervention effects) combined with robust in vitro mechanistic evidence.
Source
Acute-Phase Serum Amyloid A: An Inflammatory Adipokine and Potential Link between Obesity and Its Metabolic Complications
Rongze Yang et al. · PLoS Medicine · 2006
DOI 10.1371/journal.pmed.0030287
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