Hindsight: Adipose Tissue and Cardio-Renal DiseaseSaturday, March 17, 2012
Back in 2000, we were still in the early years of recognizing that fat tissue was an important source of a wide range of molecules that can act locally (paracrine) or at remote organs (endocrine) including blood vessels, the heart, and the kidney.
At that time, Stefan Engeli and I reviewed the emerging literature on this issue in a paper we published in Hormone & Metabolism Research.
In this paper we discussed the potential role of several vasoactive factors, including non-esterified fatty acids, angiotensin II, prostaglandins, and nitric oxide, which were by then all known to be produced and secreted by adipose tissue and could all have important local or paracrine effects.
In addition, we also discussed the central nervous system actions of the adipose tissue-derived hormone leptin, which had been discovered to increase sympathetic nervous system activity, which is typically found to be elevated in obesity. We postulated that enhanced leptin-driven renal sympathetic out-flow, in combination with low atrial natriuretic peptide plasma levels possibly due to over-expression of the natriuretic peptide clearance receptor in adipocytes, may enhance sodium retention and volume expansion, both key features in the pathophysiology of obesity-associated hypertension.
Since then, we have learnt much more about how factors produced in adipose tissue can affect a wide range of physiological functions, and new factors, collectively often called ‘adipokines’, continue to be discovered at a steady pace.
According to Google Scholar, this paper has been cited 80 times.