Journal article
Marked resistance of femoral adipose tissue blood flow and lipolysis to adrenaline in vivo
- Abstract:
- Aims/hypothesis Fatty acid entrapment in femoral adipose tissue has been proposed to prevent ectopic fat deposition and visceral fat accumulation, resulting in protection from insulin resistance. Our objective was to test the hypothesis of femoral, compared with abdominal, adipose tissue resistance to adrenergic stimulation in vivo as a possible mechanism. Methods Regional fatty acid trafficking, along with the measurement of adipose tissue blood flow (ATBF) with 133Xe washout, was studied with the arteriovenous difference technique and stable isotope tracers in healthy volunteers. Adrenergic agonists (isoprenaline, adrenaline [epinephrine]) were infused either locally by microinfusion or systemically. Localmicroinfusion of adrenoceptor antagonists (propranolol, phentolamine) was used to characterise specific adrenoceptor subtype effects in vivo. Results Femoral adipose tissue NEFA release and ATBF were lower during adrenaline stimulation than in abdominal tissue (p<0.001). Mechanistically, femoral adipose tissue displayed a dominant a-adrenergic response during adrenaline stimulation. The a-adrenoceptor blocker, phentolamine, resulted in the 'disinhibition' of the femoral ATBF response to adrenaline (p<0.001). Conclusions/interpretation Fatty acids, once stored in femoral adipose tissue, are not readily released upon adrenergic stimulation. Femoral adipose tissue resistance to adrenaline may contribute to the prevention of ectopic fatty acid deposition. © Springer-Verlag 2012.
Actions
Authors
- Journal:
- Diabetologia More from this journal
- Volume:
- 55
- Issue:
- 11
- Pages:
- 3029-3037
- Publication date:
- 2012-11-01
- DOI:
- EISSN:
-
1432-0428
- ISSN:
-
0012-186X
- Pubs id:
-
pubs:356605
- UUID:
-
uuid:e054a652-32ad-4e60-ae20-1d1c55c57a16
- Local pid:
-
pubs:356605
- Source identifiers:
-
356605
- Deposit date:
-
2013-11-16
Terms of use
- Copyright date:
- 2012
If you are the owner of this record, you can report an update to it here: Report update to this record