Format

Send to

Choose Destination
Diabetologia. 2012 Nov;55(11):3029-37. doi: 10.1007/s00125-012-2676-0. Epub 2012 Aug 17.

Marked resistance of femoral adipose tissue blood flow and lipolysis to adrenaline in vivo.

Author information

1
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK. k.manolopoulos@bham.ac.uk

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 (133)Xe 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. Local microinfusion 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 α-adrenergic response during adrenaline stimulation. The α-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.

PMID:
22898765
DOI:
10.1007/s00125-012-2676-0
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center