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Adipose tissue, inflammation and insulin resistance
Helen Roche
Professor of Nutrigenomics, UCD School of Public
Health; UCD Conway Institute of Molecular Medicine,
University College Dublin, Ireland
The
Metabolic Syndrome (Met Syn) is a very common condition
that often precedes T2DM and is associated with a
greater risk of CVD. It is characterized by abdominal
obesity, insulin resistance, dyslipidaemia and
hypertension. There is always a concomitant sub-acute
pro-inflammatory state which must impede insulin
signalling. Therefore this presentation will focus on
the interaction between dietary fat composition, insulin
sensitivity and inflammatory stressors on the Met Syn.
The complex roles of nutrient sensitive transcription
factors, within the context of insulin resistance will
be explored.
Obesity is characterised by the infiltration of
macrophages into adipose tissue, a key organ which
probably explains the sub-acute pro-inflammatory state
associated with insulin resistance. Our group have
addressed this interaction between adipose tissue,
inflammation and insulin sensitivity from a number of
perspectives. New preliminary data show that mice with a
compromised macrophage response become obese but not
insulin resistant to high-fat diet-induced obesity
(unpublished data). Furthermore we have demonstrated
that feeding anti-inflammatory fatty acids to obese mice
confer an insulin sensitive state, despite remaining
obese. This observation was associated with key changes
in the anti-inflammatory profile of adipose tissue (Moloney
et al. 2007).
Our results suggest that manipulating the inflammatory
components of adipose tissue may represent an
alternative strategy in terms of reducing the metabolic
risk factors associated with obesity. The challenge will
be to validate this hypothesis in man.
Moloney F, Toomey S Noone E,
Nugent A, Allan B, Loscher CE & Roche HM (2007)
Anti-diabetic effects of cis-9, trans-11 conjugated
linoleic acid may be mediated via anti-inflammatory
effects in white adipose tissue.
Diabetes 56(3): 574-82.
The work described in this abstract was supported by The
Welcome Trust, UK. (2000-2005) and Science Foundation
Ireland Principal Investigator
Programme (2007-2011).
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