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1 Discovery Technologies Area, Novartis Institutes for Biomedical Research, Inc., Cambridge, MA, USA
2 the Diabetes and Metabolism Area, Novartis Institutes for Biomedical Research, Inc., Cambridge, MA, USA
* To whom correspondence should be addressed. E-mail: didier.laurent{at}pharma.novartis.com.
High visceral adiposity and intramyocellular lipid levels (IMCL) are both associated with the
development of type 2 diabetes. The relationship between visceral adiposity and IMCL levels
was explored in a diet-induced and a glucocorticoid-induced model of insulin resistance. In
the diet-induced model, lean and fa/fa Zucker rats were fed either a normal or a high-fat (HF)
chow over a 4-week period. Fat distribution, IMCL content in the tibialis anterior (IMCLTA)
muscle and whole-body insulin resistance were measured prior to and following the 4-week
period. The HF diet-induced increase in IMCLTA was strongly correlated with visceral fat
accumulation and greater glucose intolerance in both groups of rats. The increase in IMCLTA
to visceral fat accumulation was three-fold greater for fa/fa rats. In the glucocorticoid-induced
model, insulin sensitivity was impaired using dexamethasone. In-vivo adiposity and IMCLTA
content measurements were combined with ex-vivo analysis of plasma and muscle tissue.
Dexamethasone treatment had minimal effect on visceral fat accumulation, while increasing
IMCLTA levels by ~30% (p<0.05) compared to controls. Dexamethasone increased plasma
glucose by 2-fold, and increased the saturated fatty acid content of plasma lipids (fatty acid
(CH2)n/
CH3 ratio +15%, p<0.05). The lipid composition of the TA muscle was unchanged by
dexamethasone treatment indicating that the relative increase in IMCLTA observed in-vivo
resulted from a decrease in lipid oxidation. Visceral adiposity may influence IMCL
accumulation in the context of dietary manipulations; however a "causal" relationship still
remains to be determined. Dexamethasone-induced insulin resistance likely operates under a
different mechanism, i.e. independently of visceral adiposity.
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