Abstract
Hyperglycaemia has a deferred detrimental effect on glucose metabolism, termed “metabolic memory”. Elevated saturated fatty acids promote insulin resistance, hyperglycaemia and associated atherosclerotic complications, but their effect on “metabolic memory” is unknown. Therefore we investigated whether basal and insulin-stimulated (10 −6 M for 12 h) glucose (2-deoxy- d-[ 3H]-glucose) uptake was affected by palmitate pre-treatment human THP-1 monocytes. Palmitate-induced a time-dependent and concentration-dependent inhibition of insulin-stimulated glucose uptake, showing almost complete abolition of the insulin-stimulatory effect with 300 μM palmitate. Basal glucose uptake was unaffected by palmitate. When palmitate was washed out, the inhibitory effect on insulin-stimulated glucose uptake persisted for at least 60 h.
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