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Abstract
Hypothesis: Pathological hypertrophy is associated with whole body insulin-resistance and the development of heart failure. Physiological hypertrophy is not. We compared substrate oxidation patterns and the effect of insulin in isolated working rat hearts with physiological or pathological hypertrophy. Methods: Physiological hypertrophy was induced by treadmill- running of male Sprague-Dawley-rats for 10 weeks (TR). Pathological hypertrophy was induced by aortic-banding for 10 weeks (AoB). Contractile function and hypertrophy-grade was assessed by echocardiography. Glucose (GO) and fatty-acid-oxidation (FAO) with or without insulin stimulation were assessed in the isolated working heart with radioactive tracers. Results: Both interventions caused significant hypertrophy (LVPWD +26%TR, p<0,05; +56% AoB, p<0,01). There were no changes in EF among groups: (AoB71±10%, TR69±2%; Control71±6%). Isolated hearts had lowest cardiac power after AoB (mW/gdry: 8,7±4,14 vs. 35,5±7,4 in Control, p<0.01). TR did not affect cardiac power. Decreased power after AoB was associated with the lowest FAO-rates (µmolOleat/min/gdry AoB: 0,36±0,10, TR:0,92±0,27, Control:0,91±0,23, p<0,01). GO was significantly decreased in both hypertrophy groups (µmolGlucose/min/gdry: AoB: 0,24±0,12; TR:0,20±0,13; Control: 0,39±0,18, p<0.02). Insulin stimulation increased GO in all groups (µmolGlucose/min/gdry: AoB to 0,54±0,21; TR to 0,75±0,41; Control: to 1,31±0,54). The relative increase was greatest in TR (+356%) and smallest in AoB (+161%). Insulin caused a reduction in FAO, which was similar in all groups (AoB: –49%, TR: –54%, Control: –54%). Conclusions: Physiological hypertrophy is associated with normal function and insulin sensitivity. The unexpected decrease in basal glucose oxidation was similar to the pathological state and warrants further investigation. Hearts with pathological hypertrophy had poor function and were insulin resistant.
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