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1 Department of Medical Physiology, University of Tromsoe, Tromsoe, Norway
* To whom correspondence should be addressed. E-mail: anned{at}fagmed.uit.no.
Hearts from type 2 diabetic (db/db) mice demonstrate altered substrate utilization with high rates of fatty acid oxidation, decreased functional recovery following and reduced cardiac efficiency. Although db/db mice show overall insulin resistance in vivo, we recently reported that insulin induces a marked shift towards glucose oxidation in isolated perfused db/db hearts. We hypothesize that such a shift in metabolism should improve cardiac efficiency and consequently increase functional recovery following low-flow ischemia. Hearts from db/db and non-diabetic (db/+) mice were perfused with 0.7 mM palmitate plus either 5 mM glucose (G), 5 mM glucose and 300 µU/ml insulin (GI) or 33 mM glucose and 900 µU/ml insulin (HGHI). Rates of substrate oxidation and post-ischemic recovery were only moderately affected by GI and HGHI in db/+ hearts. In contrast, GI and particularly HGHI markedly increased glucose oxidation and improved post-ischemic functional recovery in db/db hearts. Cardiac efficiency was significantly improved in db/db, but not in db/+ hearts, in the presence of HGHI. In conclusion, insulin and glucose normalize cardiac metabolism, restore efficiency and improve post-ischemic recovery in type 2 diabetic mouse hearts. These findings may in part explain the beneficial effect of GIK (glucose-insulin-potassium) therapy in diabetic patients with cardiac complications.
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