Abstract
Aims/HypothesisRecent evidence suggests a link between myocardial steatosis and diabetic cardiomyopathy. Insulin, as a lipogenic and growth-promoting hormone, might stimulate intramyocardial lipid (MYCL) deposition and hypertrophy. Therefore, the aim of the present study was to investigate the short-term effects of insulin therapy (IT) on myocardial lipid content and morphology in patients with T2DM.MethodsEighteen patients with T2DM were recruited (age 56±2 years; HbA1c: 10.5±0.4%). In 10 patients with insufficient glucose control under oral medication IT was initiated due to secondary failure of oral glucose lowering therapy (IT-group), while 8 individuals did not require additional insulin substitution (OT-group). In order to assess MYCL and intrahepatic lipid (IHLC) content as well as cardiac geometry and function magnetic resonance spectroscopy (MRS) and imaging (MRI) examinations were performed at baseline (IT and OT) and 10 days after initiation of IT. Follow up measurements took place 181±49 days after IT.ResultsInterestingly, basal MYCLs were 50% lower in IT- compared to OT-group (0.41±0.12 vs. 0.80±0.11% of water signal; p = 0.034). After 10 days of IT, an acute 80%-rise in MYCL (p = 0.008) was observed, while IHLC did not change. Likewise, myocardial mass (+13%; p = 0.004), wall thickness in end-diastole (+13%; p = 0.030) and concentricity, an index of cardiac remodeling, increased (+28%; p = 0.026). In the long-term MYCL returned to baseline, while IHCL significantly decreased (−31%; p = 0.000). No acute changes in systolic left ventricular function were observed.Conclusions/InterpretationThe initiation of IT in patients with T2DM was followed by an acute rise in MYCL concentration and myocardial mass.
Highlights
The pathogenesis of diabetic heart disease is multi-factorial and complex
The present study shows that the initiation of insulin therapy (IT) in patients with long standing type-2 diabetes mellitus (T2DM) and bad metabolic control due to secondary failure of oral glucose lowering therapy is associated with an acute but transient rise in might stimulate intramyocardial lipid (MYCL) content and myocardial wall thickness
The observed changes were initially linked to myocardial hypertrophy with preservation of cardiac function
Summary
The pathogenesis of diabetic heart disease is multi-factorial and complex. Putative mechanisms include metabolic disturbances, myocardial fibrosis and small vessel disease [1]. High dietary intake of free fatty acids may result in intracellular accumulation of potentially toxic intermediates of the lipid metabolism, all of which lead to impaired myocardial performance and morphological changes [2,3]. At the late stage of the disease myocyte loss and replacement fibrosis is increased, indicating cardiac remodeling in patients with type-2 diabetes mellitus (T2DM) [4,5]. Assessment of cardiac lipid metabolism by means of magnetic resonance spectroscopy in obese patients with T2DM and non-ischemic cardiomyopathy demonstrated increased intramyocardial lipid content (MYCL) [6,7,8]. To date contradictive results have been published concerning the short term effects of MYCL accumulation (steatosis) on cardiac function [7,9]
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