Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

Abstract

BackgroundAlcoholic cardiomyopathy (CMP) is one of the major complications of chronic excessive alcohol consumption. The pathogenic mechanisms implicated are diverse, inducing functional and structural changes in the myocardium. Insulin-like Growth Factor 1 (IGF-1) plays an important role in modulating the cell cycle, and helps the differentiation and proliferation of cardiac tissue inhibiting apoptosis. Experimental studies have suggested the role of IGF-1 in alcohol-induced cardiac damage. The aim of the present study was to determine the effect of chronic alcohol consumption on IGF-1 myocardial expression and to compare this expression in cases of hypertension and other cardiac diseases.MethodsWe studied heart samples from human organ donors: 10 healthy donors, 16 with hypertension, 23 with chronic alcohol consumption and 7 with other causes of cardiac disease. IGF-1 myocardial expression was evaluated with a specific immunohistochemistry assay using a semi-quantitative method.ResultsA significant decrease in IGF-1 myocardial expression was observed comparing all the cases included with control donors. This decrease in IGF-1 myocardial expression was significantly lower in the group of donors with chronic alcohol consumption compared to controls. On group evaluation according to the presence of CMP, donors with chronic alcohol consumption without CMP presented significantly lower IGF-1 expression than controls, whereas donors with chronic alcohol consumption with CMP showed a downward trend without achieving significance.ConclusionsChronic alcohol consumption significantly reduces IGF-1 myocardial expression. This decrease induced by alcohol is partially compensated in the presence of structural myocardial damage.

Myostatin and insulin-like growth factor-1 in hypertensive heart disease

“…One event corroborating this differential myocyte effect of IGF-1 and myostatin is the absence of a significant correlation between myostatin and IGF-1 myocardial activities in the whole sample of the organ donors evaluated in the present study. The present study also corroborates the previously described effects of alcohol consumption on IGF-1 and myostatin myocardial expression [13,29]. Thus, donors with alcohol consumption showed a non-significant increase in myostatin myocardial expression compared to control donors.…”

“…A steady increase in local cardiac myocyte IGF-1 activity may counterbalance the cardiac damaging effect induced by the haemodynamic factors in AHT with the local protector effect of IGF-1. This situation in HHD is also similar to that reported by our group in previous studies on alcoholic dilated cardiomyopathy [29]. In experimental studies, IGF-1 has demonstrated a beneficial therapeutic effect on the myocardial dysfunction caused by excessive alcohol consumption [25].…”

“…In the presence of CMP, high levels of circulating IGF-1 have been reported in patients with essential hypertension, suggesting the up-regulation of IGF-1 in hypertensive CMP [27,28]. In a recent study, we observed a non-significant downward trend of IGF-1 myocardial expression in AHT compared to the non-hypertensive controls [29]. No other clinical investigations have studied the direct effect of AHT on myocardial IGF-1 expression in humans.…”

Cardiovascular risks and benefits of moderate and heavy alcohol consumption

“…45,81 Ethanol also disturbs cardiac repair mechanisms, increasing the activity of myostatin 82 and decreasing IGF-1 myocardial expression, leading to inhibition of myocyte proliferation. 83 In this situation, alcohol consumption impairs cardiac adaptation and repair mechanisms. 83 …”

Alcoholic Cardiomyopathy: Old and New Insights

“…This is mediated by interference with myokines (FGF-21) and local hormones and growth-factors such as myostatin [33], IGF-1 [34], ghrelin [35] and leptin [36]. Thus, ethanol decreases the myocyte proliferation rate probably by myostatin up-regulation [33] and modifies the mechanisms of cardiac plasticity [37].…”