Insulin resistance does not predict myocardial steatosis in women
MedWire News: Women with insulin resistance (IR) are no more likely than women who are insulin sensitive (IS) to have myocardial steatosis, show study results.
Michael Krebs (Medical University of Vienna, Austria) and colleagues investigated links between IR and myocardial steatosis and function in 34 women with variable insulin sensitivity.
They reasoned that IR is associated with lipid accumulation in skeletal muscle and the liver and could therefore also predict cardiac steatosis, an important factor in the development of diabetic cardiomyopathy.
To test their theory, the team recruited 11 IS, 10 IR, six impaired glucose tolerant (IGT), and seven Type 2 diabetic women to take part in their study. The women were aged 48 years on average and all had a mean body mass index between 25 and 28 kg/m2.
Krebs et al focused on women with abnormal glucose metabolism, as previous studies have suggested they have almost double the risk for developing diabetic cardiomyopathy compared with their male counterparts.
Magnetic resonance imaging and spectroscopy techniques were used to evaluate myocardial lipid accumulation and function.
As reported in the journal Diabetologia, only women with Type 2 diabetes had significantly elevated myocardial lipid content, at 0.7%, compared with 0.4%, 0.4%, and 0.5%, in women who were IS, IR, and IGT, respectively.
Regarding myocardial function, women with IR had significantly lower stroke volume (-15%) and a higher heart rate (+11%) than IS women. Their myocardial function was better than that of women with Type 2 diabetes, however, who had a 27% lower stroke volume and a 14% higher heart rate than IS women.
Krebs and team say that their results show that although "intramyocardial lipid stores were clearly higher in women with overt hyperglycemia (ie, Type 2 diabetes), IR as such was not associated with increased myocardial lipid content."
The team suggests further research in both men and women is needed to confirm their findings.
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By Helen Albert