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Fatty liver in uncomplicated type 2 DM is associated with impaired myocardial HEP metabolism, modulated by myocardial glucose uptake

Purpose

To study the associations between fatty liver (FL), insulin resistance, myocardial high-energy-phosphate (HEP) and glucose metabolism, and heart function in patients with uncomplicated type 2 diabetes mellitus (T2DM).

Materials and methods

We studied 35 T2DM patients (Mean ± SD Hba1c = 7.0 ± 0.8%) without coronary artery disease or heart failure, as determined by echocardiography. 1H-MRS of the liver for the assessment of liver fat, myocardial 31P-MRS for assessment of myocardial HEP metabolism and MRI to determine left ventricular function were performed. Furthermore, a hyperinsulinemic, euglycemic clamp was performed to establish whole body insulin sensitivity. Moreover, PET with H215O (fasting conditions) and [18F]-2-fluoro-2-deoxy-D-glucose (clamp conditions) were used to determine myocardial blood flow (MBF) and myocardial metabolic rate of glucose uptake (MMRglu) in a subgroup of 28 patients.

Results

Patients with FL (liver: fat/water ratio>5%, n = 17) showed increased body mass index (29.5 ± 3.2 vs 27.2 ± 2.8 kg/m2, p < 0.05), reduced whole body insulin sensitivity (0.45 ± 0.48 vs 0.74 ± 0.44 (mg/kg·min)/(pmol/L), p < 0.05), and reduced MMRglu (0.21 ± 0.13 vs 0.34 ± 0.14 mmol/mL/min, p < 0.05), as compared with patients without FL, while MBF was not different. The ratio of phosphocreatine over adenosine triphosphate, a marker of myocardial HEP metabolism, was reduced in patients with FL (1.90 ± 0.35 versus 2.27 ± 0.29; p < 0.05), also after adjustment for BMI, and correlated to MMRglu (r = 0.43, p < 0.05). LV systolic and diastolic function were not statistically significantly different. Figure 1

Figure 1
figure1

Myocardial HEP metabolism in patients with DM2. PCr/ATP ratio = ratio of phosphocreatine over adenosine triphosphate. *P < 0.05.

Conclusion

Fatty liver in patients with uncomplicated T2DM is associated with decreased myocardial HEP metabolism. In addition myocardial HEP metabolism is modulated by myocardial glucose uptake.

Author information

Correspondence to Jacqueline T Jonker.

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Keywords

  • Coronary Artery Disease
  • Adenosine
  • Glucose Uptake
  • Fatty Liver
  • Diastolic Function