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PubMed1991

[Abnormal left ventricular function in diabetic patients, with special reference to abnormal diastolic function. Preclinical findings through diabetic cardiomyopathy].

In order to elucidate the nature of cardiovascular involvement in diabetes mellitus (DM), we analyzed a high-resolution time-activity cure obtained from a gated equilibrium radionuclide left ventriculography (RLVG) in 50 cases consisting of 3 groups; G-C: normal controls (n = 17, male 10 and female 7, age 49.6 +/- 9.6 years old), G-DM: patients with DM without clinical signs of ischemic heart disease (n = 17, male 13 and female 4, age 58.3 +/- 9.9 years old), and G-DM + MI: patients with DM complicated myocardial infarction (n = 16, male 14 and female 2, age 59.5 +/- 10.0 years old). Indexes of cardiac performance during both systole and diastole obtained from RLVG were as follows: ejection fraction (EF), peak ejection rate (PER), peak filling rate (PFR), time from the start of systole to PER (T-PER1), time from end-systole to PFR (T-PFR2), diastolic relaxation rate (DRR) during the first third of diastole (DRRe) and during the whole diastole (DRRt). There were no significant differences in EF and PER (systolic parameters) between G-C and G-DM. These parameters were significantly lower only in G-DM +/- MI. However, DRRe and DRRt (diastolic parameters) were significantly smaller, and T-PFR1 and T-PFR2 were longer in G-DM and G-DM + MI than in G-C. PFR was significantly lower in G-DM + MI than in the other two groups and there was no significant difference between G-DM and G-C. In addition, DRRe was significantly lower in patients with retinopathy than in patients without retinopathy in both G-DM and G-DM + MI. It is concluded that DM can cause impairment of diastolic relaxation of the left ventricle before the appearance of distinct cardiac dysfunction during systole and that it might be probably due to microangiopathy. These results suggest a poor prognosis of MI in patients with DM.

Adult↗
PubMed1993

Abnormal activation of glycogen synthesis in fibroblasts from NIDDM subjects. Evidence for an abnormality specific to glucose metabolism.

To determine whether the tendency for NIDDM to run in families could relate to genetically determined defects in insulin stimulation of glycogen synthesis, skin fibroblasts from subjects with a strong family history of NIDDM were studied. Fibroblasts from nondiabetic subjects without any family history of NIDDM were studied as control subjects. The cells were studied after 7-16 passages in culture. Rates of glycogen synthesis were lower in fibroblasts from NIDDM subjects both basally and with maximal insulin stimulation (0.77 +/- 0.11 vs. 0.46 +/- 0.04 pmol.well-1 x h-1 [P < 0.02] and 1.49 +/- 0.26 vs. 0.69 +/- 0.05 pmol.well-1 x h-1 +adP < 0.01]). Rates of glycogen synthesis were stimulated 1.9 +/- 0.2-fold above basal in the control cells and 1.5 +/- 0.1-fold above basal in the NIDDM cells (P < 0.02). Rates of [3H]thymidine uptake were similar in control and NIDDM fibroblasts (basal, 28.3 +/- 2.8 vs. 39.2 +/- 8.0; maximum, 50.9 +/- 7.2 vs. 69.3 +/- 16.9 dpm x 10(-3), respectively). Rates of uptake increased similarly in control and NIDDM cells by 1.8 +/- 0.1- and 1.7 +/- 0.1-fold above basal. Maximum specific fibroblast insulin binding was similar for control and NIDDM subjects (194.0 +/- 29.2 vs. 176.1 +/- 24.9 fmol 125I-labeled insulin bound/mg protein respectively). The tyrosine kinase activity of insulin receptors isolated from the control and NIDDM fibroblasts was similar (basal, 135 +/- 30 vs. 149 +/- 33; submaximal, 153 +/- 28 vs. 155 +/- 30; and maximal insulin, 191 +/- 45 vs. 213 +/- 48 dpm.mg protein-1 x min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗