Key result
Global myocardial glucose metabolism was significantly reduced in subjects with 1-hour postload hyperglycemia (23.7 vs 32.8 mmol/min/100 mg; P=0.024) and impaired glucose tolerance (16.4; P<0.0001).
Why the study?
Whether cardiac insulin resistance is present in individuals at risk for type 2 diabetes, such as those with impaired glucose tolerance or normal glucose tolerance with 1-h postload glucose >=155 mg/dL, remained uncertain.
Does impaired glucose tolerance or 1-h postload hyperglycemia reduce myocardial glucose metabolism in subjects without coronary artery disease?
Cross-Sectional (n=30)
Does impaired glucose tolerance or 1-h postload hyperglycemia reduce myocardial glucose metabolism in subjects without coronary artery disease?
Absolute Event Rate: 23.7% vs 32.8%
p-value: p=0.024
Myocardial insulin resistance is an early defect detectable in individuals with dysglycemic conditions (IGT and NGT 1-h high) prior to the onset of type 2 diabetes.
May signal early myocardial metabolic impairment in prediabetes; leaves open links to cardiomyopathy and requires prospective validation.
OBJECTIVE Impaired insulin-stimulated myocardial glucose uptake has occurred in patients with type 2 diabetes with or without coronary artery disease. Whether cardiac insulin resistance is present remains uncertain in subjects at risk for type 2 diabetes, such as individuals with impaired glucose tolerance (IGT) or those with normal glucose tolerance (NGT) and 1-h postload glucose ≥155 mg/dL during an oral glucose tolerance test (NGT 1-h high). This issue was examined in this study. RESEARCH DESIGN AND METHODS The myocardial metabolic rate of glucose (MRGlu) was measured by using dynamic 18F-fluorodeoxyglucose positron emission tomography combined with a euglycemic-hyperinsulinemic clamp in 30 volunteers without coronary artery disease. Three groups were studied: 1) those with 1-h postload glucose <155 mg/dL (NGT 1-h low) (n = 10), 2) those with NGT 1-h high (n = 10), 3) and those with IGT (n = 10). RESULTS After adjusting for age, sex, and BMI, both subjects with NGT 1-h high (23.7 ± 6.4 mmol/min/100 mg; P = 0.024) and those with IGT (16.4 ± 6.0 mmol/min/100 mg; P < 0.0001) exhibited a significant reduction in global myocardial MRGlu; this value was 32.8 ± 9.7 mmol/min/100 mg in subjects with NGT 1-h low. Univariate correlations showed that MRGlu was positively correlated with insulin-stimulated whole-body glucose disposal (r = 0.441; P = 0.019) and negatively correlated with 1-h (r = −0.422; P = 0.025) and 2-h (r = −0.374; P = 0.05) postload glucose levels, but not with fasting glucose. CONCLUSIONS This study shows that myocardial insulin resistance is an early defect that is already detectable in individuals with dysglycemic conditions associated with an increased risk of type 2 diabetes, such as IGT and NGT 1-h high.
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Succurro et al. (2020) conducted a cross-sectional in Impaired glucose tolerance and 1-hour postload hyperglycemia (n=30). 1-hour postload hyperglycemia (NGT 1-h high) vs. Normal glucose tolerance (NGT 1-h low) was evaluated on Global myocardial metabolic rate of glucose (MRGlu) (p=0.024). Global myocardial glucose metabolism was significantly reduced in subjects with 1-hour postload hyperglycemia (23.7 vs 32.8 mmol/min/100 mg; P=0.024) and impaired glucose tolerance (16.4; P<0.0001).
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