Key result
Impaired glucose tolerance in overweight individuals was associated with higher hepatic uptake of postprandial fatty acids over 6 hours compared to normal glucose tolerance (97 vs 68 mmol/6 h; P=0.03).
Why the study?
Cardiac and hepatic total postprandial fatty acid uptake of nonesterified and dietary fatty acids had never been reported in prediabetes with overweight.
Does impaired glucose tolerance increase postprandial hepatic and cardiac fatty acid uptake in individuals with overweight compared to normal glucose tolerance?
Cross-Sectional (n=39)
Does impaired glucose tolerance increase postprandial hepatic and cardiac fatty acid uptake in individuals with overweight compared to normal glucose tolerance?
In individuals with overweight, prediabetes is associated with increased postprandial hepatic fatty acid uptake, which is insufficiently curbed by adipose tissue trapping.
Answers are grounded in this paper and cite their sources.
May signal early hepatic lipid dysregulation in overweight prediabetes; hypothesis-generating for steatosis progression and requires prospective validation.
Excessive lean tissue uptake of fatty acids (FAs) is important in the development of insulin resistance and may be caused by impaired dietary FA (DFA) storage and/or increased nonesterified FA (NEFA) flux from adipose tissue intracellular lipolysis. Cardiac and hepatic total postprandial FA uptake of NEFA+DFA has, however, never been reported in prediabetes with overweight. In this study, 20 individuals with impaired glucose tolerance (IGT) and 19 participants with normal glucose tolerance (NGT) and normal fasting glucose underwent postprandial studies with whole-body positron emission tomography/computed tomography (PET/CT) with oral [18F]fluoro-thia-heptadecanoic acid and dynamic PET/CT with intravenous [11C]palmitate. Hepatic (97 [range 36-215] mmol/6 h vs. 68 [23-132] mmol/6 h, P = 0.03) but not cardiac (11 [range 4-24] mmol/6 h vs. 8 [3-20] mmol/6 h, P = 0.09) uptake of most sources of postprandial FA (NEFA + DFA uptake) integrated over 6 h was higher in IGT versus NGT. DFA accounted for lower fractions of total cardiac (21% [5-47] vs. 25% [9-39], P = 0.08) and hepatic (19% [6-52] vs. 28% [14-50], P = 0.04) uptake in IGT versus NGT. Increased adipose tissue DFA trapping predicted lower hepatic DFA uptake and was associated with higher total cardiac FA uptake. Hence, enhanced adipose tissue DFA trapping in the face of increased postprandial NEFA flux is insufficient to fully curb increased postprandial lean organ FA uptake in prediabetes with overweight (ClinicalTrials.gov; NCT02808182).
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Ye et al. (2022) conducted a cross-sectional in Prediabetes with overweight (n=39). Impaired glucose tolerance (IGT) vs. Normal glucose tolerance (NGT) was evaluated on Hepatic uptake of postprandial fatty acids (NEFA + DFA) integrated over 6 hours (p=0.03). Impaired glucose tolerance in overweight individuals was associated with higher hepatic uptake of postprandial fatty acids over 6 hours compared to normal glucose tolerance (97 vs 68 mmol/6 h; P=0.03).
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