Key result
Higher childhood visceral and subcutaneous adiposity is linked to lower insulin sensitivity and compensatory insulin secretion.
Why the study?
Most prior studies linked visceral and hepatic adiposity to diabetes risk in youth with obesity or impaired glucose tolerance, leaving gaps in early risk markers across a wider adiposity range.
Cross-Sectional (n=45)
Answers are grounded in this paper and cite their sources.
In pre-adolescent children, greater total adiposity is associated with reduced insulin sensitivity and compensatory increases in insulin secretion before the onset of dysglycemia.
Introduction and Objective: Visceral and hepatic adiposity are linked to diabetes risk, but most prior studies focused on youth with obesity or impaired glucose tolerance, leaving gaps in early risk markers. We examined whether abdominal fat depots and liver fat relate to insulin sensitivity, secretion, and glycemia in children across a range of adiposity, aiming to identify metabolic vulnerabilities before overt dysglycemia develops. Methods: 45 children (mean age 11.3±1 years; 62% female) underwent abdominal MRI and 3-hour OGTT. Exposures: visceral adipose tissue volume (VAT), abdominal subcutaneous adipose tissue volume (ASAT), and liver fat percent (LF%). BMI and % body fat assessed overall adiposity. Outcomes: whole-body insulin sensitivity index (ISI), insulinogenic index (InsIndex30), and glucose measures. Data was log-transformed. Spearman partial correlations adjusted for age and sex; InsIndex30 additionally adjusted for ISI. Results: Mean (SD): BMI 22.9 (5.96), % body fat 30.8 (11.52), VAT 1.2 (0.81) cm³, ASAT 5.5 (3.60) cm³, and LF% 5.3 (6.58). Greater VAT, ASAT, and LF% were associated with lower insulin sensitivity (VAT: ρ=-0.60, p<0.0001; ASAT: ρ=-0.62, p<0.0001; LF%: ρ=-0.19, p=0.27) and higher InsIndex30 (VAT: ρ=0.63, p<0.0001; ASAT: ρ=0.61, p<0.0001; LF%: ρ=0.22, p=0.19). % body fat was similarly associated with lower ISI (ρ=0.63, p<0.0001) and higher InsIndex30 (ρ=0.59, p<0.0001). InsIndex30 associations did not persist after ISI adjustment (VAT: ρ=0.28, p=0.09; ASAT: ρ=0.22, p=0.195; LF%: ρ=0.12, p=0.48, % body fat ρ=0.18, p=0.29), indicating compensatory insulin secretion. Glycemia was largely preserved with no associations for fasting glucose, 2-hr glucose, or glucose AUC. Conclusion: In children before diabetes onset, greater total adiposity (including subcutaneous, visceral, and hepatic) is associated with reduced insulin sensitivity and compensatory increases in insulin secretion, while glycemia is largely maintained. At this pre-adolescent stage, total adiposity is an early contributor to the development of T2D.
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Morgan et al. (2026) conducted a cross-sectional in Adiposity and emerging diabetes risk (n=45). Visceral, subcutaneous, and hepatic adiposity was evaluated on Whole-body insulin sensitivity index (ISI) and insulinogenic index (InsIndex30) (Spearman ρ=-0.60 for VAT and ISI, p=<0.0001). Greater visceral and subcutaneous adiposity in children was associated with lower insulin sensitivity and compensatory insulin secretion.
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