Associations of MRI-derived adrenal lipid content with hepatic and pancreatic steatosis and insulin resistance

Abstract

Aim: Adrenal adenomas are frequent incidental findings, and even non-functioning adrenal adenomas (NFAAs) may be linked to subtle metabolic alterations. According to the lipid overflow hypothesis, excess lipids accumulate in non-adipose organs, such as the liver, pancreas, and adrenal glands, potentially reflecting systemic metabolic stress. This study aimed to investigate the association between MRI-derived adrenal lipid indices and hepatic and pancreatic fat and to assess their correlation with the triglyceride-glucose (TyG) index as a marker of insulin resistance.

Materials and Methods: This retrospective study included 201 patients with lipid-rich adrenal adenomas [Adrenal Signal Intensity Index (ASII) ≥ 20%] identified on 1.5T MRI. Signal intensities were measured in adrenal lesions, liver, pancreas, and spleen using dual-echo sequences. ASII and adrenal-to-spleen chemical-shift imaging (CSI) ratios were calculated. Hepatic and pancreatic fat fractions were derived from signal intensity differences. The TyG index was computed from fasting triglyceride and glucose levels. Correlation and multivariable regression analyses were performed.

Results: Adrenal lipid indices showed significant correlations with hepatic (r = 0.32 and –0.30) and pancreatic fat fractions (r = 0.19 and –0.18) (p<0.01). These associations remained significant after adjustment for age and sex. However, no meaningful correlation was found between adrenal lipid indices and the TyG index; regression models explained only a minimal amount of the variation in TyG values (R² = 0.025).

Conclusion: MRI-derived adrenal lipid indices are associated with ectopic fat accumulation in the liver and pancreas but do not reflect systemic insulin resistance. These findings suggest that adrenal lipid content may serve as a marker of regional fat redistribution rather than global metabolic dysfunction.