Key result
Pancreatic and muscle fat show no independent link to insulin secretion after adjusting for hepatic fat.
Why the study?
The relationship between subclinical alterations in insulin secretion and sensitivity and intra-pancreatic and postural muscle fat, independent of hepatic fat, in individuals at high risk for type 2 diabetes required better understanding.
Does intra-pancreatic and postural muscle ectopic fat deposition correlate with subclinical alterations in insulin secretion, insulin sensitivity, and beta cell function in individuals at high risk for type 2 diabetes?
Cross-Sectional (n=80)
Single-blind
Yes
Does intra-pancreatic and postural muscle ectopic fat deposition correlate with subclinical alterations in insulin secretion, insulin sensitivity, and beta cell function in individuals at high risk for type 2 diabetes?
In individuals at high risk for type 2 diabetes, neither intra-pancreatic nor postural muscle fat was independently associated with insulin secretion or sensitivity after accounting for liver fat, highlighting hepatic steatosis as the primary driver of early metabolic dysfunction.
Hepatic fat may confound muscle fat associations with insulin dynamics; leaves open independent roles of pancreatic and muscle fat in type 2 diabetes risk.
Aims/hypothesis We investigated the association between multi-organ ectopic fat and glucose metabolism in individuals at high risk for type 2 diabetes. We aimed to better understand subclinical alterations in insulin secretion and sensitivity, and their relation to intra-pancreatic and postural muscle fat while adjusting for hepatic fat. Methods This cross-sectional study included 80 individuals with a BMI between 23 and 40 kg/m 2 and at least one metabolic alteration: increased fasting triglycerides or insulin, plasma glucose, HbA 1c and/or high waist circumference. Participants underwent abdominal MRI and a 3 h 75 g OGTT. Ectopic fat in the liver, pancreas and psoas and paraspinal muscles was quantified using mDIXON. Insulin sensitivity, insulin secretion and pancreatic beta cell function were determined with the oral minimal model. Results The median age of participants was 56 (IQR 39–64) years and 63% were women. Pancreatic fat fraction and paraspinal muscle fat fraction did not correlate with glucose metabolism indices. Psoas muscular fat fraction was negatively associated with static insulin secretion ( r = − 0.23, p = 0.04) and static disposition index ( r = − 0.23, p = 0.04) and positively associated with HOMA2-IR ( r = 0.25, p = 0.03), independent of age, sex and BMI. The associations did not remain significant when adding hepatic fat as a covariable. Conclusions/interpretation These results suggest that intra-pancreatic and postural muscle fat are not associated with insulin secretion and resistance in individuals at risk for type 2 diabetes. Liver fat could be a main contributor of early risk for type 2 diabetes development.
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Berteaux et al. (2026) conducted a cross-sectional in High risk for type 2 diabetes with mild metabolic alterations (n=80). Intra-pancreatic and postural muscle (psoas and paraspinal) ectopic fat fraction quantified by MRI was evaluated on Partial correlation between psoas muscular fat fraction and static insulin secretion, static disposition index, and HOMA2-IR (adjusted for age, sex, and BMI) (r = -0.23 (static insulin secretion and disposition index); r = 0.25 (HOMA2-IR), p=0.04). Intra-pancreatic and postural muscle fat fractions were not independently associated with insulin secretion or sensitivity after adjusting for hepatic fat in adults at risk for type 2 diabetes.
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