Diabetes, obesity & metabolism · 2026
Associations of Fasting Glucagon and the Glucagon-Alanine Index With Hepatic Steatosis and Liver Stiffness in Japanese Individuals With Type 2 Diabetes.
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Hattori Tomohiro, Hamaguchi Masahide, Hashimoto Yoshitaka, Kitagawa Noriyuki, Osaka Takafumi, Okada Hiroshi, Sasano Ryoichi, Kobayashi Masaki, Kitamura Tadahiro, Fukui Michiaki
Аннотация
BACKGROUND: In type 2 diabetes, impaired glucagon action in the liver (hepatic glucagon resistance) may disrupt the liver-α-cell axis. We examined the associations of fasting glucagon and a modified glucagon-alanine index (GAI) with imaging-derived hepatic steatosis and liver stiffness in Japanese individuals with type 2 diabetes.
METHODS: This was a cross-sectional analysis of baseline data from the KAMOGAWA-DM cohort. Among patients with type 2 diabetes with fasting glucagon measured, 46 participants were included after exclusions. Liver steatosis was assessed by abdominal ultrasonography using a liver steatosis score, and liver stiffness was quantified by shear-wave elastography (E-value, kPa). Fasting glucagon was measured using a Mercodia enzyme-linked immunosorbent assay (ELISA). The modified GAI was calculated as fasting glucagon (pmol/L) × alanine (arbitrary units) and log-transformed (Base = 10) for analyses. Group comparisons, correlation analyses, and exploratory receiver operating characteristic (ROC) analyses were performed.
RESULTS: Twenty-three participants had metabolic dysfunction-associated steatotic liver disease (MASLD) and 23 did not. Fasting glucagon levels and the GAI were significantly higher in MASLD group, whereas alanine alone did not differ significantly between groups. Log-transformed fasting glucagon and log-transformed GAI were positively correlated with the ultrasonographic liver steatosis score; log-transformed fasting glucagon was also positively correlated with liver stiffness. In exploratory ROC analyses, log-transformed fasting glucagon cutoff of 1.511 yielded 82.6% sensitivity and 65.2% specificity, and log-transformed GAI of 4.036 yielded 73.9% sensitivity and 81.8% specificity for discriminating MASLD.
CONCLUSIONS: In Japanese individuals with type 2 diabetes, higher fasting glucagon and a higher modified GAI were associated with greater imaging-derived liver steatosis. Higher fasting glucagon was also associated with greater liver stiffness. These cross-sectional findings are compatible with, but do not establish, hepatic glucagon resistance or disruption of the liver-α-cell axis.
METHODS: This was a cross-sectional analysis of baseline data from the KAMOGAWA-DM cohort. Among patients with type 2 diabetes with fasting glucagon measured, 46 participants were included after exclusions. Liver steatosis was assessed by abdominal ultrasonography using a liver steatosis score, and liver stiffness was quantified by shear-wave elastography (E-value, kPa). Fasting glucagon was measured using a Mercodia enzyme-linked immunosorbent assay (ELISA). The modified GAI was calculated as fasting glucagon (pmol/L) × alanine (arbitrary units) and log-transformed (Base = 10) for analyses. Group comparisons, correlation analyses, and exploratory receiver operating characteristic (ROC) analyses were performed.
RESULTS: Twenty-three participants had metabolic dysfunction-associated steatotic liver disease (MASLD) and 23 did not. Fasting glucagon levels and the GAI were significantly higher in MASLD group, whereas alanine alone did not differ significantly between groups. Log-transformed fasting glucagon and log-transformed GAI were positively correlated with the ultrasonographic liver steatosis score; log-transformed fasting glucagon was also positively correlated with liver stiffness. In exploratory ROC analyses, log-transformed fasting glucagon cutoff of 1.511 yielded 82.6% sensitivity and 65.2% specificity, and log-transformed GAI of 4.036 yielded 73.9% sensitivity and 81.8% specificity for discriminating MASLD.
CONCLUSIONS: In Japanese individuals with type 2 diabetes, higher fasting glucagon and a higher modified GAI were associated with greater imaging-derived liver steatosis. Higher fasting glucagon was also associated with greater liver stiffness. These cross-sectional findings are compatible with, but do not establish, hepatic glucagon resistance or disruption of the liver-α-cell axis.