Hyperglucagonemia in patients with transjugular intrahepatic portosystemic stent-shunts (TIPS)

Roggenbuck, Dirk; Rossbach, C; Buchwald, A.; Scholz, K. H.; Ramadori, Giuliano; Nolte, W.

doi:10.1055/s-2004-819117

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here, steatosis might-through hepatic glucagon resistance along with impaired hepatocyte function-lead to the disruption of the liver alpha cell axis, a direct feedback mechanism between hepatic amino acid metabolism and pancreatic glucagon secretion. The finding of hyperglucagonemia in patients with cirrhosis has been described in several studies (Junker et al, 2015;Raddatz et al, 2004;Yoshida et al, 1998) and proposed to be related to glucagon receptor signaling in the liver (Dean et al, 2017;Longuet et al, 2013). Secondly, we found an exaggerated postprandial metabolic response after the meal intervention in both patients with NAFLD and cirrhosis.…”

Section: Healthysupporting

confidence: 83%

Postprandial dysfunction in fatty liver disease

Grandt

Jensen

Werge

et al. 2023

Physiological Reports

View full text Add to dashboard Cite

Fatty liver disease has mainly been characterized under fasting conditions. However, as the liver is essential for postprandial homeostasis, identifying postprandial disturbances may be important. Here, we investigated postprandial changes in markers of metabolic dysfunction between healthy individuals, obese individuals with non‐alcoholic fatty liver disease (NAFLD) and patients with cirrhosis. We included individuals with biopsy‐proven NAFLD (n = 9, mean age 50 years, mean BMI 35 kg/m2, no/mild fibrosis), cirrhosis with hepatic steatosis (n = 10, age 62 years, BMI 32 kg/m2, CHILD A/B) and healthy controls (n = 10, age 23, BMI 25 kg/m2), randomized 1:1 to fasting or standardized mixed meal test (postprandial). None of the patients randomized to mixed meal test had type 2 diabetes (T2D). Peripheral blood was collected for 120 min. After 60 min, a transjugular liver biopsy and liver vein blood was taken. Plasma levels of glucose, insulin, C‐peptide, glucagon, and fibroblast growth factor 21 (FGF21) were measured. Postprandial peak glucose and C‐peptide were significantly increased in NAFLD, and cirrhosis compared with healthy. Patients with NAFLD and cirrhosis had hyperglucagonemia as a potential sign of glucagon resistance. FGF21 was increased in NAFLD and cirrhosis independent of sampling from the liver vein versus peripheral blood. Glucagon levels were higher in the liver vein compared with peripheral blood. Patients with NAFLD and cirrhosis without T2D showed impaired glucose tolerance, hyperinsulinemia, and hyperglucagonemia after a meal compared to healthy individual. Postprandial characterization of patients with NAFLD may be important to capture their metabolic health.

show abstract