Serum alanine transaminase is predictive of fasting and postprandial insulin and glucagon concentrations in type 2 diabetes.

The liver plays a key role in glucose homeostasis. Serum liver enzyme levels, including alanine transaminase (ALT), aspartate transaminase (AST) and gamma-glutamyl transferase (GGT), are reportedly predictive of the risk of type 2 diabetes (T2D). However, the link between the liver enzyme profile and metabolic derangements in T2D, particularly the secretion of both insulin and glucagon, is not clear. This study evaluated its relationships with glycemia, insulin and glucagon both during fasting and after an oral glucose load or a mixed meal in T2D. 15 healthy and 43 T2D subjects ingested a 75 g glucose drink. 86 T2D subjects consumed a mixed meal. Venous blood was sampled for measurements of blood glucose and plasma insulin, C-peptide and glucagon. Blood glucose, plasma insulin, C-peptide and glucagon concentrations, both fasting and after oral glucose, correlated directly with ALT, while fewer and weaker correlations were observed with GGT or AST. Subgroup analysis in T2D subjects ascertained that plasma insulin, C-peptide and glucagon concentrations after oral glucose were higher with increasing ALT. Similar findings were observed in the T2D subjects who received a mixed meal. In conclusion, serum liver enzyme profile, particularly ALT, reflects dysregulated fasting and nutrient-stimulated plasma insulin and glucagon concentrations in T2D.

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Déclaration de conflit d'intérêts

Conflict of Interest NJWA has received speaker fees from Mercodia and MSD, and research support from Mercodia and Novo Nordisk, and acts on advisory boards on Boehringer Ingelheim. KLJ has received research funding from Sanofi Aventis and AstraZeneca and is a share-holder for Glyscend. MH has participated in the advisory boards and/or symposia for Novo Nordisk, Sanofi, Novartis, Eli Lilly, Merck Sharp & Dohme, Boehringer Ingelheim, Inova and AstraZeneca and has received honoraria for this activity, and is a share-holder for both Satiogen and Glyscend. CKR has received research funding from AstraZeneca, Merck Sharp & Dohme, Eli Lilly, Novartis, and Sanofi, and is a share-holder for both Satiogen and Glyscend. TW has received travel support from Novartis and Sanofi and research funding from Novartis and AstraZeneca. None of the other authors has any personal or financial conflict of interest to declare.