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Abstract
Background
Coffee consumption has been associated with reduced risk of developing type 2 diabetes mellitus (T2DM) however, the mechanism for this association has yet to be elucidated. Non-alcoholic fatty liver disease (NAFLD) characterizes and predicts T2DM yet the relationship of coffee with this disorder remains unclear. Our aim was to investigate the associations of coffee with markers of liver injury in 1005 multi-ethnic, non-diabetic adults in the Insulin Resistance Atherosclerosis Study.
Methods
Dietary intake was assessed using a validated 114-item food frequency questionnaire. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and fetuin-A were determined in fasting blood samples and the validated NAFLD liver fat score was calculated. Multivariate linear regression assessed the contribution of coffee to variation in markers of liver injury.
Results
Caffeinated coffee showed significant inverse associations with ALT (β = −0.08, p = 0.0111), AST (β = −0.05, p = 0.0155) and NAFLD liver fat score (β = −0.05, p = 0.0293) but not with fetuin-A (β = 0.04, p = 0.17). When the highest alcohol consumers were excluded, these associations remained (ALT β = −0.11, p = 0.0037; AST β = −0.05, p = 0.0330; NAFLD liver fat score β = −0.06, p = 0.0298). With additional adjustment for insulin sensitivity, the relationship with ALT remained significant (ALT β = −0.08, p = 0.0400; AST β = −0.03, p = 0.20; NAFLD liver fat score β = −0.03, p = 0.27). There were no significant associations of decaffeinated coffee with liver markers.
Conclusions
These analyses indicate a beneficial impact of caffeinated coffee on liver morphology and/or function, and suggest that this relationship may mediate the well-established inverse association of coffee with risk of T2DM.
Full text here: http://www.biomedcentral.com/1471-230X/15/88#
Background
Coffee consumption has been associated with reduced risk of developing type 2 diabetes mellitus (T2DM) however, the mechanism for this association has yet to be elucidated. Non-alcoholic fatty liver disease (NAFLD) characterizes and predicts T2DM yet the relationship of coffee with this disorder remains unclear. Our aim was to investigate the associations of coffee with markers of liver injury in 1005 multi-ethnic, non-diabetic adults in the Insulin Resistance Atherosclerosis Study.
Methods
Dietary intake was assessed using a validated 114-item food frequency questionnaire. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and fetuin-A were determined in fasting blood samples and the validated NAFLD liver fat score was calculated. Multivariate linear regression assessed the contribution of coffee to variation in markers of liver injury.
Results
Caffeinated coffee showed significant inverse associations with ALT (β = −0.08, p = 0.0111), AST (β = −0.05, p = 0.0155) and NAFLD liver fat score (β = −0.05, p = 0.0293) but not with fetuin-A (β = 0.04, p = 0.17). When the highest alcohol consumers were excluded, these associations remained (ALT β = −0.11, p = 0.0037; AST β = −0.05, p = 0.0330; NAFLD liver fat score β = −0.06, p = 0.0298). With additional adjustment for insulin sensitivity, the relationship with ALT remained significant (ALT β = −0.08, p = 0.0400; AST β = −0.03, p = 0.20; NAFLD liver fat score β = −0.03, p = 0.27). There were no significant associations of decaffeinated coffee with liver markers.
Conclusions
These analyses indicate a beneficial impact of caffeinated coffee on liver morphology and/or function, and suggest that this relationship may mediate the well-established inverse association of coffee with risk of T2DM.
Full text here: http://www.biomedcentral.com/1471-230X/15/88#
