Fetuin-A is a gycoprotein secreted by the liver and released in high concentrations. It plays a role as a physiological inhibitor of insulin receptor tyrosine kinase associated with insulin resistance. It has been associated with metabolic syndrome and atherosclerosis . Many authors suggest that fetuin-A may be an independent risk factor for type 2 diabetes and marker of diabetes complications.
Nevertheless the value of fetuin-A as an independent predictor of diabetes in chronic liver diseases has not been evaluated. Is it possible that fetuin-A is involved in genesis of diabetes and induction of bad outcome in patients with liver cirrhosis?
Yes, this may happen if patients with metabolic syndrome and hepatic steatosis time and poor control of their metabolism, reaching developing DM2, and simultaneously continue to hepatic steatosis hepatitis and eventually cirrhosis without intervention another etiologic agent as would be the case in other patients who have concomitant chronic active viral hepatitis (B or C) or liver damage by alcohol.
Yes, this may happen if patients with metabolic syndrome and hepatic steatosis time and poor control of their metabolism, reaching developing DM2, and simultaneously continue to hepatic steatosis hepatitis and eventually cirrhosis without intervention another etiologic agent as would be the case in other patients who have concomitant chronic active viral hepatitis (B or C) or liver damage by alcohol.
Dear Professor,
This is an important topic as it will have impact on investigation and management of diabetes mellitus (DM) in the future. One of your publications in 2009 advocated a new paradigm called "hepatogenous diabetes" as there are interrelations between liver and pathogenesis of DM. On the other hand, I have read a medical case in New England Journal of Medicine about glycogenic hepatopathy which illustrates the interrelations between complication of DM on the liver. These evidences may trigger more research about interrelations of DM and liver.
I would like to follow and participate in this discussion. Thank you.
According to the etiopathogenic relationship between obesity, metabolic syndrome, type 2 diabetes and liver disease (steatosis to cirrhosis) by the mechanisms described above, or others to be discovered.
It is an exciting field and open to current research
The author of the question that animates this discussion, it has published about it.
Dear Drs and collegues Cheong Wong and Garcia Vigil
Thanks for your comments. As you have pointed out, the association Diabetes- Cirrhosis is more complex than it was thought. There are still many lines of research for completely understand the nature of this association. Nevertheless, in the last ten years we have made some progress. Currently it is known that DM may produce liver disease and that DM may be a complication of liver cirrhosis. Pathophysiology of liver cirrhosis induced by DM is partially understood and at the same time there are some observations regarding the mechanism of diabetes after liver cirrhosis. In the near future I am sure that some concepts regarding the association DM-Liver cirrhosis will change:
1.- Hepatogenous diabetes will be recognized as a different entity. ( Up to date it is not accepted)
2.- Hepatogenous diabetes will be recognized as a complication of liver cirrhosis in the same way as hepatic encephalopathy, ascites, portal hypertension , etc
3.- DM will be widely accepted as adverse predictor of chronic liver disease. Induce complications and reduce surevival
4.- Therapeutic guidelines of DM in liver cirrhosis will be published. Incretin based therapies will be largely studied in this context. (In fact this year appeared the first publication (1))
5.- DM will be taken into account in HCV infected patients for prognosis and prediction of response to treatment with old and new antivirals.( The first publication with new oral antivirals will appear soon in J Clin Gastoenterol 2016)
6.- DM will be taken into account in patients waiting to be transplanted
And finally more biological markers for predicting expression of DM will be studied such as fetuin-A protein, in order to monitor patients.
I recommend you to read our last review appeared one month ago.(2)
It was the reason of my question
Best regards
1.- Hamed AE et al. J Endocrinol Diabetes Obes 2015;3:1073
2.- Garcia-Compean D . Dig Dis Sci 2015 (In press) [PMID: 26462490 DOI 10.1007/s10620-015-3907-2]
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