Abstract
Hepatic encephalopathy is the main cognitive dysfunction in cirrhotic patients associated with impaired prognosis. Hyperammonemia plus inflammatory response do play a crucial role on hepatic encephalopathy. However, in some patients HE appeared without hyperammonemia and patients with increased levels of ammonia could not show cognitive dysfunction. This has led to investigate other factors that could act in a synergistic way. Diabetes mellitus and insulin resistance are characterized by releasing and enhancing these pro-inflammatory cytokines and, additionally, has been related to hepatic encephalopathy. Indeed, patients with diabetes showed raised risk of over hepatic encephalopathy in comparison with non-cirrhotics. Type 2 diabetes mellitus could impair hepatic encephalopathy by different mechanisms that include: a) increasing glutaminase activity; b) impairing gut motility and promoting constipation, intestinal bacterial overgrowth and bacterial translocation. Despite of insufficient clarity about the practicability of anti-diabetic therapy and the most efficacious therapy, we would have to pay a special attention to the management of type 2 diabetes mellitus and insulin resistance in cirrhotic patients.
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Abbreviations
- HE:
-
Hepatic encephalopathy
- DM:
-
Diabetes mellitus
- T2DM:
-
Type 2 diabetes mellitus
- HD:
-
Hepatogenous diabetes
- TNFα:
-
Tumor necrosis factor alpha
- IL-6:
-
Interleukin 6
- GLS:
-
Glutaminase
- KGLS:
-
Kidney-type glutaminase
- LGLS:
-
Liver-type glutaminase
- BBB:
-
Blood brain barrier
- IR:
-
Insulin resistance
- SIBO:
-
Small intestine bacterial overgrowth
- MHE:
-
Minimal hepatic encephalopathy
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Ampuero, J., Ranchal, I., del Mar Díaz-Herrero, M. et al. Role of diabetes mellitus on hepatic encephalopathy. Metab Brain Dis 28, 277–279 (2013). https://doi.org/10.1007/s11011-012-9354-2
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DOI: https://doi.org/10.1007/s11011-012-9354-2