Does consuming high-sucuble carbohydrates help protect the brain in times of acute stress?

Chronic low glucose in the blood can in extreme cases even lead to fatty liver disease and peripheral neuropathy but the mechanisms that cause this are currently unknown. When cognitive function is affected this type of liver injury is thought to be triggered by inflammation (pathological changes to the connective tissues) and also from the release of toxins (exogenous or endogenous) from damage to the brain.

In a recently published article in PNAS researchers of the Department of Neurology Pharmacology and Neurosurgery of MedUni Viennas Center for Neurodegenerative Diseases have analyzed data from chronic low-grade gliomas (CLGs) in animal models and have now reported novel insights. They were surprised that an inflammatory process apparently plays an important role in the development of the liver damage.

Latently metastatic gliomas (or almost exclusively lymphomas) are most common tumors in adults. They are characterized by a very low number of cells and a very high tumor-forming ability which is regulated by the tumor suppressor gene TREM2. It is known that these tumors are frequently treated with the antiproliferative drug gemcitabine.

The study was led by Dr. Christian Hoffmann and involves the transient use of gemcitabine in animal models with CRLG. In the latter stage several FK506 inhibitors (possible combinations) have been combined. This has led to permanent reduction in tumor size and consolidation of the tumors in the background. The only cause for concern for doctors has been the discovery of hematological malignancies which resulted from an unusual number of therapy failures. As a result this group of patients is considered highly resistant to gemcitabine treatment.

Within the context of the current study which was recently published in the prestigious German magazine Cell Reports the authors conclude that patients with the basal-like CRLG have a dramatic increase in the tumor growth potential after treatment with gemcitabine. They go on to prove that amyloid-beta deposition in patients with this type of CRLG is also a significant prognostic factor in the post-translational development of liver diseases.

These findings offer a new natural approach for the management of CLGs. The authors hope that the studies on human troughs will be leveraged as a basis for developing specific therapies against CRLG or other patients. These data will also play an important role in the development of novel therapies against excess inflammation and the proliferation of pathological cells in the liver.

Findings.

The authors identified two types of patients who were resistant to gemcitabine treatment and who did not respond to any other anti-inflammatory or immuno-suppressive medicines. These patients had aberrant deposits of hematopoietic progenitors in the small intestine which react abnormally to immunosuppressive drugs and lead to chronic inflammation. Three of these patients eventually developed hepatocellular carcinoma an aggressive type of liver cancer.


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