Researchers set to investigate new diabetes treatments tumbled on new findings indicating excess production of neurotransmitters in the human liver could play a key role in the onset of insulin resistance in Type-II diabetes. The recent findings shine a light on novel preventive treatments for diabetes.

Type-II Diabetes Explained

Type-II Diabetes
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According to the US National Library of Medicine, Type-II diabetes is categorized as a lifelong chronic disease where a person struggles with high levels of glucose in the blood and is the most common form of diabetes.

Insulin is a hormone produced by beta cells, specialized pancreas cells. The pancreas, located behind the stomach provides the insulin that the body needs to move sugar in the blood into cells later stored as energy.

A patient with Type-II diabetes has muscle, liver, and fat cells that do not respond efficiently to insulin. As a result, blood sugar does not get into cells to be stored as energy. When sugar is unable to penetrate cells, a high level of sugar builds up in the patient's blood.

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Livers Key Role in Diabetes-II

The link between diabetes and fat in the liver has long been known to researchers, the mystery lies in how the liver plays a key role in insulin sensitivity. The new study published in the journal Cell Reports, entitled "Hepatocyte membrane potential regulates serum insulin and insulin sensitivity by altering hepatic GABA release" focuses on Gamma-aminobutyric acids that are known to inhibit central nervous system neurotransmitters.

High production of GABA decreases nerve activity, a mechanism that researchers hypothesize as to the liver's influence on blood sugar levels.

Benjamin Renquist, lead author from the School of Animal and Comparative Biomedical Sciences, University of Arizona explains that when the human liver produces GABA, it decreases the activity of liver nerves that run to the brain. Hence, fatty liver, linked closely to type-II diabetes, by producing GABA decreases the firing of brain activity. The decrease is sensed by the central nervous system that changes outgoing signals affecting glucose homeostasis.

GABA production in the body's liver is overseen by enzymes known as GABA transaminase. Researchers blocked the production of enzymes in type-II diabetic animal models to test out the mechanism's role in insulin resistance.

Researchers note that the inhibition of excess GABA production in the liver restores insulin sensitivity in the models within days. Long-term inhibition of GABA-transaminase resulted in a decrease in food intake and weight loss.

To confirm the novel findings in humans, the team looked at GABA-related gene activity in patients diagnosed with type-II diabetes. A link was detected between insulin resistance and increased expression of the gene in the patient's liver known to play a key role in GABA production.

GABA transaminase inhibitors are already existent in the market, despite primarily being designed as anti-convulsant medication. Clinical trials are now underway to further investigate whether one of the already approved GABA transaminase inhibitors could improve insulin sensitivity in obese patients.

Renquist explain that the trials are more about investigating the role the enzyme plays in particular pathways in Type-II diabetes instead of improving pre-existing drugs New Atlas reports.



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