How Signaling Between Alpha and Beta Cells May Help In Treating Diabetes

With new technology and research, many diseases of the past are no longer common or a global threat today. For instance,  tuberculosis and leprosy cases are extremely rare. Even if there is a diagnosis of either of the two, the treatment is easily available.

However, despite such advancements, some conditions are particularly hard to control even today. New global health challenges are present now, replacing the old ones. Many of these are due to the nature of the lifestyles today which is characterized by sedentary routines and stress.

These conditions are also among the top killers worldwide. For example, diabetes is one of the most common health issues in the world now. Experts have cited it as a global pandemic. No matter how much awareness there is regarding health today, the number of diabetes diagnosis seems to go up.

Consequently, there is now a lot of research on the problem of diabetes and its potential treatments. There have been various suggestions for the treatment of both diabetes type 1 and type 2 and the prevention of the latter as well.

Though both of the types have their variations, it is the insulin-producing cells in the pancreas that are affected. New research on this subject takes a different path and shows another way of treatment – to boost the body so it can heal itself and get rid of diabetes.

What Does the Research Highlight?

Regulation of blood-sugar levels and production of insulin are the main functions of the pancreas. In order to perform these, three types of cells in the organ actively work.

These are called alpha cells, which make glucagon, beta cells, that make insulin for regulation of the glucagon, and the delta cells that produce a hormone called somatostatin which looks over the activity of the other two cells.

Malfunctioning in beta-cell activity is present in both type 1 and type 2 diabetes. The new research focuses on this part and suggests the boosting the cells may push the body to adjust and start producing the required amount of insulin again.

The study was conducted by researchers from the University of Bergen in Norway and its findings are published in the journal Nature Cell Biology.

Read the findings of the study here. 

One of the authors of the study  Luiza Ghila from the Raeder Research Lab in the Department of Clinical Science at the University of Bergen comments:

“We are possibly facing the start of a totally new form of treatment for diabetes, where the body can produce its own insulin, with some start-up help”

How Can the Body Heal Itself?

According to research, every type of cell present in the body carries a function. But the function and the identity of the cell is not always fixed. Some of the mature cells are also able to change and learn functions of other cells in accordance with the need.

This can happen in a number of situations. For example, in case of an injury where other type of cells are required in a higher number. In a mouse-model, the researchers in this research, looked at a similar phenomena in alpha and beta cells.

It was noted that alpha cells are affected by signals from beta cells especially when they are injured. In fact, many of the alpha cells transform and adapt to replace damaged beta cells.

Thus, the signaling between these two types of cells can be impacted using a compound in order to maximize the number of beta cells by 5%. This can be the first step towards adapting an approach to use the body’s own capabilities to fight diabetes.

The researchers state that these findings are particularly important and hint that further investigation is required in this field for new treatment. They add that developments in such as treatment can also ensure cures for other conditions such as Alzheimer’s disease.


Areeba Hussain

Areeba is an independent medical and healthcare writer. For the last three years, she is writing for Tophealthjournal. Her prime areas of interest are diseases, medicine, treatments, and alternative therapies. Twitter @Areeba94789300

Leave a Reply

Your email address will not be published. Required fields are marked *


Adblock Detected

Please consider supporting us by disabling your ad blocker