Groundbreaking research unveils a crucial gene that regulates post-meal blood sugar levels, shining a new light on Type 2 diabetes mechanisms.

Scientists have made remarkable strides in understanding what exactly goes wrong when a person is diagnosed with Type 2 diabetes, unlocking possible treatment in the future.

The condition, affecting millions globally, is characterised by an individual’s struggle to regulate glucose levels due to insufficient insulin secretion or reduced insulin sensitivity, often referred to as insulin resistance.

In a radical departure from conventional research approaches, which generally focus on insulin resistance in the fasting state, a team from the University of Cambridge delved into the mechanisms that trigger insulin resistance post a meal or sugar intake— a key contributing factor to Type 2 diabetes.

The new insights, revealed after studying over 55,000 individuals worldwide, could unlock groundbreaking treatments for this widespread disease.

The findings of the study are published in the renowned journal, Nature Genetics.

Professor Sir Stephen O’Rahilly, the co-director of the Wellcome-MRC Institute of Metabolic Science, clarified the novelty of their research approach.

“We know there are some people with specific rare genetic disorders in whom insulin works completely normally in the fasting state, where it’s acting mostly on the liver, but very poorly after a meal, when it’s acting mostly on muscle and fat,” he said.

“What has not been clear is whether this sort of problem occurs more commonly in the wider population and whether it’s relevant to the risk of getting Type 2 diabetes.”

How can it help?

An international consortium of scientists aggregated genetic data from 28 studies, aiming to identify genetic variants that influence insulin levels after a glucose challenge.

They discovered 10 new loci (regions of the genome) associated with insulin resistance. Notably, eight of these regions were also tied to an elevated risk of Type 2 diabetes, underscoring their importance in disease development.

Within these genetic regions, the team pinpointed a gene associated with GLUT4, a vital protein that facilitates glucose transport from the bloodstream into cells after eating.

They found that reduced levels of GLUT4 in muscle tissues corresponded with this genetic variant.

Further investigations using cell lines from mice unveiled 14 genes crucial to GLUT4 trafficking and glucose uptake. Nine of these genes were previously unknown in the context of insulin regulation.

These genes were found to influence the movement of GLUT4 from the cell interior to its surface, thereby affecting the cell’s capacity to remove glucose from the blood.

These groundbreaking findings shine a new light on the intricacies of blood glucose regulation and potentially open the doors to innovative therapeutic strategies.

Early detection of post-meal glucose regulation issues can serve as a warning sign of increased Type 2 diabetes risk. By deciphering the basic mechanisms underlying common diseases like Type 2 diabetes, the research may guide the way towards precision healthcare and tailored treatments.