By: Jamie Morton

Genetic changes hidden among our so-called junk DNA have helped New Zealand scientists uncover a suspected missing link between type 2 diabetes and obesity. Photo / File

Genetic changes hidden among our so-called junk DNA have helped New Zealand scientists uncover a suspected missing link between type 2 diabetes and obesity.

Nearly a third of Kiwis live with obesity, which is considered a major risk factor for type 2 diabetes and other disorders.

The fact obesity and diabetes so often affect the same people has led scientists to suspect that similar genes are contributing to the development of the disorders, which are both on the rise in populations around the world.

Untangling the genetic links has been a challenge for scientists, but a just-published study by Kiwi researchers has revealed how certain genetic changes found in regions of DNA that are non-coding and associated with the disorders can act together to alter how genes behave.

Techniques developed in the new study could provide medical researchers with new information and a fresh way to attack the puzzle, which may lead to better treatment, or even prevention, of the disorders.

The study, led by Dr Justin O’Sullivan, a molecular biologist at the University of Auckland’s Liggins Institute, focused on regions of DNA that commonly vary between individuals and that have been linked to a disease.

Called single nucleotide polymorphisms, or SNPs, some of these fall inside genes, but most fall outside them, in segments once believed to be little more than inactive spacers between genes.

It was believed SNPs outside genes were brought into contact with, and influenced the working of, far-off genes through the way DNA was tightly coiled inside the cell nucleus.

DNA, the long molecules inside our cells containing our entire genetic blueprint, are around 2m long, but packed into a cell nucleus only 10 micrometres across – equivalent to a 100th of a millimetre.

“SNPs offer a key to unlock the riddles of many diseases and disorders that can be passed from parent to child, but do not seem to pass directly through the genes,” O’Sullivan said.

SNPs that predisposed people to obesity were different from the ones linked to diabetes.

But using their new technique, the Auckland team revealed for the first time there were many instances where a SNP for obesity and a SNP for diabetes were both in contact with, and changed the functioning of, the same gene.

“We can’t tell from this study if the SNPs themselves are causing the disorders through changing the way the genes work, or if it is something nearby on that same DNA segment,” said study co-author and Liggins PhD student Tayaza Fadason.

“But it is clear that these SNPs we have identified are markers of DNA segments that are somehow altering the functioning of the genes they come into contact with.”

O’Sullivan pointed out another remarkable finding of the study, just published in the international journal Frontiers in Genetics.

“Many of the regulatory SNP-gene connections we pinpointed affect body tissues not usually thought of as driving obesity or type-2 diabetes – breast tissue, brain tissue from the cerebellum, skin and blood, the fat that sits just beneath the skin.

“On the other hand, while visceral fat has a big contribution to diabetes, we found few SNP-gene connections in that tissue.”

This suggested researchers may need to broaden their hunt for genetic drivers of obesity and diabetes beyond “the usual suspects”, he said.

It also lent weight to a new way of thinking, now gaining traction among geneticists, which recognised there was more to genetics than the sequence of genes.

“We also need to understand the other forms of information in DNA – including how it’s folded – that affect how genes are read and used.”

The research team also included Cameron Ekblad and William Schierding from the Liggins Institute, and John Ingram from the New Zealand Institute of Plant and Food Research.

The team is currently looking at SNP-gene connections’ role in type-1 diabetes, muscle wasting and the relationships between other medical disorders.

Diabetes campaign kicks off

The study comes as Diabetes NZ this week launches its Diabetes Action Month.

Almost a quarter of a million New Zealanders have been diagnosed with diabetes, while another 100,000 are estimated to have the disease without knowing it.

The November-long awareness campaign features a range of national campaigns and regional events highlighting the differences between type 1 and 2 diabetes, what symptoms to look out for, and what to do if you or someone close to you shows the symptoms.

While type 2 diabetes is affected by lifestyle and is mostly diagnosed later in life, type 1 was an autoimmune disease mostly diagnosed in childhood.

About 10 per cent of people with diabetes had type 1, with more than 20,000 in New Zealand, including 2500 children under 18.

Diabetes NZ will also start distributing an educational toy called Jerry the Bear – including features that enable augmented-reality play with a smartphone app – to children between 4 and 10 who were newly diagnosed with type 1 diabetes.

Multisport athlete and type 1 diabetic Emily Wilson will be taking Jerry on a tour across the country, travelling by bike, kayak, raft, by foot and swimming.

People will further be able to download a new free app allowing access to Diabetes NZ’s Take Control Toolkit, which has 60 resources to help people manage their health, even if they don’t have diabetes.

Source: NZ Herald

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