Big breakthrough: Genetic link between obesity-diabetes

Auckland researchers have a made a ‘‘major leap’’ in understanding why obesity and type 2 diabetes often go hand-in-hand.

Scientists from University of Auckland’s Liggins Institute have found DNA markers linked to diabetes and obesity can act together to alter how other genes behave.

The study, published in international journal Frontiers in Genetics, could answer why some people develop type 2 diabetes and others don’t, study lead and molecular biologist Dr Justin O’Sullivan said.

More than 260,000 New Zealanders live with type 2 diabetes, where the body does not produce enough insulin, or the cells in the body do not recognise insulin is present, leading to high levels of glucose in the blood.

The 2015/2016 New Zealand Health Survey found that almost one in three adults were obese (32 per cent), and a further 35 per cent of adults were overweight.

The fact that obesity and diabetes so often affect the same people suggests similar genes are contributing

‘‘If you can put people into groups you can understand how the treatments affect them and what these genetic features are, then you can move towards a much more precise way of dealing with people: Preventing these disorders and treating people.’’ Dr Justin O’Sullivan

to the development of both the disorders, O’Sullivan said.

But until now, scientists have struggled to ‘‘untangle’’ the link between the two.

‘‘The techniques we developed in this study provide medical researchers with new information and a different viewpoint from which to look at the genetics behind obesity and diabetes, which could ultimately help us better treat and even prevent them,’’ O’Sullivan said. Some people become obese and don’t become diabetic and some are thin but do develop diabetes, he said, so the question is, why some people and not others? The researchers identified SNP – pronounced ‘‘snips’’ – single nucleotide polymorphisms, change the activity of faroff genes they come into contact with. SNPs that predispose people to obesity are different from the ones linked to

diabetes. But the team found for the first time that there are many instances where a SNP for obesity and a SNP for diabetes are both in contact with, and change the functioning of, the same gene.

‘‘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.

O’Sullivan said the study was significant in increasing awareness of why some people respond to particular treatments and others don’t.

‘‘If you can put people into groups you can understand how the treatments affect them and what these genetic features are, then you can move towards a much more precise way of dealing with people: Preventing these disorders and treating people.’’

The study shows researchers need to broaden their hunt for genetic drivers of obesity and diabetes beyond the usual suspects, he said.

Also involved in the study were Tayaza Fadason, Cameron Ekblad and William Schierding from the Liggins Institute, and John Ingram from The New Zealand Institute of Plant and Food Research.

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