Wednesday June 19, 2019

Genes Tied to Obesity May Lower Risk of Diabetes

"Meanwhile, some lean or normal weight individuals develop diseases like Type-2 diabetes," Yaghootkar noted

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Diabetes
Representational image. Pixabay

Certain genetic factors may impact our body in intriguingly paradoxical ways. A team of scientists has identified 14 new genetic variations that were linked with higher Body Mass Index (BMI) but have the potential to lower risk of diabetes, lower blood pressure and lower heart disease risk.

According to researchers, it is because the location — around middle or round the liver — where surplus fat is stored could be genetically determined.

This location is more important than the amount when it comes to insulin resistance and risk of diabetes and other conditions.

“There are some genetic factors that increase obesity, but paradoxically reduce metabolic risk. It is to do with where on the body the fat is stored,” said Brunel Alex Blakemore, Professor at the Brunel University London.

The findings revealed that as they gain weight, people who carry these genetic factors store it safely under the skin, and so have less fat in their major organs such as the liver, pancreas and kidneys.

Diabetes
Representational image. Pixabay

“Directly under the skin is better than around the organs or especially, within the liver,” Blakemore added.

For the study, published in the journal Diabetes, the team examined more than 500,000 people aged between 37 and 73.

They used Magnetic Resonance Imaging (MRI) scans of these people’s waists to match where they stored extra fat with whether they showed signs of Type-2 diabetes, heart attack and risk of stroke.

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“There are many overweight or obese individuals who do not carry the expected metabolic disease risks associated with higher BMI,” explained Hanieh Yaghootkar from the University of Exeter in Britain.

“Meanwhile, some lean or normal weight individuals develop diseases like Type-2 diabetes,” Yaghootkar noted. (IANS)

Next Story

Researchers Find Drug to Delay Type-1 Diabetes by Two Years

The effects of the drug were greatest in the first year after it was given, said the study published online in The New England Journal of Medicine

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Diabetes
Representational image. Pixabay

In a first, researchers have found that a treatment affecting the immune system effectively slowed the progression to clinical Type-1 diabetes in high risk individuals by two years or more.

“The results have important implications for people, particularly youth, who have relatives with the disease, as these individuals may be at high risk and benefit from early screening and treatment,” said Lisa Spain, Project Scientist from US National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

The study, involving treatment with an anti-CD3 monoclonal antibody (teplizumab), was conducted by Type 1 Diabetes TrialNet, an international collaboration aimed at discovering ways to delay or prevent Type-1 diabetes.

Participants were randomly assigned to either the treatment group, which received a 14-day course of teplizumab, or the control group, which received a placebo.

All participants received glucose tolerance tests regularly until the study was completed, or until they developed clinical Type-1 diabetes – whichever came first.

During the trial, 72 per cent of the people in the control group developed clinical diabetes, compared to only 43 per cent of the teplizumab group.

diabetes
“Although Type-1 and Type-2 diabetes in parents are well-established risk factors for diabetes, we show that gestational diabetes mellitus may be a risk indicator for diabetes in the mother’s children before age 22,” . Pixabay

The median time for people in the control group to develop clinical diabetes was just over 24 months, while those who developed clinical diabetes in the treatment group had a median time of 48 months before progressing to diagnosis.

“The difference in outcomes was striking. This discovery is the first evidence we’ve seen that clinical Type-1 diabetes can be delayed with early preventive treatment,” Spain added.

Type-1 diabetes develops when the immune system’s T cells mistakenly destroy the body’s own insulin-producing beta cells.

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Insulin is needed to convert glucose into energy. Teplizumab targets T cells to lessen the destruction of beta cells.

The effects of the drug were greatest in the first year after it was given, said the study published online in The New England Journal of Medicine. (IANS)