Fat enzyme breakthrough kept mouse thin on 'pizza and burgers diet'

Photo / Getty Images

An obesity breakthrough appears to have been made by Danish researchers who say they've found a way to keep weight off while eating a "pizza and burgers diet".

Pizza chips and burgers can be consumed without gaining weight if a certain enzyme is reduced, new research has discovered.

Copenhagen University scientists claim eliminating the NAMPT enzyme — at least in mice — made it impossible for the rodents to gain weight, reports news.com.au.

They tested mice with the deleted NAMPT enzyme along control mice, who became obese on the same 12 week diet which "more or less" matches eating pizza and burgers.

The slim mice had their NAMPT — short for nicotinamide phosphoribosyltransferase — enzyme removed from their fat cells.

The trial of mice by the Danish researchers revealed for the first time that NAMPT deficiency in fat cells is a protector against diet-induced obesity.

The premise of the study by the University's Faculty of Health and Medical Sciences was that human bodies are extremely efficient at storing fat from food into our fat tissue.

A report of the study in Science Daily said that large amounts of NAMPT had been found in the blood and stomach fat tissue of overweight or obese people.

"However, this study provides the first evidence that NAMPT is absolutely required to become overweight or obese and that lack of NAMPT in fat tissue fully protects against obesity.." Science Daily wrote.

The research team led by Karen Nørgaard Nielsen, of the Novo Nordisk Foundation Center for Basic Metabolic Research genetically deleted NAMPT from the test mice.

Fat-specific NAMPT knockout (FANKO) mice were completely resistant to high fat diet-induced obesity, even on the very fatty diet which made the control mice obese.

"We gave the mice a diet that more or less corresponds to continuously eating burgers and pizza," Ms Nielsen said.

"Still, it was impossible for them to expand their fat tissue.

"Our ultimate goal is that by understanding these fundamental underpinnings of how we become obese, we can apply our finding to the development of novel treatment strategies for metabolic disease."

Ms Nielsens's team also trialled both sets of mice on a healthier, lower-fat diet, which resulted in no weight gain after 12 weeks.

It was after they were switched to the high fat diet that the "normal" unmodified mice became very obese.

In addition, the mice with the genetically deleted NAMPT maintained better control of blood glucose than normal mice when eating high-fat food.

Insulin is the hormone which helps humans control blood glucose and it is a lack of insulin that signifies diabetes.

Prior to the new study, the presence of NAMPT was regarded as beneficial for such things as liver and skeletal muscle and critical for fat tissue function, but principally for storing fat.

"NAMPT in fat tissue was likely once an extraordinary benefit to our ancestors," said Ms Nielsen's co-author of the study, Novo Nordisk Associate Professor Zachary Gerhart-Hines.

"But in today's society full of high-fat, calorically-dense foods, it may now pose a liability."

Professor Gerhart-Hines said, however, that genetically diminishing NAMPT in humans risked harmful consequences in other human body tissues.

He hoped further research might eventually reveal how NAMPT is biologically linked to fat gain, and that could be targeted.