Thaindian News

Washington, Mar 9 (ANI): While metabolic syndrome is apparently related to obesity, researchers have said that the link is not just negative.

Metabolic syndrome is characterised by-insulin resistance, high cholesterol, fatty liver, and a greater risk for diabetes, heart disease, and stroke- all of which are related to obesity.

But, Roger Unger of the University of Texas Southwestern at Dallas, said that obesity is the body’s way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids’ toxic effects.

It is when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn’t be, and the cascade of symptoms known as metabolic syndrome sets in.

It is known that Americans since the 1950s eat too much high-calorie food loaded with carbs and fat (what Unger calls “potent adipogenic nutrient mixtures”) and, thanks to modern technology, we move far too little.

Unger said that until that changes, he doesn’t see any end to the growing epidemic of metabolic syndrome.

“We are pushing our homeostatic capability to the maximum. Overnutrition used to be rare-reserved for those in the castle. Today, it’s just the opposite. Bad calories are so cheap that anyone can afford to get overweight,” said Unger.

Unger cites plenty of evidence in support of a protective role for obesity- genetic manipulations in mice that increase or decrease fat formation have provided evidence that adipogenesis, meaning the generation of fat cells, delays other metabolic consequences of overeating.

He wrote that the reverse is also true-obesity-resistant mice have in some cases been found to develop severe diabetes upon eating too much, as a result of lipid accumulation in tissues other than fat.

Unger noted that there is some disagreement about whether insulin resistance is a primary cause of metabolic syndrome or just one of its features.

But he said that insulin resistance is not the cause of metabolic syndrome, it is a “passive byproduct” of fat deposition in the liver and muscle once storage in fat cells begins to fail.

He also claimed that cells that have already taken on too much fat would begin to exclude glucose, causing its levels in blood and urine to rise.

Once in cells, glucose becomes a substrate for the production of more fat.

“The body is doing what we should have done-keep excess calories out-and it may be protective,” said Unger.

The study has been published in the latest issue of the Cell Press publication Trends in Endocrinology and Metabolism. (ANI)