Diabetes and obesity in young people is now linked to how muscles handle a high-fat diet. Watch to find out more on this week’s Weight Loss Surgery News. Read the full story

Corn Syrup: Safe or Scary?

High fructose corn syrup, or HFCS – a mixture of glucose and fructose – is in almost everything that we eat, from soda to salad dressing. Many people say it’s harmless, just another form of sugar. Others, however, claim that HFCS in food products may contribute to the development of diabetes. Some conspiracy theorists even posit that high fructose corn syrup is being deliberately pushed on the American people to keep them hooked on sweet treats.

But is it true? Not according to a supplement to appear in the June issue of the Journal of Nutrition, which cites the results of a scientific summary published by a joint conference held in March 2008 by the International Life Sciences Institute of North America and the U.S. Department of Agriculture.

The report says it’s time critics of HFCS quit singling out high fructose corn syrup as the bad guy of the American diet and the cause of our nation’s obesity epidemic.

Critics claim that high fructose corn syrup and plain old sugar – sucrose – affect satiety, energy use and insulin levels. Scientists who attended the conference disagree, saying that little evidence exists to back such claims. Sugar is sugar is the message of the ILSI researchers, adding that high fructose corn syrup is no more likely to affect obesity than is table sugar, honey or sugar in any other form.

While this research finding would seem to put the controversy over the health effects of HFCS to rest, it’s important to note that the author and publisher of the report, the International Life Sciences Institute is a Washington, D.C.-based “educational and research organization” that is funded in part by a vast list of “member organizations” – a list that just happens to include some of the biggest producers and users of high fructose corn syrup in America, such as ADM, Cargill, ConAgra, the Coca-Cola Company and others.

Make of this what you will.

Genetically Identical Cells Can Respond Differently

Scientists may be a step closer to knowing why cells within the same body often seem to be at odds with each other.

For example, take any two genetically identical cells in a person’s body: odds are, one cell will store away the fat it receives from the bloodstream like a squirrel storing nuts for the winter. Meanwhile, the other cell burns the fat off, or passes it on to the waste management division.

That’s right: the two cells do the exact opposite of one another, even though they’re identical twins. A group of U.S. researchers thinks they know why.

Scientists at Purdue University’s Weldon School of Biomedical Engineering say that a recent study shows that a cell that processes insulin quickly tends to store up fat faster than other cells.

The researchers focused on a type of genetically identical cells called 3T3-L1 cells. They found that the variability in the cells’ fat storage behavior depended on their individual exposure to insulin, a hormone that triggers cells to take in glucose from the bloodstream and convert it to stored fat.  Cells that were subject to increased and prolonged insulin stimulation stacked away the fat like nobody’s business; cells that missed out on the insulin drenching didn’t.

What makes this important is that these researchers think it might be possible to develop a drug that will short-circuit the reaction that makes insulin-exposed cells hoard fat – and thus help people with obesity.

Researchers Find Gene that Turns Carbs into Fat

A team of U. S. researchers at the University of California, Berkeley, who are performing a study of the formation, development and storage of fat at the molecular level, made a surprise find.

One of the researchers isolated a gene, called DNA-PK, and found that it contributes to the body’s metabolic process in the liver, which is turning that plate of pasta directly into fat.

Typically, after a meal high in carbohydrates, the body’s blood glucose level becomes elevated, which triggers the secretion of insulin.  Excess glucose stored in the liver is then turned into fatty acids, which turn into fat.

This process has long been understood, but the exact molecular pathway had been a mystery.  Until now.The researchers determined that DNA-PK was acting as a signaling molecule in a metabolic chain-reaction in which insulin binds to liver cell receptors. To test their theory, the team bred mice with a disabled version of DNA-PK and basically carbo-loaded them.

The results?  These genetically altered mice were leaner and had 40% less body fat than the control group. Not only did these mice not get fat on a high-carb diet, but they also had lower levels of cholesterol, a major proponent of heart disease.

So what does that mean for us humans? Well, since humans and mice share this same gene, the researchers hope that the findings will help in the understanding of how the body metabolizes carbohydrates, how they contribute to obesity, and most importantly, lead to a drug that can prevent obesity.