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Slimming Effects of Fatty Diets May Be Possible
Published August 2008
In a fast-paced world of even faster food options, persuading people to eat healthy and exercise has become increasingly difficult.
Because of that, scientists and foodies alike are constantly looking for ways to combat weight gain and perhaps even lessen the negative health effects associated with the ever-prevalent high-fat diets.
Results of a recently published study suggest that may actually be possible.
UC researchers along with colleagues from the Spanish National Cancer Research Center have found that higher levels of a specific protein called Sirt1 can actually reduce liver inflammation caused by high-fat diets and improve the liver’s tolerance to glucose. (Glucose intolerance is often referred to as pre-diabetes.)
The researchers also found that activation of the Sirt1 pathway may prevent non-alcoholic fatty liver disease—a condition often diagnosed in overweight or obese individuals, particularly those with diabetes and higher cholesterol levels.
The results of the rodent study are published in the June 30, 2008, online edition of the journal Proceedings of the National Academy of Sciences.
“This pathway seems to work like an internal shield against the damaging consequences of a highfat diet,” says Matthias Tschöp, MD, senior author and professor in UC’s psychiatry department.
“It appears to be particularly effective in the liver,” he adds, “but we are still far from understanding in detail how this pathway works.”
Sirt1 (silent information regulator 1) is a type of sirtuin—a protein found in many organisms, from humans to bacteria.
Previous studies of rodents have shown that Sirt1 can be activated by a naturally occurring chemical called resveratrol, which is found in red wine. In very high doses, resveratrol has been shown to promote glucose control and calorie burning.
The authors say that the design of previous tests of elevated Sirt1 may have led to the activation of other sirtuins and pathways, so a more direct and specific study of Sirt1 was needed to prove its reported implications.
This new study of Sirt1 took a more direct look at the protein’s actions by introducing a transgenic copy of it directly into the mouse genome—keeping the elevated concentration contained where it could not directly impact other tissues or organs.
Mice with elevated Sirt1 levels who were exposed to high-fat diets had fat gain similar to mice with normal Sirt1 levels, but were better protected from fat-induced inflammation, glucose intolerance and fatty-liver disease.
“Thus, activation of Sirt1 may represent a promising strategy for preventing and treating metabolic syndrome,” the authors write. Paul Pfluger, PhD, lead author and member of UC’s Obesity Research Center, cautions that more research is needed before this animal study could be extrapolated to humans, but, he says, “Determining exactly how Sirt1 works is an important step towards understanding how the effects of high-fat diets can be tempered pharmacologically.”
Coauthors from the Spanish National Cancer Research Center include Daniel Herranz, Susana Velasco and Manual Serrano. The U.S.-based portion of this study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases.