Health & Medicine
The Complex Regulation Behind Lipid Metabolism: It's All in the Genes
Kathleen Lees
First Posted: Apr 30, 2014 01:44 PM EDT
That four letter 'F Word.' Food.
It's on our mind's constantly. We need it to survive, thrive and function. And sometimes, it doesn't hurt if it tastes nice, too.
Yet too much high-energy, high-fat food can often lead to overweight or even obese individuals (as so many studies show.) But there's a lot more to it than that, according to researchers. Of course, it all comes down to another four letter word, only this time it begins with a 'G.'
Genes are responsible for much of what identifies us as human. (We'll skip the nature vs. nurture theory for this article.) For this study in particular, researchers from the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Japan, discovered that the Sirt7 gene plays a critical role in regulating metabolism energy.
For the study, researchers worked to identify a protein from the sirtuin group that holds a critical function in a high fat diet and how this determines the formation of fat deposits. For this, researchers carried out a wide range of tests on mice who lacked the sirtuin SIRT7. These Sirt7-knockout mice were then fed high-fat pellets over the span of several months.
"We established that Sirt7-knockout mice put on significantly less weight than the control group. On the contrary, they maintained their normal weight," said Eva Bober, a scientist at the MPI. Moreover, compared with the non-genetically-modified mice, these animals tended to have lower triglyceride and cholesterol levels in their livers and normal insulin levels, via a press release. "Everything pointed to the fact that the animals which lacked SIRT7 were able to process the excess energy in the food better and did not build up any pathological fat depots."
While examining liver cells, scientists discovered that SIRT7 activates a large number of genes for lipid metabolism. For mice without SIRT7, this gene remains largely unactivated--thus creating fewer fat deposits in the rodents.
"We discovered a second mechanism as well," Bober added, via the release. "SIRT7 also inhibits the degradation of certain proteins. Because they are then active for longer, these proteins also make a greater contribution to energy storage than is actually intended." Conversely, if SIRT7 is missing, these proteins are degraded and fewer fat depots are formed.
With further studies, researchers hope to find new therapeutic approaches for treating metabolic issues.
More information regarding the study can be seen via the journal Cell Metabolism.
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First Posted: Apr 30, 2014 01:44 PM EDT
That four letter 'F Word.' Food.
It's on our mind's constantly. We need it to survive, thrive and function. And sometimes, it doesn't hurt if it tastes nice, too.
Yet too much high-energy, high-fat food can often lead to overweight or even obese individuals (as so many studies show.) But there's a lot more to it than that, according to researchers. Of course, it all comes down to another four letter word, only this time it begins with a 'G.'
Genes are responsible for much of what identifies us as human. (We'll skip the nature vs. nurture theory for this article.) For this study in particular, researchers from the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Japan, discovered that the Sirt7 gene plays a critical role in regulating metabolism energy.
For the study, researchers worked to identify a protein from the sirtuin group that holds a critical function in a high fat diet and how this determines the formation of fat deposits. For this, researchers carried out a wide range of tests on mice who lacked the sirtuin SIRT7. These Sirt7-knockout mice were then fed high-fat pellets over the span of several months.
"We established that Sirt7-knockout mice put on significantly less weight than the control group. On the contrary, they maintained their normal weight," said Eva Bober, a scientist at the MPI. Moreover, compared with the non-genetically-modified mice, these animals tended to have lower triglyceride and cholesterol levels in their livers and normal insulin levels, via a press release. "Everything pointed to the fact that the animals which lacked SIRT7 were able to process the excess energy in the food better and did not build up any pathological fat depots."
While examining liver cells, scientists discovered that SIRT7 activates a large number of genes for lipid metabolism. For mice without SIRT7, this gene remains largely unactivated--thus creating fewer fat deposits in the rodents.
"We discovered a second mechanism as well," Bober added, via the release. "SIRT7 also inhibits the degradation of certain proteins. Because they are then active for longer, these proteins also make a greater contribution to energy storage than is actually intended." Conversely, if SIRT7 is missing, these proteins are degraded and fewer fat depots are formed.
With further studies, researchers hope to find new therapeutic approaches for treating metabolic issues.
More information regarding the study can be seen via the journal Cell Metabolism.
See Now: NASA's Juno Spacecraft's Rendezvous With Jupiter's Mammoth Cyclone