The enzyme, MGAT2, determines whether dietary fat is used to generate energy or stored under the skin around the waist. The discovery of its role could be the key to preventing obesity, diabetes and heart disease
Scientists found that mice missing the gene for MGAT2 were able to feast on a high fat diet without becoming flabby or overweight. Mice lacking MGAT2 were also protected against glucose intolerance - a precursor to diabetes - high cholesterol and a build up of fat in liver cells.
Enzymes are biological catalysts that are essential for numerous biological functions MGAT2 is one of three MGAT enzymes found in the intestines of both mice and humans. Cutting MGAT activity with drugs could be another way to combat obesity, the scientists believe.
Dr Robert Farese, from the University of California at San Francisco, and colleagues, reduced MGAT activity in mice by more than half by knocking out MGAT2. On a low fat diet, the mice developed in just the same way as normal animals. But on a 60 per cent fat diet, they gained much less weight.
After 16 weeks, the experimental mice weighed 40 per cent less than mice with functioning MGAT2 genes and the amount of fat they carried was more than 50 per cent lower. Further studies showed that mice lacking MGAT2 had less insulin in their blood and better glucose tolerance after prolonged high-fat feeding than normal mice.
They also had reduced concentrations of harmful cholesterol in their blood. A high level of low density lipoprotein (LDL), known as "bad", cholesterol, is a major risk factor for heart disease.A chief reason for the current obesity epidemic is thought to be that the human body still behaves as it did many thousands of years ago when food was far more scarce.
The excess calories eaten today are stored away as fat to help in leaner times which never arrive. MGAT enzymes appear to play an important role in this energy storage process.Reporting their findings in the journal Nature Medicine, the researchers wrote: "Our studies identify MGAT2 as a key determinant of energy metabolism in response to dietary fat and suggest that the inhibition of this enzyme may prove to be a useful strategy for treating obesity and other metabolic diseases associated with excessive fat intake."
Scientists found that mice missing the gene for MGAT2 were able to feast on a high fat diet without becoming flabby or overweight. Mice lacking MGAT2 were also protected against glucose intolerance - a precursor to diabetes - high cholesterol and a build up of fat in liver cells.
Enzymes are biological catalysts that are essential for numerous biological functions MGAT2 is one of three MGAT enzymes found in the intestines of both mice and humans. Cutting MGAT activity with drugs could be another way to combat obesity, the scientists believe.
Dr Robert Farese, from the University of California at San Francisco, and colleagues, reduced MGAT activity in mice by more than half by knocking out MGAT2. On a low fat diet, the mice developed in just the same way as normal animals. But on a 60 per cent fat diet, they gained much less weight.
After 16 weeks, the experimental mice weighed 40 per cent less than mice with functioning MGAT2 genes and the amount of fat they carried was more than 50 per cent lower. Further studies showed that mice lacking MGAT2 had less insulin in their blood and better glucose tolerance after prolonged high-fat feeding than normal mice.
They also had reduced concentrations of harmful cholesterol in their blood. A high level of low density lipoprotein (LDL), known as "bad", cholesterol, is a major risk factor for heart disease.A chief reason for the current obesity epidemic is thought to be that the human body still behaves as it did many thousands of years ago when food was far more scarce.
The excess calories eaten today are stored away as fat to help in leaner times which never arrive. MGAT enzymes appear to play an important role in this energy storage process.Reporting their findings in the journal Nature Medicine, the researchers wrote: "Our studies identify MGAT2 as a key determinant of energy metabolism in response to dietary fat and suggest that the inhibition of this enzyme may prove to be a useful strategy for treating obesity and other metabolic diseases associated with excessive fat intake."
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