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Researchers discover molecular 'switch' that tells body to store or burn fat

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"These data establish that SCD-1 is an important biological modulator of lipid metabolism," adds Ntambi.

Obese (leptin-deficient) mice also have massively fatty livers, which is corrected when the mice are given leptin. The lack of SCD-1 in the mutant mice also caused their livers to be normal and not fatty.

"Inhibiting SCD-1 could be of potential use for reducing weight and for reducing fat content in liver, which is also an important clinical problem," says Friedman. Fatty liver, clinically known as steatosis, often develops in people who are obese, who abuse alcohol or other drugs, or who are diabetic.

The researchers caution however that completely eliminating SCD-1 could cause other medical and health problems as evidenced by the abnormalities of asebia mice. Mice which completely lack the SCD-1 enzyme suffer from corneal dryness, which can lead to corneal opacities, as well as the condition known as scarring dermatitis. Inhibition of SCD-1 could also increase tissue-damaging free radicals, a potential sequelae of increased oxidative metabolism.

A key question is whether a partial reduction in SCD-1 activity rather than a complete loss of the enzyme's activity as in asebia mice could alter metabolism without incurring unwanted side effects.

The answer appears to be yes, according to Ntambi and co-author Makoto Miyazaki, Ph.D., a biochemist at the University of Wisconsin at Madison, who have shown in separate studies that mutant mice with half the level of the enzyme appear normal.

"Still, many more studies will be necessary to confirm that molecules that inhibit SCD-1 have an acceptable therapeutic index," cautions Friedman.

How Does SCD-1 work?

Fat in liver generally can be stored, exported in very low-density lipoprotein (VLDL) particles or burned for energy.

"Our experiments show that fat storage and export of fat via VLDL in the obese mice lacking SCD-1 were reduced,"
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Contact: Joseph Bonner
bonnerj@mail.rockefeller.edu
212-327-8998
Rockefeller University
11-Jul-2002


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