Metabolic syndrome, a collection of related abnormalities like hypertension, obesity, insulin resistance, and excess cholesterol, poses a major risk for developing heart disease and diabetes.
Individuals with a genetic predisposition to high cholesterol (familial hyperlipidemia or FH) can be especially vulnerable to metabolic syndrome, but researchers have now found that blocking the enzyme stearoyl-CoA desaturase-1 (SCD1), which helps synthesize unsaturated fatty acids, greatly improves the profile of FH-mice affected by metabolic syndrome.
Previous mouse studies on SCD1 found that blocking this enzyme could reduce obesity in normal mice; Michael Hayden and colleagues wondered whether such a protective effect would extend to mice with excess cholesterol levels.
They mimicked FH in mice by knocking out the LDL receptor, causing a cholesterol buildup. When fed a high-fat Western diet, these mice develop obesity and diabetes in adulthood. However, when the researchers also knocked out SCD1, the mice improved dramatically, accumulating far less fat in their liver, which in turn led to fewer triglycerides in the blood, increased insulin sensitivity, and less weight gain.
These results highlight that SCD1 might be a potential drug target for FH individuals who have developed other components of metabolic syndrome
The above post is reprinted from materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.
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