Why the study?
Does hepatic Trib1 overexpression or deficiency alter plasma lipid levels and VLDL production in mice?
Does hepatic Trib1 overexpression or deficiency alter plasma lipid levels and VLDL production in mice?
Trib1 regulates hepatic lipogenesis and VLDL production in mice, providing a functional mechanism for its genetic association with plasma lipids and myocardial infarction risk in humans.
Does not alter clinical lipid management; hypothesis-generating for Trib1 as a target in human dyslipidemia.
Recent genome-wide association studies have identified a genetic locus at human chromosome 8q24 as having minor alleles associated with lower levels of plasma triglyceride (TG) and LDL cholesterol (LDL-C), higher levels of HDL-C, as well as decreased risk for myocardial infarction. This locus contains only one annotated gene, tribbles homolog 1 (TRIB1), which has not previously been implicated in lipoprotein metabolism. Here we demonstrate a role for Trib1 as a regulator of lipoprotein metabolism in mice. Hepatic-specific overexpression of Trib1 reduced levels of plasma TG and cholesterol by reducing VLDL production; conversely, Trib1-knockout mice showed elevated levels of plasma TG and cholesterol due to increased VLDL production. Hepatic Trib1 expression was inversely associated with the expression of key lipogenic genes and measures of lipogenesis. Thus, we provide functional evidence for what we believe to be a novel gene regulating hepatic lipogenesis and VLDL production in mice that influences plasma lipids and risk for myocardial infarction in humans.
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Burkhardt et al. (2010) studied this question.
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