Medicine. HDL miR-ed down by SREBP introns

Abstract

Animal cells must maintain a membrane cholesterol-to-phospholipid ratio within tight limits for normal function. Elaborate mechanisms control the cellular input of cholesterol from endogenous synthesis or uptake from plasma lipoproteins. Much less is known about the factors that regulate the output of cholesterol from cells. On pages 1566 and 1570 of this issue, Najafi-Shoushtari et al. (1) and Rayner et al. (2) show that cholesterol output is controlled by the same genes that regulate cholesterol input, but in a reciprocal manner and through an unexpected mechanism.

Potential dual role of SREBP in metabolic syndrome

In obese subjects with metabolic syndrome, insulin resistance leads to elevated insulin, which activates transcription of SREBP-1c in the liver. This leads to increased VLDL triglycerides and decreased HDL cholesterol in the blood. miR-33b is encoded in intron 17 (red); exons are in blue.