Jongsook Kim Kemper, Associate Professor of Molecular and Integrative Physiology, authored a study about cholesterol regulation published in the most recent issue of Genes and Development.
The Kemper lab and its partners have detailed how the activity of a small protein, named Small Heterodimer Partner (SHP), is controlled to modulate the conversion of cholesterol to bile acids.
Cholesterol is an important constituent of cell membranes and is used by the liver to make bile acids.
Bile acids play important dietary roles in the body, including the absorption of fat-soluble nutrients during digestion and regulating fat and glucose metabolism. Excessive amounts of cholesterol and bile acids, however, can lead to cardiovascular disease and metabolic ailments.
When bile acid levels are too high, SHP is made to stop the conversion of cholesterol into new bile acid.
The Kemper Lab found when bile acid levels are low, SHP is rapidly broken down in liver cells to allow for the production of more bile acids. Then, when bile acid levels increase, SHP remains stable and can halt the conversion of cholesterol into new bile acids.
In another interesting discovery, obese mice were found to have very stable SHP compared to their non-obese counterparts. Mice fed a chronic western diet had more than twice the levels of stable SHP than those that had normal diets.
“Abnormal stabilization of SHP may be associated with metabolic disorders, including obesity and diabetes,” according to the paper. “The mechanism underlying elevated SHP stability in these obese mice is not clear, but these intriguing results provide a potential link between abnormally elevated SHP stability and metabolic disease.”