The risk for pouchitis was highest during the initial six-month period. Cumulative risk leveled off after two years but was substantial (51 percent) at four years. Less than 10 percent of patients had severe, chronic pouchitis, and only two patients (1.3 percent) had their pouches removed.

Inhibition of hepatic HMG-CoA reductase by pravastatin results in an increased expression of hepatic LDL receptors, which explains the lowered plasma levels of LDL cholesterol.

No abstract

an elevated hepatic synthesis of cholesterol, and a reduced Hepatic cholesterol metabolism was studied in operaconversion of cholesterol to bile acids or to a decreased esteritive liver biopsies from 17 morbidly obese subjects and fication rate of hepatic cholesterol. 5 Obese subjects have an compared with that in samples from 15 nonobese conincreased synthesis of cholesterol that has been established trols. The aim was to understand the mechanisms causin several previous studies. [6][7][8] In a previous study, we assayed ing the hypersecretion of cholesterol into bile. The conthe activity of the microsomal enzyme 3-hydroxy-3-methyltent of cholesteryl esters was increased threefold in the glutaryl coenzyme A (HMG CoA) reductase, that regulates liver of obese subjects compared with that of the conthe synthesis of cholesterol, and showed that the liver is a trols (P õ .0001). The activity and the messenger RNA major contributor to the increased cholesterol production in (mRNA) level of 3-hydroxy-3-methylglutaryl coenzyme obesity. 9 Bile acid formation and pool size have been reported A (HMG CoA) reductase, the rate limiting enzyme for to be normal or enhanced in obesity. 1,3,4,8 No information is cholesterol synthesis, were higher in the obese subjects available on the activity of the microsomal cholesterol 7a-compared with the nonobese subjects (75% and 140%, hydroxylase, the rate determining enzyme for catabolism of respectively; P õ .01). In the obese subjects, the activity cholesterol to bile acids, in obesity. In a recent study of obese and mRNA level of cholesterol 7a-hydroxylase, which subjects, we found the activity of the microsomal acyl coenregulates the catabolism of cholesterol to bile acids, zyme A:cholesterol acyltransferase (ACAT) which catalyzes were also increased by 140% (P õ .05) and 180% (P Å .06), the esterification of cholesterol, to be normal but the content respectively, as compared with the controls. There was of esterified cholesterol in liver homogenates was elevated in a significant correlation between the activities and the comparison with nonobese controls. 10 mRNA levels of cholesterol 7a-hydroxylase among theThe aim of the present study was to elucidate possible obese subjects (r Å /0.65, P õ .01). The activities of acylmechanisms responsible for the previously reported hypersecoenzyme A:cholesterol acyltransferase (ACAT), which cretion of biliary cholesterol in obesity. We, therefore, considgoverns cholesteryl ester formation, in obese and nonered it important to thoroughly study the hepatic metabolism obese patients were 12.5 { 1.7 and 8.1 { 1.2 pmol/min/ of cholesterol in obese subjects. We have assayed the activimg protein, respectively (P õ .05), and the low-density ties of the following three important rate-limiting enzymes: lipoprotein (LDL) receptor mRNA levels were 5.3 { 0.7 HMG CoA reductase, cholesterol 7a-hydroxylase, and ACAT. and 4.5 { 0.9 molecules of mRNA/mg of RNA, respectively.In addition, we have quantitated the mRNA levels for HMG We conclude that the activities ...