Effects of bariatric surgery on inflammatory, functional and structural markers of coronary atherosclerosis.
*Gastric Bypass; Adult; Biological Markers – Blood; Biomarkers/blood; Blood Flow Velocity – Physiology; Blood Flow Velocity/physiology; Blood Vessels – Pathology; Body Mass Index; Brachial Artery – Ultrasonography; Brachial Artery/diagnostic imaging; C-Reactive Protein – Analysis; C-Reactive Protein/analysis; Carotid Arteries – Pathology; Carotid Arteries/pathology; Cholesterol – Blood; Cholesterol/blood; Coronary Arteriosclerosis – Blood; Coronary Arteriosclerosis – Pathology; Coronary Arteriosclerosis – Physiopathology; Coronary Artery Disease/*blood/pathology/*physiopathology; Female; Follow-Up Studies; Gastric Bypass; Human; Humans; Male; Muscle; Prospective Studies; Smooth – Pathology; Triglycerides – Blood; Triglycerides/blood; Tunica Intima/pathology; Tunica Media/pathology; Ultrasonography; Vasodilation – Physiology; Vasodilation/physiology
This study was designed to assess the effects of bariatric weight loss surgery on structural, functional, and inflammatory markers of coronary atherosclerosis. Obesity is a worldwide epidemic and an independent risk factor for coronary atherosclerosis. It remains unclear whether surgically induced weight loss reduces cardiovascular risk. This prospective study enrolled 50 consecutive subjects with morbid obesity who underwent Roux-en-Y gastric bypass surgery (GBS) after failed attempts at medical weight loss. Subjects were recruited through a comprehensive weight loss center affiliated with an academic tertiary care hospital. All subjects had body mass indexes \textgreater or =40 kg/m(2) or body mass indexes of 35 to 40 kg/m(2) with \textgreater or =2 co-morbid obesity-related conditions. Markers of coronary atherosclerosis, including brachial artery flow-mediated dilation, carotid intima-media thickness, and high-sensitivity C-reactive protein, were measured before GBS and 6, 12, and 24 months after GBS. There were statistically significant improvements in all measured markers of coronary atherosclerosis after GBS. The mean body mass index decreased from 47 to 29.5 kg/m(2) at 24 months (p \textless0.001), the mean carotid intima-media thickness regressed from 0.84 to 0.50 mm at 24 months (p \textless0.001), mean flow-mediated dilation improved from 6.0% to 14.9% at 24 months (p \textless0.05), and mean high-sensitivity C-reactive protein decreased from 1.23 to 0.65 mg/dl at 6 months (p \textless0.001) and to 0.35 mg/dl at 24 months (p \textless0.001). In conclusion, GBS results in significant improvements in inflammatory, structural, and functional markers of coronary atherosclerosis.
Habib Phillip; Scrocco John David; Terek Megan; Vanek Vincent; Mikolich J Ronald
The American journal of cardiology
2009
2009-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.amjcard.2009.06.042" target="_blank" rel="noreferrer noopener">10.1016/j.amjcard.2009.06.042</a>
Hepatic carboxylesterase 1 is essential for both normal and farnesoid X receptor-controlled lipid homeostasis.
*Homeostasis; *Lipid Metabolism; Animals; Carboxylic Ester Hydrolases/*physiology; Cholesterol/blood; Cytoplasmic and Nuclear/*physiology; Fatty Acids/metabolism; Inbred C57BL; Lipogenesis; Liver/*enzymology; Mice; Receptors; Sterol Regulatory Element Binding Protein 1/physiology; Triglycerides/metabolism
UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is one of the major health concerns worldwide. Farnesoid X receptor (FXR) is considered a therapeutic target for treatment of NAFLD. However, the mechanism by which activation of FXR lowers hepatic triglyceride (TG) levels remains unknown. Here we investigated the role of hepatic carboxylesterase 1 (CES1) in regulating both normal and FXR-controlled lipid homeostasis. Overexpression of hepatic CES1 lowered hepatic TG and plasma glucose levels in both wild-type and diabetic mice. In contrast, knockdown of hepatic CES1 increased hepatic TG and plasma cholesterol levels. These effects likely resulted from the TG hydrolase activity of CES1, with subsequent changes in fatty acid oxidation and/or de novo lipogenesis. Activation of FXR induced hepatic CES1, and reduced the levels of hepatic and plasma TG as well as plasma cholesterol in a CES1-dependent manner. CONCLUSION: Hepatic CES1 plays a critical role in regulating both lipid and carbohydrate metabolism and FXR-controlled lipid homeostasis.
Xu Jiesi; Li Yuanyuan; Chen Wei-Dong; Xu Yang; Yin Liya; Ge Xuemei; Jadhav Kavita; Adorini Luciano; Zhang Yanqiao
Hepatology (Baltimore, Md.)
2014
2014-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/hep.26714" target="_blank" rel="noreferrer noopener">10.1002/hep.26714</a>