Search Results
Search for other papers by Wonsuk Choi in
Google Scholar
PubMed
Search for other papers by Joon Ho Moon in
Google Scholar
PubMed
Search for other papers by Hail Kim in
Google Scholar
PubMed
transporters (VMAT), with the remaining free 5-HT in portal blood being primarily metabolized in the liver. Thus, >95% of 5-HT is stored in platelets, with free 5-HT levels being low in peripheral blood ( Holmsen 1989 , Richter et al. 1989 , El-Merahbi et
Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA
Research and Development Division, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA
Search for other papers by Rita E Roberts in
Google Scholar
PubMed
Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA
Research and Development Division, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA
Search for other papers by Jacqueline Cavalcante-Silva in
Google Scholar
PubMed
Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
Search for other papers by Rhonda D Kineman in
Google Scholar
PubMed
Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA
Research and Development Division, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA
Search for other papers by Timothy J Koh in
Google Scholar
PubMed
wound healing, IGF-1 is present at high levels in the circulation and the liver is the major source of circulating IGF-1 in mice ( Yakar et al. 1999 ). In humans, IGF-1 levels in wounds are correlated with those in blood, suggesting that blood is the
Search for other papers by Gabriel Forn-Cuní in
Google Scholar
PubMed
Search for other papers by Monica Varela in
Google Scholar
PubMed
Search for other papers by Conrado M Fernández-Rodríguez in
Google Scholar
PubMed
Search for other papers by Antonio Figueras in
Google Scholar
PubMed
Search for other papers by Beatriz Novoa in
Google Scholar
PubMed
diseases are part of a condition termed metabolic syndrome. The hepatic component of metabolic syndrome is non-alcoholic fatty liver disease (NAFLD). This term comprises a wide range of progressive liver injuries including bland steatosis, variable degrees
Search for other papers by S Eleswarapu in
Google Scholar
PubMed
Search for other papers by H Jiang in
Google Scholar
PubMed
Introduction Growth hormone (GH) is a pituitary polypeptide hormone that plays a central role in animal growth and metabolism ( Harvey et al. 1995 ). A major target organ of GH is the liver, where GH regulates the expression of
Search for other papers by Ya Liu in
Google Scholar
PubMed
Search for other papers by Xiaoqing Zhou in
Google Scholar
PubMed
Search for other papers by Ye Xiao in
Google Scholar
PubMed
Search for other papers by Changjun Li in
Google Scholar
PubMed
Search for other papers by Yan Huang in
Google Scholar
PubMed
Search for other papers by Qi Guo in
Google Scholar
PubMed
Search for other papers by Tian Su in
Google Scholar
PubMed
Search for other papers by Lei Fu in
Google Scholar
PubMed
Search for other papers by Liping Luo in
Google Scholar
PubMed
Introduction Nonalcoholic fatty liver disease (NAFLD), characterized mainly by hepatic steatosis, is the most common liver disease worldwide ( Birkenfeld & Shulman 2014 , Meex & Watt 2017 ). It is reported that NAFLD is closely associated
Search for other papers by Alyce M Martin in
Google Scholar
PubMed
Search for other papers by Emily W Sun in
Google Scholar
PubMed
Nutrition and Metabolism, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
Search for other papers by Damien J Keating in
Google Scholar
PubMed
pathogenesis of human metabolic disorders. Gut hormone regulation of metabolism The regulation of whole-body metabolism involves the integrated activity of multiple metabolically active tissues, including the GI tract, pancreas, adipose tissue, liver
Search for other papers by Sung-Soo Park in
Google Scholar
PubMed
Search for other papers by Yeon-Joo Lee in
Google Scholar
PubMed
Search for other papers by Sooyeon Song in
Google Scholar
PubMed
Search for other papers by Boyong Kim in
Google Scholar
PubMed
Search for other papers by Hyuno Kang in
Google Scholar
PubMed
Search for other papers by Sejong Oh in
Google Scholar
PubMed
Search for other papers by Eungseok Kim in
Google Scholar
PubMed
Introduction Excessive fat accumulation in key metabolic tissues, including the liver and adipose tissue, is closely associated with metabolic disorders such as obesity, insulin resistance, diabetes, nonalcoholic hepatic steatosis
Search for other papers by Tina Seidu in
Google Scholar
PubMed
Search for other papers by Patrick McWhorter in
Google Scholar
PubMed
Search for other papers by Jessie Myer in
Google Scholar
PubMed
Search for other papers by Rabita Alamgir in
Google Scholar
PubMed
Search for other papers by Nicole Eregha in
Google Scholar
PubMed
Search for other papers by Dilip Bogle in
Google Scholar
PubMed
Search for other papers by Taylor Lofton in
Google Scholar
PubMed
Search for other papers by Carolyn Ecelbarger in
Google Scholar
PubMed
Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
Search for other papers by Stanley Andrisse in
Google Scholar
PubMed
triglycerides and free fatty acids (FFA), thus driving lipid accumulation mainly in the liver ( Samuel & Shulman 2016 ). Previous work has shown that low-dose DHT female mice displayed obesity-independent impaired glucose tolerance, insulin resistance, and
Search for other papers by H. ADLERCREUTZ in
Google Scholar
PubMed
CONTENTS
Introduction
Biological inactivation and metabolism of oestrogens in the normal liver of animals
Biological inactivation and metabolism of oestrogens in the damaged liver of animals
Biological inactivation and metabolism of oestrogens in the normal human liver
The role of conjugation of oestrogens in their biological inactivation
Role of the enterohepatic circulation in the biological inactivation and metabolism of oestrogens in human subjects
Oestrogen metabolism in human subjects with liver disease
Studies in vitro
Studies on urinary excretion of oestrogens using biological and chemical methods
Studies on the biological effects of oestrogens on the vaginal smear and urinary sediment in liver disease
Studies on the mechanism leading to increased oestrogen excretion and to symptoms of increased oestrogen activity in the organism
The relation of the disturbed metabolism of oestrogens to the clinical symptoms seen in liver disease
Conclusions
References
INTRODUCTION
The nature of the changes in oestrogen metabolism in liver
Search for other papers by R P Rhoads in
Google Scholar
PubMed
Search for other papers by J W Kim in
Google Scholar
PubMed
Search for other papers by M E Van Amburgh in
Google Scholar
PubMed
Search for other papers by R A Ehrhardt in
Google Scholar
PubMed
Search for other papers by S J Frank in
Google Scholar
PubMed
Search for other papers by Y R Boisclair in
Google Scholar
PubMed
despite elevated plasma growth hormone (GH; Block et al. 2001 , Rhoads et al. 2004 ). This fall in plasma IGF-I is thought to reflect decreased GH-stimulated IGF-I transcription in liver as a consequence of GH receptor (GHR) loss ( Radcliff et al
