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
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Alyce M Martin, Emily W Sun, and Damien J Keating
Sung-Soo Park, Yeon-Joo Lee, Sooyeon Song, Boyong Kim, Hyuno Kang, Sejong Oh, and Eungseok Kim
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
Tina Seidu, Patrick McWhorter, Jessie Myer, Rabita Alamgir, Nicole Eregha, Dilip Bogle, Taylor Lofton, Carolyn Ecelbarger, and Stanley Andrisse
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
H. ADLERCREUTZ
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
R P Rhoads, J W Kim, M E Van Amburgh, R A Ehrhardt, S J Frank, and Y R Boisclair
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
Christopher J Delvecchio and John P Capone
Introduction The liver X receptors (LXRs; α and β subtypes) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors and are activated by oxidized cholesterol metabolites known as oxysterols ( Janowski et al
Paola Venditti, Angela Bari, Lisa Di Stefano, and Sergio Di Meo
). Accumulating evidence has demonstrated that in the liver such effects are primarily due to increased tissue content of mitochondrial respiratory chain components ( Brand & Murphy 1987 ), including autoxidizable electron carriers ( Venditti et al . 2003 ). This
Giuseppe Calamita, Maria Moreno, Domenico Ferri, Elena Silvestri, Patrizia Roberti, Luigi Schiavo, Patrizia Gena, Maria Svelto, and Fernando Goglia
synthesis ( Roodyn 1965 , Goglia et al. 1988 ), the turnover ( Gross 1971 ), and the functional capacity of mitochondrial components. Liver mitochondria from hypothyroid rats have a decreased activity of membrane-associated electron transport enzymes and
E. TUERKISCHER and E. WERTHEIMER
A decrease in the glycogen content of the diabetic liver is often considered to be the direct result of the diabetic disturbance in metabolism, caused either by an increased glycogenolysis or by a decreased ability to synthesize glycogen. In previous experiments [Tuerkischer & Wertheimer, 1946] it was observed that the livers of alloxandiabetic rats and of pair-fed, normal rats contained equal amounts of glycogen. The liver glycogen of alloxan-diabetic rats starved for 24 hr. was actually considerably higher than that of normal, control rats, a fact also reported shortly thereafter by Weber [1946]. Additional burdening of the carbohydrate metabolism with complete exhaustion of the carbohydrate reserves (by phloridzin or swimming) caused increased glycogenesis in the diabetic rat, starved for 24 hr., with an increased deposition of glycogen in the liver. This increase in liver glycogen was only found in non-comatose, alloxan-diabetic rats. It was therefore assumed that the decrease in
María Cecilia Ramirez, Guillermina María Luque, Ana María Ornstein, and Damasia Becu-Villalobos
metabolism, thus increasing the susceptibility to develop later disease. In rodents, GH regulates the sexually dimorphic patterns of a large number of liver-expressed genes, including many receptors, signaling molecules, and enzymes of steroid and drug
