Endocrine Abstracts

Men have a higher prevalence and risk of non-alcoholic fatty liver disease (NAFLD) than age-matched women and this may, in part, be related to differences in fatty acid oxidation. Fasting and postprandial fatty acid oxidation was investigated in 11 healthy men and 11 healthy women matched for age (46±2 years vs 46±2 years (mean±S.E.M.)), BMI (28.0±1 vs 27.0±1 kg/m2) and liver fat content (3.4±0.9 vs 3.9±0.7%) measure...

Hepatic steatosis, accumulation of intracellular triglyceride (TG) (>5% of hepatic tissue), is the prerequisite for the development of non-alcoholic fatty liver disease (NAFLD). NAFLD represents a spectrum of liver diseases and is associated with obesity and obesity-related metabolic diseases such as type 2 diabetes and cardiovascular disease. Steatosis occurs due to an imbalance between fatty acid input and removal (fatty acid partitioning) which can be affected by geneti...

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic disease. 5β-reductase (AKR1D1) is highly expressed in human liver where it inactivates steroid hormones and catalyzes a fundamental step in bile acid synthesis. Steroid hormones, including glucocorticoids, as well as bile acids are established regulators of metabolic phenotype. We hypothesized that AKR1D1 plays a crucial regulatory role in hepatic metabolic homeostasis. Genetic manipulatio...

Non-alcoholic fatty liver disease is the hepatic manifestation of metabolic disease. 5β-reductase (AKR1D1) is highly expressed in human and rodent liver where it inactivates steroid hormones and catalyzes a fundamental step in bile acid synthesis. Steroid hormones, including glucocorticoids, as well as bile acids are established regulators of metabolic phenotype. We have hypothesized that AKR1D1 plays a crucial regulatory role in hepatic metabolic homeostasis.<p class...

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic disease. Steroid hormones and bile acids are established regulators of metabolic phenotype. 5β-reductase (AKR1D1) is highly expressed in human liver where it inactivates steroid hormones and catalyzes a fundamental step in bile acid synthesis. We hypothesized that AKR1D1 plays a key role in hepatic metabolic homeostasis. Genetic manipulation of AKR1D1 ...

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic disease. Steroid hormones and bile acids are established regulators of metabolic phenotype. 5β-reductase (AKR1D1) is highly expressed in human liver where it inactivates steroid hormones and catalyzes a fundamental step in bile acid synthesis. We hypothesized that AKR1D1 plays a key role in hepatic metabolic homeostasis. Genetic manipulation of AKR1D1 ...

Steroid hormones and BAs are established regulators of metabolic phenotype. 5β-reductase (AKR1D1) is highly expressed in the liver where it inactivates steroid hormones and catalyses a fundamental step in bile acid (BA) synthesis. We have hypothesised that AKR1D1 plays a crucial regulatory role in hepatic metabolic homeostasis. Genetic manipulation of AKR1D1 was performed in human liver HepG2 and Huh7 cells. Expression changes were confirmed by qPCR and western blotting, ...

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic disease. 5β-reductase (AKR1D1) is highly expressed in human liver where it inactivates steroid hormones and, in parallel, catalyzes a fundamental step in bile acid synthesis. Steroid hormones, including glucocorticoids, as well as bile acids (BAs) are established regulators of metabolic phenotype. We have hypothesized that AKR1D1 plays a crucial regulatory role in hepatic metabolic homeost...

Objective: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome. Steroid hormones and bile acids are potent regulators of hepatic carbohydrate and lipid metabolism. Steroid 5β-reductase (AKR1D1) is highly expressed in human liver where it inactivates steroid hormones and catalyzes a fundamental step in bile acid synthesis.Methods: Human liver biopsies were obtained from 34 obese patients and AKR1D1 mRNA expres...