Endocrine Abstracts

Primary human hepatocytes are considered the ‘gold standard’ to explore metabolic phenotype within the liver, however they come with limitations, such as donor variability, lack of proliferation and rapid phenotype loss. The human hepatoma cell line, HepG2, has been used extensively in cell-based metabolic studies but there are significant limitations including their malignant origin and inherent low rates of triglyceride secretion. The aim of this study was to inves...

Introduction: Excessive consumption of free sugars (glucose and fructose) is linked to an increased risk of developing chronic metabolic diseases. Current knowledge of fructose metabolism has focussed on the liver where it is implicated in impaired insulin sensitivity, increased fat accumulation and dyslipidaemia. The long-term effects of elevated fructose consumption on human health are poorly defined and fructose metabolism in subcutaneous adipose tissue, the largest human f...

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...

Background and Aim: Hepatic de novo lipogenesis (DNL) has been implicated in the development of non-alcoholic fatty liver disease (NAFLD). Supplementation with the omega-3 fatty acids (FA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decreases intrahepatic triacylglycerol (IHTAG) and plasma TAG concentrations, which is suggested to be mediated through changes in hepatic DNL. We investigated the effects of omega-3 FA supplementation on intrahepatic DNL an...

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 ...

Non-alcoholic fatty liver disease is the hepatic manifestation of the global epidemic of metabolic disease. Steroid hormones, including glucocorticoids and sex steroids, regulate metabolic phenotype, and in addition, bile acids have recently been identified as potent metabolic regulators. 5β-reductase (AKR1D1) is predominantly expressed in the liver and is a crucial regulator of steroid hormone clearance as well as bile acid synthesis. Its role in pathogenesis of metaboli...

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, ...