Endocrine Abstracts

Introduction: Efficient fuel selection between glucose and fatty acids in insulin-sensitive organs is a key feature which determines metabolic health in humans. In skeletal muscle, lipid storage and utilisation can differ between healthy and diseased individuals, however to date there are limited in vitro models to explore this. Therefore, aim of this work was to investigate the effects of nutrition on engineered skeletal muscle health and metabolism.<p class="abs...

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...

Introduction: Glucocorticoids (GC) are prescribed to 2–3% of the population of the UK and USA. Their use is associated with a significant side effect profile that includes the development of central obesity, insulin resistance and type 2 diabetes. 5α-reductase (5αR) inhibitors (Finasteride and Dutasteride) are also commonly prescribed in the context of prostate disease, where they inhibit the conversion of testosterone to dihydrotestosterone. Additionally, they ...

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...

The health burden associated with non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, continues to escalate. Not only is NAFLD associated with significant liver-specific and cardiovascular morbidity and mortality, but patients are at risk of the development of hepatocellular carcinoma (HCC); a malignancy where the incidence continues to rise and there are very limited therapeutic strategies.Aldo-keto reductase ...

Background: Intrahepatic triglyceride (IHTG) accumulation, a cardiometabolic disease risk factor, is greater in individuals consuming saturated-fat (SFA) compared to polyunsaturated-fat (PUFA) enriched diets. We have demonstrated that compared to SFA, PUFA are preferentially partitioned into oxidation pathways, which may, in part, explain the divergence in IHTG accumulation. However, it remains unclear if this preferential handling is maintained when hepatocel...

Background: Fasting hyperglycaemia and hypertriglyceridemia are characteristic of insulin resistance (IR), type 2 diabetes, and non-alcoholic fatty liver disease, but the underlying mechanisms remain unclear. Rodent work has suggested this is due to selective hepatic IR; defined by increased hepatic gluconeogenesis (GNG) and de novo lipogenesis (DNL). The aim of this study was to determine if signatures of selective hepatic IR were associated with hyp...

The incidence of non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, continues to rise. NAFLD is associated with significant liver-specific and cardiovascular morbidity and mortality, including hepatocellular carcinoma (HCC). Currently, there are no licensed therapies, highlighting the importance of understanding the pathogenic mechanisms that drive the condition. Cytochrome p450 oxidoreductase (POR) plays an essential role in activa...

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 ...