The role of bile acids in regulating glucose and lipid metabolism.

In recent years, bile acids (BAs) are increasingly being appreciated as signaling molecules beyond their involvement in bile formation and fat absorption. The farnesoid X receptor (FXR) and the G protein-coupled bile acid receptor 1 (GPBAR1, also known as TGR5) are two dominating receptors through which BAs modulate glucose and lipid metabolism. FXR is highly expressed in the intestine and liver. GPBAR1 is highly expressed in the intestine. The present study reviews the metabolism and regulation of BAs, especially the effects of BAs on glucose and lipid metabolism by acting on FXR in the liver and intestine, and GPBAR1 in the intestine. Furthermore, it explains that fibroblast growth factor 15/19 (FGF15/19), ceramide, and glucagon like peptide-1 (GLP-1) are all involved in the signaling pathways by which BAs regulate glucose and lipid metabolism. This article aims to provide an overview of the molecular mechanisms by which BAs regulate glucose and lipid metabolism, and promote further scientific and clinical research on BAs.

Liver dysfunction induced by Levothyroxine Sodium Tablets (Euthyrox®) in a hypothyroid patient with Hashimoto's thyroiditis: case report and literature review.

A 49-year-old woman with hypothyroidism developed liver dysfunction after increasing dose of levothyroxine (L-T4) (Euthyrox®) from 25 µg to 50 µg. Viral hepatitis, autoimmune hepatitis and non-alcoholic steatohepatitis (NASH) were ruled out with examinations. She had no concurrent medication and had no history of infectious, chronic or any other autoimmune diseases. After cessation of Levothyroxine Sodium Tablets (Euthyrox®), liver enzymes gradually returned to normal. She was diagnosed levothyroxine-induced liver injury, based on criteria proposed in "Diagnosis and treatment guideline on drug-induced liver injury" issued by the Chinese Medical Association (2015). As an alternative 25 µg qod of Levothyroxine Sodium Tablets (Letrox®) was tried and increased gradually up to 75 µg daily. Since then liver enzymes have remained within normal range. The main difference of additive for both tablets is whether it contains lactose or not: Euthyrox® contains lactose which caused no liver injury, thus excluding the possibility that an additive of Euthyrox® contributed to liver injury. The relatively quicker and larger replacement with synthetic T4 for hypothyroidism inducing transient thyrotoxicosis was suspected, although thyroid function was normal. Immune-mediated drug-induced liver injury (DILI) was also not excluded. This is a rare case of drug-induced liver injury due to levothyroxine tablets. It reminded us that when replacement with synthetic T4 for hypothyroidism is done, smaller-dose initiation and slower-speed increase may be useful for treatment of cases similar to genetically susceptible individuals.

Effects of chronic ethanol consumption on levels of adipokines in visceral adipose tissues and sera of rats.

AIM: To investigate the effects of ethanol on adipokines (leptin, adiponectin, resistin, visfatin and cartonectin) levels in visceral adipose tissue (VAT) and sera, and explore the correlation between VAT and serum adipokine levels. METHODS: Forty-eight Wistar rats were randomly divided into control, low, middle and high ethanol treatment groups that received 0, 0.5, 2.5, or 5.0 g of ethanol x kg(-1) x d(-1), respectively, via gastric tubes for 22 weeks. The levels of fasting blood glucose (FBG) and fasting serum insulin (FINS) were measured and homeostasis model assessment of insulin resistance (HOMA-IR) values were calculated. Adipokines in perirenal and epididymal VAT and sera were measured by enzyme-linked immunosorbent assays (ELISAs). RESULTS: High-dose treatments of ethanol (vs control group) significantly increased FINS (eg 37.86%) and HOMA-IR values (eg 40.63%). In VAT, levels of leptin, resistin and visfatin in the middle- and high-dose groups were significantly elevated, whereas adiponectin and cartonectin levels decreased. In sera, changes in adipokine levels were similar to that observed in VAT, with the exception of cartonectin. These ethanol-induced effects were dose-dependent. A positive correlation existed between VAT and serum adipokine levels, except for cartonectin. CONCLUSION: Chronic ethanol consumption affects adipokine levels in VAT and sera in a dose-dependent manner, with the exception of serum cartonectin. The altered levels of adipokines in VAT and sera are positively correlated.