Fish Oil Increases Diet-Induced Thermogenesis in Mice.

Increasing energy expenditure (EE) is beneficial for preventing obesity. Diet-induced thermogenesis (DIT) is one of the components of total EE. Therefore, increasing DIT is effective against obesity.

Different expressions of clock genes in fatty liver induced by high-sucrose and high-fat diets.

Sucrose consumption can cause obesity and nonalcoholic fatty liver disease (NAFLD). NAFLD is associated with the disruption of circadian rhythms. We compared the alterations in NAFLD circadian rhythms induced by a high-sucrose diet (HSD) with those induced by a high-fat diet (HFD) in mice.

A novel method for measuring diet-induced thermogenesis in mice.

Diet-induced thermogenesis (DIT) refers to energy expenditure (EE) related to food consumption. Enhancing DIT can lead to weight loss. Factors that increase DIT are expected to lower body mass index and body fat mass.

Effective Food Ingredients for Fatty Liver: Soy Protein β-Conglycinin and Fish Oil.

Obesity is prevalent in modern society because of a lifestyle consisting of high dietary fat and sucrose consumption combined with little exercise. Among the consequences of obesity are the emerging epidemics of hepatic steatosis and nonalcoholic fatty liver disease (NAFLD). Sterol regulatory element-binding protein-1c (SREBP-1c) is a transcription factor that stimulates gene expression related to de novo lipogenesis in the liver.

Soya protein β-conglycinin ameliorates fatty liver and obesity in diet-induced obese mice through the down-regulation of PPARγ.

Diets high in fat can result in obesity and non-alcoholic fatty liver disease (NAFLD). The improvement of obesity and NAFLD is an important issue. β-Conglycinin, one of the soya proteins, is known to prevent hyperlipidaemia, obesity and NAFLD.

PTPRJ Inhibits Leptin Signaling, and Induction of PTPRJ in the Hypothalamus Is a Cause of the Development of Leptin Resistance.

Leptin signaling in the hypothalamus plays a crucial role in the regulation of body weight. Leptin resistance, in which leptin signaling is disrupted, is a major obstacle to the improvement of obesity. We herein demonstrated that protein tyrosine phosphatase receptor type J (Ptprj) is expressed in hypothalamic neurons together with leptin receptors, and that PTPRJ negatively regulates leptin signaling by inhibiting the activation of JAK2, the primary tyrosine kinase in leptin signaling, through the dephosphorylation of Y813 and Y868 in JAK2 autophosphorylation sites.

Dietary β-conglycinin prevents acute ethanol-induced fatty liver in mice.

Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. β-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether β-conglycinin feeding has an effect on the prevention of acute ethanol-induced fatty liver in mice.

Knockdown of aquaporin-8 induces mitochondrial dysfunction in 3T3-L1 cells.

Background: Aquaporin-8 (AQP8), a member of the aquaporin water channel family, is expressed in various tissue and cells, including liver, testis, and pancreas. AQP8 appears to have functions on the plasma membrane and/or on the mitochondrial inner membrane. Mitochondrial AQP8 with permeability for water, HO and NH has been expected to have important role in various cells, but its information is limited to a few tissues and cells including liver and kidney.

Wild-type and specific mutant androgen receptor mediates transcription via 17β-estradiol in sex hormone-sensitive cancer cells.

We previously encountered regulatory processes wherein dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)α, but not the androgen receptor (AR), in breast cancer MCF-7 cells. Here, we investigated whether such aberrant ligand-nuclear receptor (NR) interaction is present in prostate cancer LNCaP cells. First, we confirmed that LNCaP cells expressed large amounts of AR at negligible levels of ERα/β or progesterone receptor.