The invention provides a non-human animal model for non-alcoholic steatohepatitis (NASH)-induced heptocellular carcinoma, methods of screening for agents for treating heptocellular carcinoma, methods of screening for targets useful in suppressing NASH progression to heptocellular carcinoma, methods of treating heptocellular carcinoma, and compositions for treating the same.

The presently disclosed subject matter relates to methods of improving insulin sensitivity in cells, tissues, and subjects, as well as methods of reducing insulin resistance, improving glucose homeostasis, reducing hepatic tryglyceride levels, reducing food intake, and treating metabolic disorders, such as those occurring in individuals who are obese, diabetic, and/or have hepatic steatosis.

The present invention relates to an animal model having hypoparathyroidism and a method for producing the same. According to the present invention, the animal model having hypoparathyroidism is economical and efficient in that it can demonstrate a pathophysiology of hypoparathyroidism and maintain a survival of animals without any distortion of the pathophysiology by supplying an optimal calcium content diet.

Provided is a gene in drosophila designated as dSLC5A1. This gene is responsible for taste independent nutrient sensing. Activation of neurons expressing this gene results in hunger behavior. Provided are compositions and methods for identifying agents that can interfere with hunger behavior.

Described are alcohol-induced liver cancer model mice, methods of generating the alcohol-induced liver cancer model mice, and methods of using the alcohol-induced liver cancer model mice. Methods of treating alcoholic liver disease, including hepatocellular carcinoma, are also described.

Methods and compositions for the prevention and treatment of liver damage or disease in a subject in need thereof are provided. The methods involve providing the sulfated oxysterol 25-hydroxycholesterol-3-sulfate (25HC3S) to the subject e.g. by 1) administering 25HC3S to the subject; or 2) overexpressing, in the subject, the hydroxysterol sulfotransferase enzyme SULT2B1b, which catalyzes the sulfation of 25-hydroxycholesterol (25HC) to form 25HC3S.

Fatty liver was induced by administering agents for inducing organ inflammation to experimental animals to evoke insulin resistance and by rearing them with high-fat diets. As a result, steatohepatitis was successfully induced in the animals. The animals show pathological findings similar to those of humans. By using these model animals, substances for treating or preventing diseases can be efficiently screened and the efficacy of medicinal substances can be effectively evaluated.

The present invention provides methods, agents, compounds, and compositions useful for administering to subjects having or at risk of having anemias. In certain embodiments, methods herein comprise administering two agents to a subject, which are useful for the treatment of an anemia.

A nucleic acid for the controlled expression of a nucleic acid encoding a pro-apoptotic protein in an individual, including: a regulatory polynucleotide including a minimal promoter and at least one AARE (amino acid response element) nucleic acid, the regulatory polynucleotide being activated in an individual upon consumption of a diet deficient in at least one essential amino acid; and a nucleic acid encoding a pro-apoptotic protein, which is placed under the control of the regulatory polynucleotide.

Provided is a polynucleotide, including a cis-regulatory element and a nucleotide sequence encoding a vestigial like 4 protein, wherein the cis-regulatory element includes an uncoupling protein 1 enhancer and an uncoupling protein 1 promoter. Also provided is a viral vector including said polynucleotide. Also provided is a method of transfecting a cell or a subject with said polynucleotide or said viral vector.