Abstract: Methods for the treatment or prevention of disease, such as fatty liver disease and obesity, are described including the modulation the amount of CTRP1 in a subject. Novel mouse strains are also described.

Abstract: Methods for the treatment or prevention of disease, such as fatty liver disease and obesity, are described including the modulation the amount of CTRP1 in a subject. Novel mouse strains are also described.

Abstract: 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.

Abstract: The present invention provides a method for identifying a subject having or at risk of having a metabolic disease, such as diabetes or obesity. The invention is based on an approach to identify candidate genes involved in metabolic diseases, such as obesity and type 2 diabetes (T2D) through epigenetic mechanisms. The method includes identifying in the subject genetic markers correlating differentially methylated regions (DMRs) in the genome with genetic risk loci for the subject and comparing methylation patterns of the markers with a control sample from a subject not having the disease. In another embodiment, the invention also provides a method of treating a subject having or at risk of having a metabolic disease. In another embodiment, the invention provides a method of providing a prognostic evaluation of a subject having or at risk of having a metabolic disease.

Abstract: Disclosed is the novel myokine known as myonectin (CTRP15), an isolated nucleic acid encoding the myonectin (CTRP15) gene, and the amino acid sequence encoding the myonectin (CTRP15) protein. Methods of isolation of the nucleic acid, protein, polypeptides and methods of making anybodies to myonectin (CTRP15) protein are provided. The use of myonectin (CTRP15) in the modulation of lipid and/or glucose metabolism, suppressing the expression of autophagy genes, inhibiting LC3 lipidation and autophagosome-dependent p62 degradation, and activating the Akt/mTOR pathway is also provided.

Abstract: Disclosed is the novel myokine known as myonectin (CTRP15) an isolated nucleic acid encoding the myonectin (CTRP15) gene, and the amino acid sequence encoding the myonectin (CTRP15) protein. Methods of isolation of the nucleic acid, protein, polypeptides and methods of making anybodies to myonectin (CTRP15) protein are provided. The use of myonectin (CTRP15) in the modulation of lipid and/or glucose metabolism, suppressing the expression of autophagy genes, inhibiting LC3 lipidation and autophagosome-dependent p62 degradation, and activating the Akt/mTOR pathway is also provided.

Abstract: The present invention provides substantially purified peptide portions of adipokine polypeptides, including, for example, C1q/TNF-related protein-12 (CTRP12), a functional homolog or function fragment of CTRP12, and a fusion polypeptide comprising any of the above.

Abstract: Disclosed is the novel myokine known as myonectin (CTRP15), an isolated nucleic acid encoding the myonectin (CTRP15) gene, and the amino acid sequence encoding the myonectin (CTRP15) protein. Methods of isolation of the nucleic acid, protein, polypeptides and methods of making antibodies to the myonectin (CTRP15) protein are provided. The use of myonectin (CTRP15) in the modulation of lipid and/or glucose metabolism, suppressing the expression of autophagy genes, inhibiting LC3 lipidation and autophagosome-dependent p62 degradation, and activating the Akt/mTOR pathway is also provided.

Abstract: Compositions and methods for treatment of obesity and/or Type II diabetes and related metabolic disorders are provided wherein the methods and treatments comprise an effective amount of an isolated and/or purified C1q/TNF-related Protein-9 (CTRP9) or a functional portion thereof, and a pharmaceutically acceptable carrier. Methods of screening for molecules which elevate levels of CTRP9 in vivo are also provided. The present inventors provide the first in vivo evidence linking CTRP9 to regulation of fat metabolism in liver and skeletal muscle via AMPK signaling pathway, and highlight its protective metabolic function in the context of HFD-mediated metabolic insults.

Abstract: Disclosed is the novel myokine known as myonectin (CTRP15), an isolated nucleic acid encoding the myonectin (CTRP15) gene, and the amino acid sequence encoding the myonectin (CTRP15) protein. Methods of isolation of the nucleic acid, protein, polypeptides and methods of making antibodies to the myonectin (CTRP15) protein are provided. The use of myonectin (CTRP15) in the modulation of lipid and/or glucose metabolism, suppressing the expression of autophagy genes, inhibiting LC3 lipidation and autophagosome-dependent p62 degradation, and activating the Akt/mTOR pathway is also provided.

Abstract: The present invention provides substantially purified peptide portions of adipokine polypeptides, including, for example, Clq/TNF-related protein-12 (CTRP12), a functional homologue or function fragment of CTRP12, and a fusion polypeptide comprising any of the above.