Abstract: It is disclosed here that insulin sensitivity in a human or non-human animal can be increased by reducing stearoyl-CoA desaturase-1 (SCD1) activity in the animal. This provides a new tool for treating and preventing type 2 diabetes. Also disclosed are methods for identifying agents that can increase insulin sensitivity in a human or non-human animal through determining the agents' effects on SCD1 activity.

Abstract: Methods for treating and preventing obesity, inhibiting adipocyte differentiation, inhibiting increased SCD-1 gene transcription, and/or reducing body fat in a subject include administering at least one analog of 1?,25-dihydroxyvitamin D3 or 1?,25-dihydroxyvitamin D2 or a pharmaceutical composition that includes such an analog to a subject in need thereof. The analog may be a 19-nor vitamin D analog such as a compound of formula IA, a compound of formula IB, or a mixture thereof where the variables R1, R2, and R3 have the values described herein.

Abstract: It is disclosed here that inhibiting the activity of the enzyme stearoyl-CoA desaturase (SCD1) in an animal causes the animal to have less body fat and greater lean body mass. The lower of SCD1 activity level can be accomplished by inhibiting activity of the enzyme or lowering levels of active enzyme in the subject.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: The cloning of a fourth mouse SCD gene, mSCD4, as well as its corresponding cDNA and amino acid sequences are disclosed. Mouse SCD4 is expressed mainly in the heart tissue and synthesizes the bulk of monounsaturated fatty acids in the heart. The disclosure here enables new tools (e.g., nucleic acids, polypeptides, antibodies, vectors, recombinant cells, and transgenic and knock-out animals) for studying the function of various SCD isoforms and their connection to various disease conditions. New tools for converting saturated fatty acyl-CoA to monounsaturated acyl-CoA and for identifying SCD modulators including isoform-specific modulators are also enabled. In addition, given that accumulation of lipid in the heart (fatty heart) can have deleterious consequences, the present invention also provides a new prevention and treatment target for fatty heart as well as methods for screening candidate drugs.

Abstract: It is disclosed here that inhibiting the activity of the enzyme stearoyl-CoA desaturase (SCD1) in an animal causes the animal to have less body fat and greater lean body mass. The lower of SCD1 activity level can be accomplished by inhibiting activity of the enzyme or lowering levels of active enzyme in the subject.

Abstract: The cloning of a fourth mouse SCD gene, mSCD4, as well as its corresponding cDNA and amino acid sequences are disclosed. Mouse SCD4 is expressed mainly in the heart tissue and synthesizes the bulk of monounsaturated fatty acids in the heart. The disclosure here enables new tools (e.g., nucleic acids, polypeptides, antibodies, vectors, recombinant cells, and transgenic and knock-out animals) for studying the function of various SCD isoforms and their connection to various disease conditions. New tools for converting saturated fatty acyl-CoA to monounsaturated acyl-CoA and for identifying SCD modulators including isoform-specific modulators are also enabled. In addition, given that accumulation of lipid in the heart (fatty heart) can have deleterious consequences, the present invention also provides a new prevention and treatment target for fatty heart as well as methods for screening candidate drugs.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: It is disclosed here that insulin sensitivity in a human or non-human animal can be increased by reducing stearoyl-CoA desaturase-1 (SCD1) activity in the animal. This provides a new tool for treating and preventing type 2 diabetes. Also disclosed are methods for identifying agents that can increase insulin sensitivity in a human or non-human animal through determining the agents' effects on SCD1 activity.

Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 (“hSCD1”) in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases.

Abstract: It is disclosed here that inhibiting the activity of the enzyme stearoyl-CoA desaturase (SCD1) in an animal causes the animal to have less body fat and greater lean body mass. The lower of SCD1 activity level can be accomplished by inhibiting activity of the enzyme or lowering levels of active enzyme in the subject.