Abstract: Described are benzoimidazole indolyl methane compounds, pharmaceutical compositions containing them, and use of the compounds to inhibit PCSK9-mediated ailments.

Abstract: Described are benzoimidazole indolyl methane compounds, pharmaceutical compositions containing them, and use of the compounds to inhibit PCSK9-mediated ailments.

Abstract: The present invention relates to a recognition that an analog of ?KG can increase glucose-induced insulin secretion in vitro and in vivo in animals, particularly in mammals, and more particularly in humans and in rodents. By employing the methods of the invention, insulin secretion can be increased.

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: 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 present invention relates to a recognition that an analog of ?KG can increase glucose-induced insulin secretion in vitro and in vivo in animals, particularly in mammals, and more particularly in humans and in rodents. By employing the methods of the invention, insulin secretion can be increased.

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 present invention relates to a recognition that an analog of ?KG can increase glucose-induced insulin secretion in vitro and in vivo in animals, particularly in mammals, and more particularly in humans and in rodents. By employing the methods of the invention, insulin secretion can be increased.

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: 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: It has been discovered that the low density lipoprotein receptor (LDLR) degrades the lipoprotein apoB. Based on this observation, an artificial fusion protein has been designed containing an LDL receptor domain attached to a localization domain which causes retention of the fusion protein inside of a cell. The fusion protein is preferably retained in the endoplasmic reticulum of the cell, where the LDLR can degrade apoB. Data shows that the technique is effective in a mammal to reduce serum LDL cholesterol levels.

Abstract: A gene expression pattern analysis has identified genes the expression patterns of which are different in adipose cells of individuals who have Type 2 Diabetes Mellitus from the cells of individuals who do not have the disease. This information provides a mechanism for the genetic diagnosis of the disease.

Abstract: The invention provides a method for upregulating cholecystokinin (CCK) expression in mammalian pancreatic islets by administrating a CCK upregulating agent. The increased CCK expression activates islet cell proliferation triggering an increase in pancreatic ?-cell mass and plasma insulin levels. Accordingly, methods to produce a replenishable supply of islet cells and to ameliorate the symptoms associated with diabetes are also disclosed.

Abstract: Methods and compounds are disclosed for lowering serum LDL levels or serum cholesterol levels, or for reducing the transport of cholesterol from the gut to the blood or the lymph, based on the observation that a gene known as ABC1 is necessary in order for cholesterol to be transported from the intestinal lumen into the bloodstream. A mutant chicken phenotype, known as the WHAM chicken, characterized by low levels of serum LDL and reduced transport of cholesterol, facilitated the discovery of this function of the ABC1 gene. Techniques which act to inhibit ABC1 activity in the cells of the intestinal wall will result in lower serum cholesterol.

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: Two of the genetic bases for susceptibility to type 2 diabetes are disclosed. The alleles of the genes SorCS1 and SorCS3 that a person carries can determine whether or not that person is susceptible to type 2 diabetes.

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.