title: [What have we learned thanks to genetics in type II diabetes and its complications?].
abstract: Genetic and environmental factors contribute to the development of type 2 diabetes. However, type 2 diabetes appears to be an heterogeneous syndrome composed of sub-types strongly associated with environmental factors at one end of the spectrum, and highly genetic forms at the other end. Therefore, a first approach has been to differentiate the potential monogenic forms of diabetes, as a paradigm for genetic studies, such as maturity onset diabetes of the young (MODY) which is characterized by an early age of onset and autosomal dominant inheritance. Recent studies have shown mutations in four transcription factors, members of the hepatocyte nuclear factor family. Furthermore, some data suggest that non-MODY monofactorial forms of late-onset NIDDM, due to islet transcription factors defects exist. The positional cloning of type 2 diabetes susceptibility genes is in progress, and will help to understand the molecular basis of diabetes, first step to identify targets of new drugs that will provide a better care to diabetic patients.
authors.forename: P
authors.initials: P
authors.lastname: Froguel
mesh_terms: D000293:Adolescent; D000328:Adult; D017668:Age of Onset; D000818:Animals; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D002318:Cardiovascular Diseases / Q000209:etiology; D002648:Child; D002675:Child, Preschool; D004268:DNA-Binding Proteins; D003924:Diabetes Mellitus, Type 2 / Q000145:classification / Q000150:complications / Q000453:epidemiology / Q000235:genetics*; D003925:Diabetic Angiopathies / Q000235:genetics; D003928:Diabetic Nephropathies / Q000235:genetics; D004200:Diseases in Twins / Q000235:genetics; D005006:Ethnicity / Q000235:genetics; D020022:Genetic Predisposition to Disease; D005941:Glucokinase / Q000235:genetics; D051537:Hepatocyte Nuclear Factor 1; D051538:Hepatocyte Nuclear Factor 1-alpha; D051539:Hepatocyte Nuclear Factor 1-beta; D051557:Hepatocyte Nuclear Factor 4; D018398:Homeodomain Proteins; D006801:Humans; D007328:Insulin / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins; D007333:Insulin Resistance / Q000235:genetics; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism / Q000473:pathology; D008019:Life Style; D051379:Mice; D018345:Mice, Knockout; D018482:Muscle, Skeletal / Q000378:metabolism; D009687:Nuclear Proteins; D009765:Obesity / Q000150:complications; D010750:Phosphoproteins / Q000235:genetics; D015221:Potassium Channels / Q000235:genetics; D011972:Receptor, Insulin / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D018027:Receptors, Glucagon / Q000235:genetics; D015534:Trans-Activators / Q000235:genetics / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics
chemical_list: D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D004268:DNA-Binding Proteins; C496487:HNF1A protein, human; C496495:HNF1B protein, human; D051538:Hepatocyte Nuclear Factor 1-alpha; D051557:Hepatocyte Nuclear Factor 4; C496488:Hnf1a protein, mouse; C496496:Hnf1b protein, mouse; D018398:Homeodomain Proteins; C526292:IRS1 protein, human; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; C526295:Irs1 protein, mouse; C403128:MLX protein, human; D009687:Nuclear Proteins; D010750:Phosphoproteins; D015221:Potassium Channels; D018027:Receptors, Glucagon; C501970:Tcfl4 protein, mouse; D015534:Trans-Activators; D014157:Transcription Factors; C084010:pancreatic and duodenal homeobox 1 protein; D051537:Hepatocyte Nuclear Factor 1; D051539:Hepatocyte Nuclear Factor 1-beta; D005941:Glucokinase; D011972:Receptor, Insulin