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The β3-Adrenergic Receptor and Susceptibility to Obesity, the Insulin Resistance Syndrome, and Noninsulin-Dependent Diabetes Mellitus

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G Proteins, Receptors, and Disease

Part of the book series: Contemporary Endocrinology ((COE,volume 6))

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Abstract

Although most forms of NIDDM in humans do not exhibit simple Mendelian inheritance, the large contribution of heredity is well recognized (1-5). Progress toward an understanding of the genetic basis of NIDDM has been largely restricted to a few distinct monogenic syndromes with predictable modes of inheritance. For example, one form of autosomal-dominant maturity-onset diabetes of the young (MODY) is caused by mutations in the glucokinase (M0DY2) gene (6,7) autosomal-recessive syndromes of extreme insulin resistance are the result of mutations in the insulin receptor gene (8) and maternally inherited diabetes and deafness (MIDD) is the result of mutations in mitochondrial DNA (9). These rare subphenotypes of diabetes are examples in which single gene defects have a major influence on the phenotype and for which environmental influences on expression of the phenotype are negligible.

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Walston, J., Silver, K., Shuldiner, A.R. (1998). The β3-Adrenergic Receptor and Susceptibility to Obesity, the Insulin Resistance Syndrome, and Noninsulin-Dependent Diabetes Mellitus. In: Spiegel, A.M. (eds) G Proteins, Receptors, and Disease. Contemporary Endocrinology, vol 6. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-1802-9_18

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  • DOI: https://doi.org/10.1007/978-1-4612-1802-9_18

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