New Transcription Factors and their Role in Diabetes and its by Jacob E. Friedman (Eds.)

By Jacob E. Friedman (Eds.)

This publication comprises contributions from one of the most eminent specialists within the fields of genetics, biochemistry, and pathophysiology of diabetes. via particular examples, with vast purposes, this booklet presents a accomplished examine how transcription elements could underline the pathogenetic mechanisms of diabetes and weight problems. quantity five presents an summary of the prestige of the sphere, whereas additionally delivering helpful info of functional application to those that don't inevitably paintings during this box. the combination of easy biology with physiologically and clinically correct proteins may still give you the reader with a theoretical historical past to figuring out the innovations for brand new strength healing objectives and their program to illness. *Applies molecular biology to transcriptional legislation of metabolism and weight problems *Underscores the medical relevance of transcription elements *Provides a invaluable review of the present prestige of the sector

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29] M. , Obesity associated with a mutation in a genetic regulator of adipocyte differentiation, New Engl. J. Med. 339 (1998) 953–959. D. , Transcriptional regulation of adipogenesis, Genes Dev 14 (2000) 1293–1307. [31] R. , Differential regulation of peroxisome proliferator activated receptor gamma1 (PPARgamma1) and PPARgamma2 messenger RNA expression in the early stages of adipogenesis, Cell Growth Differ. 10 (1999) 43–48. 38 Catherine S. D. , C/EBPalpha induces adipogenesis through PPAR-gamma: a unified pathway, Genes Dev.

Lp, lipoprotein; LPL, lipoprotein lipase; FATP, fatty acid transport protein; CD36, fatty acid translocase; FFA, free fatty acids; GyK, glycerol kinase; PEPCK, phosphoenolpyruvate carboxykinase; glycerol-3-P, glycerol-3-phosphate; GLUT4, glucose transporter 4. * denotes potential sites of regulation by PPARg. so-called ‘fatty acid steal’ hypothesis), through the regulation of a panel of genes involved in FFA metabolism (Fig. 3). Adipocyte lipoprotein lipase (LPL) expression is up regulated in response to TZD treatment, thereby potentially enhancing release of FFAs from circulating lipoproteins [65].

Agarwal, A. Garg, A novel heterozygous mutation in peroxisome proliferator-activated receptor-g gene in a patient with familial partial lipodystrophy, J. Clin. Endocrinol. Metab. 87 (2002) 408–411. A. , PPARG F388L, a transactivation-deficient mutant, in familial partial lipodystrophy, Diabetes 51 (2002) 3586–3590. B. , Human metabolic syndrome resulting from dominant-negative mutations in the nuclear receptor PPARg, Diabetes 52 (2003) 910–917. [29] M. , Obesity associated with a mutation in a genetic regulator of adipocyte differentiation, New Engl.

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