By Jacob E. Friedman (Eds.)
This booklet comprises contributions from one of the most eminent specialists within the fields of genetics, biochemistry, and pathophysiology of diabetes. via particular examples, with extensive purposes, this booklet offers a complete examine how transcription components may possibly underline the pathogenetic mechanisms of diabetes and weight problems. quantity five presents an outline of the prestige of the sphere, whereas additionally delivering worthwhile info of sensible application to people who don't inevitably paintings during this box. the mixing of easy biology with physiologically and clinically proper proteins may still give you the reader with a theoretical heritage to realizing the ideas for brand new strength healing ambitions and their software to disorder. *Applies molecular biology to transcriptional law of metabolism and weight problems *Underscores the scientific relevance of transcription elements *Provides a worthwhile evaluation of the present prestige of the sphere
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Extra info for New Transcription Factors and their Role in Diabetes and its Therapy
Sci. USA 98 (2001) 5306–5311.  H. , The peroxisome proliferator-activated receptor delta promotes lipid accumulation in human macrophages, J. Biol. Chem. 276 (2001) 44258–44265.  A. , PPARd is a very low-density lipoprotein sensor in macrophages, Proc. Natl. Acad. Sci. USA 100 (2003) 1268–1273.  H. , PPAR delta functions as a prostacyclin receptor in blastocyst implantation, Trends Endocrinol. Metab. 11 (2000) 137–142. S. , Critical roles of PPAR b/d in keratinocyte response to inﬂammation, Genes Dev.
Adipose tissue, pancreatic beta cells, macrophages and vascular endothelium), albeit at low levels, while PPARg2 is expressed almost exclusively in adipose tissue . Like other nuclear receptors, PPARg has a modular structure consisting of distinct functional domains (Fig. 1a). Many of its biological effects are mediated through direct regulation of target gene transcription in a ligand-dependent manner. Following binding to speciﬁc DNA response elements (PPAR response elements (PPREs) – located in the target gene promoter) as a heterodimer with the retinoid X receptor (RXR), binding of cognate or exogenous ligand(s) induces coactivator recruitment, which in turn promotes unfolding of the chromatin structure to permit greater levels of gene transcription (Fig.
Increased glucose uptake into adipocytes contributes to whole body glucose disposal, and provides important substrate for triglyceride synthesis (see above). However, it remains to be seen whether similar direct effects on glucose uptake are also operational in skeletal muscle, where much lower levels of PPARg expression are observed, but where the majority ($80%) of glucose disposal occurs. Unfortunately, conﬂicting ﬁndings in the two existing mouse models of muscle-speciﬁc Pparg deletion have so far failed to resolve this issue [61,62].