Alternative mRNA Splicing in the Pathogenesis of Obesity.

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Term Occurence Count Dictionary
Insulin 3 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperinsulinemia 3 endocrinologydiseases
metformin 4 endocrinologydiseasesdrugs
obesity 16 endocrinologydiseases
progeria 1 endocrinologydiseases

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Insulin 7639 metabolic complications will also be discussed.2. Mis-Splicing of Metabolic Factors in Obesity2.1. Insulin ReceptorInsulin receptor belongs to a subfamily of receptor tyrosine kinases and plays an important
Insulin 7655 complications will also be discussed.2. Mis-Splicing of Metabolic Factors in Obesity2.1. Insulin Receptor Insulin receptor belongs to a subfamily of receptor tyrosine kinases and plays an important role as regulators
Insulin 40973 Variant Level in Pathological Conditions of Obese SubjectKey Changes in Metabolic PhenotypesReferences Insulin receptor (IR)Increase IR-A (skipping of exon 11) in the liverCorrelate with fasting plasma glucose and
metformin 27600 [[95],[96]].Remarkably, many Food and Drug Administration (FDA) approved marketed drugs, including metformin , affect the alternative splicing machinery [[97],[98]]. Metformin is the first-line anti-diabetic drug
metformin 27929 alters the composition of the gut microbiota [[99]]. The proposed underlying molecular mechanisms of metformin are very complicated [[100]]. A recent study tested the effect of metformin in the treatment of a “spliceopathy-associated”
metformin 28005 molecular mechanisms of metformin are very complicated [[100]]. A recent study tested the effect of metformin in the treatment of a “spliceopathy-associated” disease, myotonic dystrophy type I (also known as
metformin 28424 of the expression of the RNA-binding protein 3 (RBM3) [[98]]. It is interesting to explore whether metformin can also fix the pathological mis-splicing in obesity.In the previous section, we discussed the importance
Select Disease Character Offset Disease Term Instance
diabetes mellitus 10105 was reported by other group [[44]] and the role of insulin receptor isoforms in noninsulin-dependent diabetes mellitus remained elusive, the studies raised the possibility of cellular metabolic status alters the ratio of
hyperinsulinemia 9014 similar to that of humans, diabetic monkeys were used to explore the potential association between hyperinsulinemia and alternations in the insulin receptor mRNA splicing in 1994 [[40]]. This study provided the first
hyperinsulinemia 13204 the ligand binding [[47]]. dbPas/dbPas mice are grossly obese and exhibit hypercholesterolemia and hyperinsulinemia because soluble leptin receptor is absent [[52],[53]]. The leptin and soluble leptin receptor levels
hyperinsulinemia 34076 glucagon-producing alpha-cells within the pancreatic islets, increased number of insulin-producing beta cells, hyperinsulinemia and increased hepatic glucagon sensitivity [[126]]. In addition, in the severe SMA mouse model, subcutaneous
obesity 1402 significant changes in exon skipping and splicing factors expression levels are observed with diet-induced obesity , this review focuses on several well-known alternatively spliced metabolic factors and discusses recent
obesity 1622 in the regulation of the expressions of splice variants under the pathophysiological conditions of obesity . The potential of targeting the alternative mRNA mis-splicing for obesity-associated diseases therapies
obesity 1696 pathophysiological conditions of obesity. The potential of targeting the alternative mRNA mis-splicing for obesity -associated diseases therapies will also be discussed.1. IntroductionAlternative mRNA splicing plays
obesity 6296 metabolic diseases, especially for diabetes and cardiovascular problems. The major changes associated with obesity include positive energy balance and activation of immune system [[24]]. As alternative mRNA splicing
obesity 6507 tightly regulated by signaling pathway to cope with the physiological changes [[23]], diet-induced obesity model can be applied in the investigations of the significance of alternative mRNA splicing in the pathogenesis
obesity 6630 applied in the investigations of the significance of alternative mRNA splicing in the pathogenesis of obesity . Indeed, significant changes in the expression level of splice variants and splicing factors in association
obesity 7521 of the expression level and activity of those splicing factors as potential therapeutic targets for obesity -associated metabolic complications will also be discussed.2. Mis-Splicing of Metabolic Factors in Obesity2.1.
obesity 11592 pathological condition of obese subjects are required.2.2. Leptin ReceptorLeptin receptor (also known as obesity receptor, Ob-R) is expressed in several isoforms by alternative mRNA splicing (Figure 2) [[47]]. According
obesity 12221 OB-Rb is the only isoform that can fully activate signal transduction. The development of the early obesity phenotype in db/db mice is due to the lacking of Ob-Rb [[49]].The short leptin isoforms include Ob-Ra,
obesity 20769 subjects [[28]]. Sfrs10 heterozygous mice were generated to explore the role of RNA splicing factor in obesity -related lipogenesis. Interestingly, LPIN1 is a splicing target of SFRS10. Reduced SFRS10 favors the
obesity 22363 subjects [[29],[81],[82]]. Further investigation on the dysregulation of splicing machinery components of obesity may provide novel diagnostic and therapeutic tools for this pandemic non-communicable disease.3.1. RNA
obesity 25915 NOVA deficiency [[29]].Targeting thermogenesis in adipose tissues is a potential strategy treating obesity [[87],[88],[89]]. Adipocytes deficient in the NOVA splicing factors displayed increased thermogenesis
obesity 28480 [[98]]. It is interesting to explore whether metformin can also fix the pathological mis-splicing in obesity .In the previous section, we discussed the importance of lamin A/C mRNA level in energy metabolism [[72],[74]].
obesity 28801 protein activity [[101]]. A small molecule named as ABX300 was identified which can abrogate diet-induced obesity by modulating LMNA isoforms via serine and arginine rich splicing factor 1 (SRSF1) in HFD-fed mice [[102]].
obesity 29766 SRSF1 are 100% identical, it is interesting to explore the translational potential of ABX300 in anti- obesity treatment.Alternative splicing is regulated by differential splicing factors binding to cis-acting sequences
obesity 39552 oxygen consumption and heat productionIncreased insulin sensitivityIncreased lipid consumption and obesity -resistant metabolic phenotype[[64]]NCoR ID : contains only 1 RID–N1 and thus would be unable to interact
progeria 17989 several diseases called laminphathies (e.g., Emery-Dreifuss Muscular dystrophy and Hutchison-Gilford progeria syndrome) [[70]]. It was proposed that abnormalities in nuclear structure caused increased susceptibility

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