RGS2 C1114G polymorphism and body weight gain in hypertensive patients

Sartori, Michelangelo; Ceolotto, Giulio; Dorigatti, Francesca; Mos, Lucio; Santonastaso, Massimo; Bratti, Paolo; Papparella, Italia; Semplicini, Andrea; Palatini, Paolo

doi:10.1016/j.metabol.2007.10.021

Cited by 18 publications

(12 citation statements)

References 34 publications

(52 reference statements)

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“…Some factors may potentially interact with bariatric surgery and result in highly variable outcomes in terms of weight loss and glycemic control afterwards. Much obesity research suggests that genes are strongly implicated in obesity and weight gain [17,37,38]. Evidence also shows that genes not only affect weight gain but also interact with other medical factors to influence weight loss and glycemic control [39][40][41][42][43][44].…”

Section: Discussionmentioning

confidence: 99%

ESR1, FTO, and UCP2 Genes Interact with Bariatric Surgery Affecting Weight Loss and Glycemic Control in Severely Obese Patients

et al. 2011

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Section: Discussionmentioning

confidence: 99%

ESR1, FTO, and UCP2 Genes Interact with Bariatric Surgery Affecting Weight Loss and Glycemic Control in Severely Obese Patients

et al. 2011

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“…Human and mouse studies have also implicated RGS2, 4 and 5, in the regulation of body weight and obesity [48], [49], [50], [51]. However these RGS proteins and RGS9 likely regulate body weight through different mechanisms: RGS2, 4 and 5 are members of a different R4 subfamily of RGS proteins, have a different molecular architecture and strikingly different cellular and tissue expression patterns compared to RGS9 [18], [37], [52].…”

Section: Discussionmentioning

confidence: 99%

Association between Regulator of G Protein Signaling 9–2 and Body Weight

et al. 2011

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Regulator of G protein signaling 9–2 (RGS9–2) is a protein that is highly enriched in the striatum, a brain region that mediates motivation, movement and reward responses. We identified a naturally occurring 5 nucleotide deletion polymorphism in the human RGS9 gene and found that the mean body mass index (BMI) of individuals with the deletion was significantly higher than those without. A splicing reporter minigene assay demonstrated that the deletion had the potential to significantly decrease the levels of correctly spliced RGS9 gene product. We measured the weights of rats after virally transduced overexpression of RGS9–2 or the structurally related RGS proteins, RGS7, or RGS11, in the nucleus accumbens (NAc) and observed a reduction in body weight after overexpression of RGS9–2 but not RGS7 or 11. Conversely, we found that the RGS9 knockout mice were heavier than their wild-type littermates and had significantly higher percentages of abdominal fat. The constituent adipocytes were found to have a mean cross-sectional area that was more than double that of corresponding cells from wild-type mice. However, food intake and locomotion were not significantly different between the two strains. These studies with humans, rats and mice implicate RGS9–2 as a factor in regulating body weight.

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“…By contrast, our work has shown that the R44H variant of RGS2, although not compromising stability, did disrupt the amphipathic α-helix that is crucial for proper plasma-membrane targeting and function [38]. Notably, another mutation at the Arg 44 position, R44G, has also been shown to be associated with hypertension and higher than normal BMI (body mass index) [39], perhaps suggesting a link between RGS2 and obesity and the metabolic syndrome. In addition to those changes identified in the coding regions, the promoter region, introns and untranslated regions of RGS2 also contain several SNPs and I/D (insertion/deletion) polymorphisms, of which one has been shown to result in enhanced calcium mobilization in fibroblasts in their response to AngII [40], and one that has been linked to an increase in risk of the metabolic syndrome in white Caucasian Europeans [34].…”

Section: Clinical Hypertension: Implications For Its Association Withmentioning

confidence: 59%

RGS proteins: identifying new GAPs in the understanding of blood pressure regulation and cardiovascular function

Cifelli

Wang

et al. 2009

Clinical Science

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Understanding the mechanisms that underlie BP (blood pressure) variation in humans and animal models may provide important clues for reducing the burden of uncontrolled hypertension in industrialized societies. High BP is often associated with increased signalling via G-protein-coupled receptors. Three members of the RGS (regulator of G-protein signalling) superfamily RGS2, RGS4 and RGS5 have been implicated in the attenuation of G-protein signalling pathways in vascular and cardiac myocytes, as well as cells of the kidney and autonomic nervous system. In the present review, we discuss the current state of knowledge regarding their differential expression and function in cardiovascular tissues, and the likelihood that one or more of these alleles are candidate hypertension genes. Together, findings from the studies described herein suggest that development of methods to modulate the expression and function of RGS proteins may be a possible strategy for the treatment and prevention of hypertension and cardiovascular disease.

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RGS2 C1114G polymorphism and body weight gain in hypertensive patients

Cited by 18 publications

References 34 publications

ESR1, FTO, and UCP2 Genes Interact with Bariatric Surgery Affecting Weight Loss and Glycemic Control in Severely Obese Patients

ESR1, FTO, and UCP2 Genes Interact with Bariatric Surgery Affecting Weight Loss and Glycemic Control in Severely Obese Patients

Association between Regulator of G Protein Signaling 9–2 and Body Weight

RGS proteins: identifying new GAPs in the understanding of blood pressure regulation and cardiovascular function

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