The DD genotype of the angiotensin-converting enzyme gene occurs in very low frequency in Australian Aboriginals

Lester, Susan; Heatley, Susan L; Bardy, Peter; Bahnisch, John; Bannister, Kym M.; Faull, Randall J.; Clarkson, A. R.

doi:10.1093/ndt/14.4.887

Cited by 29 publications

(31 citation statements)

References 2 publications

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“…For the distribution of the ACE I/D polymorphism, the D allele frequency of the Koreans in the present study (39.6%) was much lower than that of African Americans (63%) 11 and Caucasians (64%), 39 but was higher than that of Australian Aborigines (12.6%) 40 and Amerindians (26.5%), 41 and similar to those described for Chinese Han (38%) 42 and mainland Japanese populations (40%). 17 Several reports have shown that ACE I/D polymorphism accounts for half of the variance of plasma ACE levels in the RAAS pathway.…”

Section: Discussionsupporting

confidence: 82%

Interaction between GNB3 C825T and ACE I/D polymorphisms in essential hypertension in Koreans

et al. 2006

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Essential hypertension (EH) is considered a typical polygenic disease, so the evaluation of gene-gene interactions rather than the determination of single gene effects is crucial to understanding any genetic influences. The G-protein b3-subunit (GNB3) 825T allele, associated with enhanced G-protein signalling, is a strong candidate for interactions with polymorphisms, such as insertion/deletion (I/D) polymorphism of angiotensin I-converting enzyme (ACE) gene. We investigated whether there is an association between GNB3 C825T and ACE I/D polymorphisms for the development of EH. We carried out a case-control study of 688 hypertensive and 924 normotensive subjects recruited from South Korea. The GNB3 C825T and ACE I/D genotypes were determined by polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism methods, respectively. The distributions of alleles and genotypes for the GNB3 C825T and ACE I/D polymorphisms were not found to be significantly associated with hypertensive status in either males or females. Logistic regression analysis indicated that the GNB3 825T allele carriers were positively associated with EH in males (odds ratio (OR) for TT/CT, 1.459; 95% confidence interval (CI), 1.048-2.033, P ¼ 0.0255). In analysis of gene-gene interaction, we found that there was a significant interaction between the GNB3 825T and ACE D alleles (Po0.05). OR for EH was significantly higher in 825T allele carriers with ACE D allele (OR, 1.490; 95% CI, 1.117-1.987, P ¼ 0.0067). A significant interaction between the GNB3 825T and the ACE D alleles may contribute to the predisposing effect for the development of EH in Koreans.

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Section: Discussionsupporting

confidence: 82%

Interaction between GNB3 C825T and ACE I/D polymorphisms in essential hypertension in Koreans

et al. 2006

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“…However, others have failed to replicate these associations (Schena, D'Altri, Cerullo, Manno, & Gesualdo, 2001;Schmidt, Schone, & Ritz, 1995). The DD genotype of the ACE gene occurs infrequently in Indigenous Australians (Lester et al, 1999), in whom no significant influence on renal disease has been demonstrated. A recent study in a remote Indigenous Australian community has, however, found an association between a common polymorphism of the p53 gene and proteinuria (McDonald et al, 2002).…”

Section: Genetic Explanationsmentioning

confidence: 99%

Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians

Cass

Cunningham

Snelling³

et al. 2004

Social Science & Medicine

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Indigenous Australians are disadvantaged, relative to other Australians, over a range of socio-economic and health measures. The age-and sex-adjusted incidence of end-stage renal disease (ESRD) -the irreversible preterminal phase of chronic renal failure -is almost nine times higher amongst Indigenous than it is amongst non-indigenous Australians. A striking gradient exists from urban to remote regions, where the standardised ESRD incidence is from 20 to more than 30 times the national incidence. We discuss the profound impact of renal disease on Indigenous Australians and their communities. We explore the linkages between disadvantage, often accompanied by geographic isolation, and both the initiation of renal disease, and its progression to ESRD. Purported explanations for the excess burden of renal disease in indigenous populations can be categorised as:(1) primary renal disease explanations; (2) genetic explanations; (3) early development explanations; and (4) socio-economic explanations.We discuss the strengths and weaknesses of these explanations and suggest a new hypothesis which integrates the existing evidence. We use this hypothesis to illuminate the pathways between disadvantage and the human biological processes which culminate in ESRD, and to propose prevention strategies across the life-course of Indigenous Australians to reduce their ESRD risk.Our hypothesis is likely to be relevant to an understanding of patterns of renal disease in other high-risk populations, particularly indigenous people in the developed world and people in developing countries. Furthermore, analogous pathways might be relevant to other chronic diseases, such as diabetes and cardiovascular disease. If we are able to confirm the various pathways from disadvantage to human biology, we will be better placed to advocate evidence-based interventions, both within and beyond the scope of the health-care system, to address the excess burden of renal and other chronic diseases among affected populations.

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“…Research on 2 different Indigenous Australian populations has indicated that the genetic regulation of both inflammatory pathways and the RAS is dramatically different to that found in Caucasians [24,25] . Recent research investigating SNPs in the RAS has shown that Indigenous Australians have different allele frequencies compared with other populations, and indeed display polymorphisms not seen in other populations [24,26] . In light of this evidence, it is reasonable to suspect that the genetic regulation of RAS and inflammatory activity is different in Indigenous Australians compared with other population groups.…”

Section: Personalised Medicinementioning

confidence: 92%

“…Research in Indigenous people from Western Australia, Central Australia, and the Tiwi Islands has shown that Indigenous Australians are genetically distinct from all other global populations [24,25,31,32] . Therefore, it is expected that if Indigenous people are to enjoy the benefits of pharmacogenomics and personalised medicine, specific genetic research must be undertaken in Indigenous Australian cohorts to identify genetic determinants of disease risk, prognosis, and response to therapy.…”

Section: The Future Of Genetic Research In Indigenous Peoplesmentioning

confidence: 99%

Personalised Medicine: A New Approach to Improving Health in Indigenous Australian Populations

Rae

Grimson

Pringle

2017

Public Health Genomics

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Personalised medicine is a newly emerging field with much to offer to all populations in improved clinical treatment options. Since the 1970s, clinicians and researchers have all been working towards improving the health of Indigenous Australians. However, there has been little research on the impact of genetics on Indigenous health, how genetic and environmental factors interact to contribute to poor health in Indigenous people, and how genetic factors specific to Indigenous people affect their responses to particular treatments. This short review highlights the urgent need for more genetic studies specific to Indigenous people in order to provide more appropriate care and to improve health outcomes. This paper explores why genetic work with Indigenous communities has been limited, how personalised medicine could benefit Indigenous communities, and highlights a number of specific instances in which personalised medicine has been critical for improving morbidity and mortality in other high-risk groups. In order to take the next step in advancing the health of Indigenous peoples, targeted research into the genetic factors behind chronic diseases is critically needed. This research may allow clinicians a better understanding of how genetic factors interact with environmental factors to influence an Indigenous Australian's individual risk of disease, prognosis, and response to therapies. It is hoped that this knowledge will produce clinical interventions that will help deliver clearly targeted, more appropriate care to this at-risk population.

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The DD genotype of the angiotensin-converting enzyme gene occurs in very low frequency in Australian Aboriginals

Abstract: The D allele of the ACE gene has little or no influence on the renal disease of Australian Aboriginals.

Cited by 29 publications

References 2 publications

Interaction between GNB3 C825T and ACE I/D polymorphisms in essential hypertension in Koreans

Interaction between GNB3 C825T and ACE I/D polymorphisms in essential hypertension in Koreans

Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians

Personalised Medicine: A New Approach to Improving Health in Indigenous Australian Populations

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