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At least 415 records · Page 23Linked to original sources
PubMed2006

Syndromic obesity and diabetes: changes in body composition with age and mutation analysis of ALMS1 in 12 United Kingdom kindreds with Alstrom syndrome.

CONTEXT: Alström syndrome (AS) is a monogenic form of infancy-onset obesity and insulin resistance, caused by ALMS1 mutations. The natural history of the insulin resistance is unknown, in particular how this relates to changes in body composition. It is also unclear how ALMS1 mutations relate to the characteristic phenotype. OBJECTIVES: Our objectives were to characterize body composition and metabolic parameters, to establish ALMS1 mutation spectrum of United Kingdom AS patients, and to determine whether a genotype-phenotype correlation exists. DESIGN AND PATIENTS: We conducted a cross-sectional cohort study of 12 unrelated subjects with AS. Age-standardized body composition was assessed by anthropometry and dual-energy x-ray absorptiometry and insulin sensitivity by homeostasis model assessment. The exons and intron-exon boundaries of ALMS1 were directly sequenced. SETTING: The study was performed during the annual Alström Syndrome UK multidisciplinary screening clinic. RESULTS: AS patients have early-onset obesity, but body mass index, waist circumference, and body fat from dual-energy x-ray absorptiometry were negatively correlated with age (r = -0.37, P = 0.2; r = -0.84, P = 0.002; and r = -0.6, P = 0.05). Despite this, insulin resistance increased, demonstrated by raised fasting insulin and fall in homeostasis model assessment insulin sensitivity with age (r = -0.64, P = 0.02). ALMS1 mutations were identified in 10 of 12 patients, with a potential founder mutation in exon 16 present in five [np 10775del (C); Del3592fs/ter3597]. No genotype-phenotype correlation was observed. CONCLUSIONS: We identified mutations in ALMS1 in more than 80% of patients with no genotype-phenotype correlation. In AS, severe childhood obesity, waist circumference, and body fat decrease with age, whereas insulin resistance increases. The abdominal obesity, insulin resistance, diabetes, hypertriglyceridemia, and hypertension suggest that AS could represent a monogenic model for the metabolic syndrome.

Absorptiometry, Photon↗
PubMed2005

Polymorphisms of the CLCN7 gene are associated with BMD in women.

UNLABELLED: Here we show that a common polymorphism causing a valine to methionine amino acid substitution at codon 418 (V418M) in the CLCN7 gene is associated with femoral neck BMD in women. Our study adds to accumulating evidence that shows that common allelic variants in monogenic bone disease genes often contribute to BMD regulation in normal subjects. INTRODUCTION: The CLCN7 gene is a strong candidate for regulation of BMD, because mutations in CLCN7 cause some forms of osteopetrosis, a disease characterized by impaired osteoclast function and increased BMD. In this study, we sought to determine whether common allelic variation within CLCN7 was associated with BMD in the normal population. MATERIALS AND METHODS: We conducted mutation screening of the exons and intron-exon boundaries in CLCN7 by DNA sequencing in 50 normal subjects. We conducted an association study between common polymorphisms in CLCN7 and haplotypes defined by these polymorphisms and BMD values at the lumbar spine and femoral neck in a population-based cohort study of 1077 Scottish women 45-55 years of age. RESULTS: We identified 24 polymorphisms, but most were rare and only 4 had allele frequencies of >5%. These were a conservative single nucleotide polymorphism (SNP) in exon 1 (rs3751884), a 50-bp tandem repeat polymorphism within intron 8, and two SNPs within exon 15 (rs12926089 and rs12926669), of which one (rs12926669) predicts an amino acid change from valine to methionine at codon 418 (V418M). The exon 15 SNPs were in strong linkage disequilibrium and were both associated with femoral neck BMD (p = 0.001-0.003). None of the other polymorphisms were associated with BMD, and long-range haplotypes showed a much weaker association with BMD than the exon 15 SNPs. The V418M polymorphism was an independent predictor of femoral neck BMD on multiple regression analysis accounting for 1% of the variance in BMD at this site. CONCLUSIONS: Our study indicates that the V418M polymorphism of CLCN7 contributes to the genetic regulation of femoral neck BMD in women and adds to accumulating evidence that indicates that subtle polymorphic variation in genes that cause monogenic bone diseases also contribute to regulation of BMD in normal subjects.

Adult↗
PubMed2004

Lipid disorders and mutations in the APOB gene.

BACKGROUND: Plasma lipoproteins are important determinants of atherosclerosis. Apolipoprotein (apo) B is a large, amphipathic glycoprotein that plays a central role in human lipoprotein metabolism. Two forms of apoB are produced from the APOB gene by a unique posttranscriptional editing process: apoB-48, which is required for chylomicron production in the small intestine, and apoB-100, required for VLDL production in the liver. In addition to being the essential structural component of VLDL, apoB-100 is the ligand for LDL-receptor-mediated endocytosis of LDL particles. CONTENT: The study of monogenic dyslipidemias has revealed important aspects of metabolic pathways. In this review, we discuss the regulation of apoB metabolism and examine how APOB gene defects can lead to both hypo- and hypercholesterolemia. The key clinical, metabolic, and genetic features of familial hypobetalipoproteinemia and familial ligand-defective apoB-100 are described. SUMMARY: Missense mutations in the LDL-receptor-binding domain of apoB cause familial ligand-defective apoB-100, characterized by hypercholesterolemia and premature coronary artery disease. Other mutations in APOB can cause familial hypobetalipoproteinemia, characterized by hypocholesterolemia and resistance to atherosclerosis. These naturally occurring mutations reveal key domains in apoB and demonstrate how monogenic dyslipidemias can provide insight into biologically important mechanisms.

Apolipoproteins B↗
PubMed2000

Estimation of penetrance from twin data.

A simple method for estimating the gene frequency p and the penetrance value K from data on polymorphic monogenic characteristics on monozygotic twin pairs is presented. In spite of the method here presented having limited value because the results it yields cannot be evaluated on their own, the estimates of p and K it provides can be indirectly tested by comparing them to the ones obtained in familial aggregates through classical segregation analysis or by using the latter to calculate the expected proportions of dominant-dominant, dominant-recessive and recessive-recessive monozygotic twin pairs. When the method is applied to data on tongue-rolling ability published in the literature, a good agreement is observed between twin and familial estimates, thus indicating that the method is reliable and that it can be used as an ancillary way of corroborating or otherwise evidence of monogenic autosomal dominant mechanism inferred from the analysis of familial data.

Chromosome Segregation↗
PubMed2026

Preimplantation genetic testing for concurrent Meckel Syndrome and hereditary breast cancer in a Chinese family harboring a novel NPHP3 pathogenic variant and a canonical BRCA2 frameshift variant.

Meckel syndrome (MKS) is a lethal autosomal recessive disease with high phenotypic and genetic heterogeneity. Defects in NPHP3 cause MKS type 7. Herein, we report a case of a Chinese family with a newborn male proband presenting with occipital encephalocele and polycystic kidneys. Whole-exome sequencing was performed on genomic DNA extracted from peripheral blood. Potential variants were assessed for pathogenicity. Two compound heterozygous variants of NPHP3 (c. 950T>C, p. Phe317Ser, and c.2694-2_2694-1delAG) were identified, which were inherited from both parents, with c.950T>C representing a novel variant. Two BRCA2 variants (c.5576_5579delTTAA, p. Ile1859Lysfs*3, and c.9357A>C,p. Leu 3119 Phe) were identified, which were inherited from the father. After the proband was diagnosed with MKS7, the couple chose preimplantation genetic testing for monogenic disorders (PGT-M) to simultaneously prevent the transmission of NPHP3 and BRCA2 pathogenic variants, leading to a successful pregnancy. Our study expands the NPHP3 variant spectrum and contributes to the molecular diagnosis and genetic counseling of MKS. This case indicates that PGT-M is a viable option for NPHP3-related MKS and BRCA-positive patients to avoid transmission while maintaining their families. Successful application of PGT-M provides a potential approach for treating other monogenic diseases.

Journal Article↗
PubMedDate not supplied

Hereditary ataxia in the Jack Russell Terrier--clinical and genetic investigations.

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.

Animals↗
PubMed2002

Maturity-onset diabetes of the young caused by a balanced translocation where the 20q12 break point results in disruption upstream of the coding region of hepatocyte nuclear factor-4alpha (HNF4A) gene.

Monogenic human disorders have been used as paradigms for complex genetic disease and as tools for establishing important insights into mechanisms of gene regulation and transcriptional control. Maturity-onset diabetes of the young (MODY) is a monogenic dominantly inherited form of diabetes that is characterized by defective insulin secretion from the pancreatic beta-cells. A wide variety of mutation types in five different genes have been identified that result in this condition. There have been no reports of a chromosome deletion or translocation resulting in MODY. We report a pedigree where MODY cosegregates with a balanced translocation [karyotype 46, XX t(3;20) (p21.2;q12)]. The chromosome 20 break point, 20q12, is within the region of one of the known MODY genes, hepatocyte nuclear factor-4alpha (HNF4A). Fluorescence in situ hybridization analysis demonstrated that the break point does not disrupt the coding region of this gene, but it lies at least 6 kb upstream of the conventional promoter (P1). We propose that this mutation disrupts the spatial relationship between the recently described alternate distal pancreatic promoter (P2) and HNF4A. This is the first case of MODY due to a balanced translocation, and it provides evidence to confirm the crucial role of an upstream regulator of HNF4A gene expression in the beta-cell.

Adolescent↗
PubMed2001

Heritability estimations for diseases, coat color, body weight, and height in a birth cohort of Boxers.

OBJECTIVE: To obtain heritability estimates for diseases and characteristics in Boxers. ANIMALS: Birth cohort of 2,929 purebred Boxers from 414 litters. PROCEDURE: Heritability estimates were determined for cheiloschisis-palatoschisis, cryptorchidism, epilepsy, stifle disorders, cardiac disorders, coat color, birth weight, and adult weight, and height. Binary traits were analyzed by use of a mixed-effects probit model. Some traits also were analyzed by use of a model that postulated monogenic inheritance. Full pedigree analyses were performed. Variation in incidences of disease among clusters of related dogs was evaluated. RESULTS: Heritability estimates were virtually zero for cardiac disorders, medium (0.17 to 0.36) for most other traits, and high (> 0.55) for coat color, birth weight, and adult height. Litter effects and risk factors affected cheiloschisis-palatoschisis, heart murmur, coat color, broadly defined epilepsy, and adult weight. Litter effects may be attributable to common environmental effects for littermates but also may be attributable to dominance variation caused by a recessive gene. Heritability estimates increased when stricter definitions for epilepsy and stifle disorders were used. The monogenic model did not reveal higher heritability estimates for 6 traits analyzed. Incidences for white coat differed significantly for 10 familial clusters, confirming high heritability and effects of familial lineage. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that genetic improvement of most traits should be feasible, except for cardiac disorders. However, because most traits are influenced by environmental effects as well as genetic effects, genetic counseling based on polygenic inheritance and use of familial information rather than strict exclusion of parents is preferred.

Animals↗
PubMedDate not supplied

Human cytochromes P-450.

Studies in vivo have provided evidence for a multiplicity of cytochromes P-450 in man, some of which are under independent monogenic control. Although the activity of cytochromes P-450 in man are generally lower than those of rat, this is by no means always the case. There are several important exceptions including the N-hydroxylation of 2-acetamidofluorene. Studies in vitro by a number of different techniques have confirmed the evidence from studies in vivo that there are multiple forms of human cytochrome P-450. In addition to differences in Vmax, the different forms of cytochrome P-450 may also exhibit marked differences in their apparent Km values. The implications that this may have for pharmacokinetics and toxicology are discussed. The polymorphism in the 4-hydroxylation of debrisoquine observed in vivo has been shown to be due to a defect in a specific form of cytochrome P-450 which appears to be under monogenic regulation. Cross-inhibition studies have enabled the specificity of this isozyme to be characterized. Such studies have also enabled the contribution of this isozyme of cytochrome P-450 to the oxidation of other substrates to be determined. Compounds investigated include bufuralol and phenytoin. Evidence from studies both in vivo and in vitro suggest that selective induction of different forms of cytochrome P-450 can occur in man. However, the number of different classes of inducer in man is not yet known. Human cytochromes P-450 have been purified to near homogeneity in several laboratories. Different forms of cytochrome P-450 purified from the same liver sample vary in molecular weight, chromatographic characteristics and substrate specificities.

Cytochrome P-450 Enzyme System↗
PubMed1996

[The mechanisms of aging and perspective for elimination of deleterious effects].

Genetic programs and age-dependent changes in DNA and protein are involved in aging. The genetic program governs body weight, longevity, aging rate, sex-maturating period and metabolic rate in mammals, and such a number of life history variables are highly correlated with body size. Monogenic age-1 and daf-2 C. elegans mutants extend life span twice. However, human monogenic progeroids shorten lifespan. The Werner syndrome gene was mapped in 8p12. Mutations in the Cockayne syndrome genes (the CSA and CSB genes acting for preferential repair of active genes by interacting with transcription factor TFIIH) and in the ataxia telangictasia gene ATM (homologous with PI-3 kinase for signal transduction) have been disclosed. All such findings suggest a strong basis for the genetic program of aging. In addition, recent evidence indicates that genetic instability, such as telomere loss, somatic and mitochondrial DNA mutations, increases with age. In addition, amounts of carbonylated protein also increase during human aging, and greatly increase in an SOD-deficient C. elegans mutant, but to a less extent in long-living age-1. Therefore, the aging process involves gene action, genetic instability and protein oxidation. Dietary restriction and elimination of deleterious excessive reactive oxygen species may improve many abnormalities due to aging.

Aging↗
PubMed1999

Evidence for a third genetic locus causing familial hypercholesterolemia. A non-LDLR, non-APOB kindred.

Monogenically inherited hypercholesterolemia is most commonly caused by mutations at the low density lipoprotein receptor (LDLR) locus causing familial hypercholesterolemia (FH) or at the apolipoprotein B (APOB) locus causing the disorder familial defective apoB (FDB). Probands from 47 kindreds with a strict clinical diagnosis of FH were selected from the Cardiovascular Genetics Research Lipid Clinic, Utah, for molecular genetic analysis. Using a combination of single-strand conformation polymorphism (SSCP) and direct sequencing, 12 different LDLR gene mutations were found in 16 of the probands. Three of the probands were carriers of the APOB R3500Q mutation. In five of the remaining 28 pedigrees where no mutation had been detected, samples from enough relatives were available to examine co-segregation with the LDLR region using the microsatellite marker D19S221, which is within 1 Mb centromeric of the LDLR locus, and D19S394, sited within 150 kb telomeric of the LDLR locus. In four of the families there was strong evidence for co-segregation between the LDLR locus and the phenotype of hypercholesterolemia, but in one large family with 18 living affected members and clear-cut bimodal hypercholesterolemia, there were numerous exclusions of co-segregation. Using length polymorphic markers within and outside the APOB gene, linkage of phenotype in this family to the APOB region was similarly excluded. In this large family, the degree of hypercholesterolemia, prevalence of tendon xanthomata, and occurrence of early coronary disease were indistinguishable from the other families studied. In summary, the data provide unequivocal evidence that a third locus can be etiological for monogenic familial hypercholesterolemia and should be reinvigorating to research in this field.

Adolescent↗
PubMed1999

Gene defects in idiopathic epilepsy.

Idiopathic epilepsies are mainly due to genetic factors. In most cases the mode of inheritance is either oligogenic or multifactorial. Only a few rare idiopathic epilepsies are single gene disorders. Monogenic epilepsies offer the chance to identify genes/gene families which might also be involved in the aetiology of common forms of the disease. The genetic basis of two monogenic epilepsies have recently been identified: autosomal dominant nocturnal frontal lobe epilepsy and benign familial neonatal convulsions.

Chromosomes, Human, Pair 20↗
PubMed2000

Diagnosis, management and prevention of the common dyslipidaemias in South Africa--clinical guideline, 2000. South African Medical Association and Lipid and Atherosclerosis Society of Southern Africa Working Group.

The optimum management of dyslipidaemia requires a comprehensive, diagnostic work-up. This, minimally, includes: Characterisation of any hyperlipidaemic disorder present. Identification of additional risk factors so as to assess overall (global) risk of future coronary heart disease (CHD). The global risk is best assessed by a calculation combining the risk factors in the individual. In severe monogenic dyslipidaemias and in patients with confirmed pre-existing CHD the risk is usually high; in most such cases the use of lipid-modifying drugs (LMDs) is indicated. Assessment of psychosocial, economic and educational factors relevant to management. Prevention and cost-effective management of even moderately dyslipidaemic patients require appropriate modification of lifestyle: avoidance of tobacco smoking, participation in regular exercise, and a health-promoting diet. Depending on individual circumstance, vigorous, personalised intervention and expert assistance from dieticians, biokineticists and other health care personnel may determine success. The correct choice of patient for drug treatment is a key therapeutic decision and is best done after full lifestyle modification. Recent evidence confirms that appropriately prescribed LMD therapy can lower morbidity and mortality from CHD as well as all-cause mortality. Patients with the following features are candidates for LMD therapy: have clinical CHD and a low-density lipoprotein cholesterol (LDLC) level > 3.0 mmol/l despite optimum non-pharmacological intervention, or suffer from familial hypercholesterolaemia (FH) or equivalent severe, monogenic disorder, or have a 10-year risk of an acute clinical coronary event of > 20% (or > 30% risk if extrapolated to the age of 60 years) owing to the presence of the hyperlipidaemia alone or in combination with contributory risk factors. The ideal target LDLC concentration is < or = 3 mmol/l, but a reduction of at least 45% should be regarded as a minimum target in severe cases who do not reach this goal. Successful therapy requires on-going attention to compliance, therapeutic response and side-effects, and may necessitate adjustment or reinforcement. Concurrent or contributory conditions, such as smoking, hypertension and diabetes mellitus, must also be treated along with the clinically manifest CHD. Severely hyperlipidaemic, complicated or unresponsive high-risk cases should be referred to an appropriate specialist or lipid clinic. Prevention of CHD in the community should be encouraged through public and professional education, the provision of community facilities for exercise and recreation, and legislation directed at reducing the use of tobacco products and ensuring the appropriate labelling of food products.

Cholestyramine Resin↗
PubMed2001

Molecular genetics of salt-sensitivity and hypertension.

For the past decade, hypertension research has shifted strongly in the direction of molecular genetics. The success stories are the monogenic hypertensive syndromes. Classic linkage analyses have located the responsible genes for glucocorticoid-remediable aldosteronism, Liddle syndrome, and apparent mineralocorticoid excess. Furthermore, a recent gain-of-function mutation has recently been described in the gene for the mineralocorticoid receptor. These genes have been cloned and their functions elucidated. Other monogenic syndromes are currently being intensively studied. However, in the area of primary hypertension, the successes have relied on the candidate gene approach. Allelic variants in the genes for angiotensinogen, alpha-adducin, the beta2-adrenergic receptor, the G-protein beta3-subunit, and the T594M mutation in the beta-subunit of the epithelial sodium channel have been identified; however, the importance of these allelic variants to primary hypertension as a whole is not yet clear. Recently, an association approach was employed to implicate the mineralocorticoid receptor gene in salt-sensitivity. Linkage approaches have been attempted and the beta-subunit of the epithelial sodium channel has been linked to hypertension and to blood pressure as a quantitative trait locus. New approaches are necessary to elucidate salt-sensitive hypertension. The analysis of multiple genes simultaneously in terms of a metabolic control analysis may provide a more promising approach.

Genetic Predisposition to Disease↗
PubMed2001

Degradation of mutant proteins, underlying "loss of function" phenotypes, plays a major role in genetic disease.

Many Mendelian monogenic disorders are caused by loss of the function of a single protein. This can result from rapid degradation of the mutant protein by cellular proteases, which reduces the steady-state concentration of the protein within the cell. The susceptibility of a protein to such proteolytic breakdown depends upon its kinetics of monomer folding and oligomer assembly and upon the intrinsic (thermodynamic) stability of its functional native-state conformation. Other cellular proteins, notably molecular chaperones, promote correct protein folding and assembly and thus provide some protection against degradation. An accumulation of recent evidence indicates that premature or accelerated degradation of mutant proteins, provoked by aberrations in their conformation, occurs in various subcellular compartments and represents a significant and prevalent pathogenic mechanism underlying genetic diseases. Inter-individual variability in proteolytic and folding systems can in part explain why "simple monogenic diseases" often display inconsistent genotype-phenotype correlations which show these disorders to be in reality quite complex. Protein folding and degradation may also be modulated artificially using exogenous small molecules. The identification or design of compounds which can interact specifically with particular target proteins, and which in so doing can exert beneficial effects on protein folding, assembly and/or stability, is beginning to open up a new and remarkably promising avenue for the treatment of diverse genetic disorders.

Genetic Diseases, Inborn↗
PubMedDate not supplied

[Application of RAPD for making DNA markers to Vrn genes].

The possibility of using the PCR with arbitrary primers to mark Vrn genes, Vrn3 in particular, was investigated. RAPD-analysis of DNA of near isogenic lines on Vrn1, Vrn2 and Vrn3 loci in genefone of four varieties of winter wheat were carried out. Monogenic dominant lines by Vrn3 locus possessed 657 b.p. polymorphic DNA fragment. The possibility of using this polymorphic DNA amplicon as a molecular marker was confirmed by results of RAPD-analysis of DNA of some commercial wheat varieties of different ecological-geographic origin possessing dominant Vrn3 alleles, as well as by RAPD-analysis of F2 population from cross of monogenic Vrn3 dominant spring line with its recurrent parent--winter wheat variety Mironovskaya 808. The results of RAPD are comparable with hybridological analysis data concerning type of development of plants from F2 population.

Base Sequence↗
PubMed2002

[Specialized genetic counseling in pediatric and adult oncology patients].

Five to ten percent of oncological diseases exhibit monogenic mode of inheritance. They occur as a consequence of the germline mutations of tumor suppressor genes and of the genes engaged in reparative processes. Most common monogenically determined oncological diseases are: AD form of breast and ovarian cancer, hereditary nonpolyposis colorectal cancer (HNPCC, Lynch sy.) and familiar adenomatous polyposis (FAP). The aim of the genetic investigation is to evaluate whether the index family deals with the hereditary form of tumor predisposition, than, if possible, to perform DNA analysis in the family and to propose preventive screening program (methods) for the probands in risk.

Adenomatous Polyposis Coli↗
PubMed2002

[Genetic analysis of mutation sy2 which causes nonhomologous meiotic synapsis in chromosomes of diploid rye Secale cereale L].

Partially nonhomologous (heterologous) synapsis of meiotic chromosomes in a spontaneous desynaptic mutant form of rye is determined by two recessive genes, sy2a and sy2b, that have independent expression and inheritance. The third gene, dominant inhibitor suppressing the mutant phenotype, has been revealed in hybrid combinations between sy2 mutants and lines segregating other meiotic mutants: sy10 (heterologous synapsis), sy1, and sy9 (asynapsis). All three genes determining desynapsis (sy2a, sy2b, and I) were shown to be nonallelic to monogenic mutations sy10, sy1, and sy9, inherited independently of them and expressed at later stages of prophase I than the sy10 gene. The possibility of modifying monogenic segregation of mutation sy2 by gametophyte selection for a locus linked to the gene expressed as sy2 at particular frequencies of recombination between this gene and selected locus is discussed.

Chromosome Pairing↗