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Biomedical subjects

K Xiang

Publications and source records attributed to K Xiang.

At least 19 recordsLinked to original sources
PubMed2006

Peroxisome proliferator-activated receptor (PPAR) delta genetic polymorphism and its association with insulin resistance index and fasting plasma glucose concentrations in Chinese subjects.

AIMS: Previous studies have shown that the peroxisome proliferator-activated receptor delta (PPARD) genetic polymorphism affects cholesterol metabolism in Whites. This association was not observed in a Korean population in a separate study, but this study showed a link between the PPARD polymorphism and body weight and fasting plasma glucose. The purpose of this study was to determine whether polymorphisms of PPARD influence glucose and cholesterol metabolism in Chinese subjects. We investigated the association between the polymorphism (-87T/C) of the human PPARD gene and phenotypes related to body weight, insulin sensitivity, glucose and lipid metabolism in Chinese subjects. METHODS: Unrelated Chinese subjects (n = 663) in Shanghai were studied; 287 had newly diagnosed Type 2 diabetes mellitus and 376 were non-diabetic control subjects over 40 years old. Clinical parameters were collected and genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: In normal glucose tolerant (NGT) subjects, the C allele carriers had higher fasting plasma glucose concentrations (P = 0.0078) and a lower insulin sensitivity index (ISI) (P = 0.0365). The C allele carriers also showed higher concentrations of low-density lipoprotein cholesterol (P = 0.0261) and percentage of body fat (P = 0.0357). There was a trend towards higher visceral adiposity in C allele carriers, but the difference was not significant (P = 0.0830). In diabetes patients, similar results were detected for plasma glucose concentrations (fasting plasma glucose P < 0.0001, 2-h plasma glucose P = 0.0052) and insulin sensitivity (homeostasis model assessment of insulin resistance P = 0.0094; ISI P = 0.0058). CONCLUSION: The PPARD-87T/C polymorphism is associated with higher fasting plasma glucose concentrations in both NGT and diabetic subjects, largely due to impaired insulin sensitivity.

Blood Glucose↗
PubMed2004

Scanning for MODY5 gene mutations in Chinese early onset or multiple affected diabetes pedigrees.

Mutation of HNF-1beta gene has been reported in early onset diabetes or MODY families and this gene has been defined as MODY5 gene. The aim of our study was to examine whether HNF-1beta mutation contribute to early onset or multiple affected diabetes pedigrees in Chinese. Molecular scanning of HNF-1beta gene promoter region, nine exons and flanking introns was performed in 154 unrelated probands from early onset and multiple affected diabetes Chinese pedigrees. The family members of probands with mutations or variants and 58 nondiabetics were also examined. Clinical examinations of renal morphology, renal function and beta-cell function were performed in the HNF-1beta gene mutation carriers and family members. Mutation of HNF-1beta gene causing the substitution S36F was found in two subjects of an early onset diabetic family. One carrier has early onset diabetes, renal function impairment and renal cyst, while the other has impaired glucose tolerance only. This is the first case of MODY5 gene mutation diabetes found in the Chinese. Three HNF-1beta variants were identified and no significant differences in allele frequencies for these variants were detected between the nondiabetic and diabetic groups. Nucleotide 66 of intron 8 of HNF-1beta gene was G in the Chinese population rather than A as noted in the GenBank sequence. These results suggest that HNF-1beta gene mutations may be associated with nondiabetic renal dysfunction and diabetes in Chinese, but they are responsible for only a small percentage of early onset or multiple affected diabetes pedigrees including MODY.

Adenine↗
PubMed2001

[The impact of calpain-10 gene combined-SNP variation on type 2 diabetes mellitus and its related metabolic traits].

OBJECTIVE: To investigate the impact of calpain-10 gene (CAPN-10) combined single nucleotide polymorphism (SNP) variation on type 2 diabetes mellitus (T2DM) and its related clinical metabolic traits in Chinese. METHODS: The study population consisted of 268 Chinese residents in Shanghai. Among them, 144 were subjects with normal glucose tolerance (NGT) and 124, with T2DM. Plasma glucose (PG), insulin (INS), c-peptide (CP) and free fatty acids (FFA) levels were measured at fasting and 30, 60, 120, and 180 minutes after oral 75 g glucose challenge. The islet beta-cell insulin secretion and tissue insulin sensitivity were assessed. CAPN-10 UCSNP44,-43,-19 and -63 were genotyped. RESULTS: (1) In Chinese NGT subjects, the major allele of UCSNP-44 was allele T (frequency=91%), of UCSNP43 was G(89%), of UCSNP-19 was I (3 repeats of a 32 bp sequence) (67%) and of UCSNP-63 was C allele (79%). Significant differences were observed in comparison of these allele frequencies in Chinese to those in other ethnic groups reported in the literature. (2) 14 genotype combinations of these four SNPs were observed in Chinese NGT subjects. 69% of the NGT population was composed of four genotype combinations, in the order of UCSNP44,-43,-19 and -63, i.e., combination A:TT-GG-DI-CC(haplotype combination was 1121/1111) (frequency=10%), combination B:TT-GA-II-CC(1121/1221)(10%), combination C:TT-GG-II-CC(1121/1121)(26%) and combination D:TT-GG-DI-CT(1121/1112)(22%).(3) The frequencies of the above mentioned SNP in single or in combinations were not different significantly between NGT and T2DM groups. (4) The variation of clinical metabolic parameter levels shifted from completely normal towards abnormal glucose intolerance among genotype combination subgroups. In comparison between combination A and combination D, subjects in the former subgroups had: higher PG levels with delayed peak after glucose challenge; less and lower decrement of FFA levels after challenge with no rising in late stage; higher insulin levels with delayed peak after challenge; and the tendency of decreased insulin sensitivity. More than half of the comparisons remained statistically significant after adjusted with age, gender, body mass index and waist circumference. CONCLUSION: The variation of calpain-10 gene has impact on the variation of clinical metabolic parameter levels related to type 2 diabetes mellitus. Such impact depends upon the haplotypes as well as the haplotype combination of calpain-10 gene variations.

Alleles↗
PubMed2001

[Dyslipidaemia and insulin resistance in Chinese in Shanghai].

OBJECTIVE: To investigate the impact of dyslipidaemia on insulin resistance in Chinese individuals in Shanghai. METHODS: 830 individuals aged over 40 years (male 300, female 530) were divided into normal and dyslipidaemia groups. The latter included 7 subgroups as follows: low high density lipoprotein (L-HDL)-subgroup I, high triglycerides (H-TG)-subgroup II, high total cholesterol or high low density lipoprotein (H-TC/H-LDL)-subgroup III, low high density lipoprotein with high triglycerides (L-HDL + H-TG)-subgroup IV, low high density lipoprotein with high total cholesterol or high low density lipoprotein (L-HDL + H-TC/H-LDL)-subgroup V, high triglycerides with high total cholesterol or high low density lipoprotein(H-TG + H-TC/H-LDL)-subgroup VI, low high density lipoprotein with high triglycerides and high total cholesterol or high low density lipoprotein (L-HDL + H-TG + H-TC/H-LDL)-subgroup VII. Homeostasis model assessment (HOMA) was applied to estimate the degree of insulin resistance (IR). RESULTS: (1) Adjusted with age, sex and body mass index (BMI), HOMA-IR was increased in the dyslipidaemia subgroups with high triglycerides. (2) Hypertriglyceridemia was more closely related to raised BMI and waist-hip ratio (WHR). (3) Both body fat (BMI, WHR) and triglycerides were independent risk factors accounting for HOMA-IR. CONCLUSION: Hypertriglycerides could be regarded as an independent risk factor for insulin resistance.

Adult↗
PubMed2000

Gene regulatory networks generating the phenomena of additivity, dominance and epistasis.

We show how the phenomena of genetic dominance, overdominance, additivity, and epistasis are generic features of simple diploid gene regulatory networks. These regulatory network models are together sufficiently complex to catch most of the suggested molecular mechanisms responsible for generating dominant mutations. These include reduced gene dosage, expression or protein activity (haploinsufficiency), increased gene dosage, ectopic or temporarily altered mRNA expression, increased or constitutive protein activity, and dominant negative effects. As classical genetics regards the phenomenon of dominance to be generated by intralocus interactions, we have studied two one-locus models, one with a negative autoregulatory feedback loop, and one with a positive autoregulatory feedback loop. To include the phenomena of epistasis and downstream regulatory effects, a model of a three-locus signal transduction network is also analyzed. It is found that genetic dominance as well as overdominance may be an intra- as well as interlocus interaction phenomenon. In the latter case the dominance phenomenon is intimately connected to either feedback-mediated epistasis or downstream-mediated epistasis. It appears that in the intra- as well as the interlocus case there is considerable room for additive gene action, which may explain to some degree the predictive power of quantitative genetic theory, with its emphasis on this type of gene action. Furthermore, the results illuminate and reconcile the prevailing explanations of heterosis, and they support the old conjecture that the phenomenon of dominance may have an evolutionary explanation related to life history strategy.

Epistasis, Genetic↗
PubMed2000

[The association between A55V variant in UCP2 gene and body fat distribution, serum lipid profile in Chinese].

OBJECTIVE: Uncoupling protein 2(UCP2) could play an important role in energy metabolism and body weight regulation. The aim of this study was to investigate Ala55Val(A55V) variant in the UCP2 gene has effects on serum lipid profile, body fat and its distribution in Chinese. METHODS: The genotypes of A55V variant in the UCP2 gene were determined by a PCR-RFLP assay in 359 unrelated Chinese [including 193 normal glucose tolerance(NGT) and 166 type 2 diabetic subjects by ADA 97' criteria]. The parameters for regional adipose tissue distribution were measured by magnetic resonance imaging(MRI). RESULTS: In NGT group, an association between A55V variant in the UCP2 gene and body mass index(BMI) (P=0.0246), as well as femoral subcutaneous adipose tissue area (FA) (P=0.0017), was noted in females. A55V variant in the UCP2 gene was also associated with serum triglyceride (TG) level (P=0.0072) in males. However, in type 2 diabetes group, an association between A55V variant in the UCP2 gene and FA (P=0.0150) was replicated in females too. Those females who were homozygotes of AA in the UCP2 gene had decreased FA not only in NGT group but also in type 2 diabetes group. Furthermore, logistic regression analysis indicated that FA (P=0.0098 in NGT females, P=0.0071 in type 2 diabetic females) and BMI (P=0.0016 in NGT females), as well as TG level (P=0.0040 in NGT males) were associated with this variant in the UCP2 gene. CONCLUSION: A55V variant in the UCP2 gene is associated not only with FA (in NGT females and type 2 diabetic females) but also with BMI (in NGT females). Therefore A55V variant in the UCP2 gene appears to play a role in body fat and its distribution in Chinese females.

Adipose Tissue↗
PubMed2000

Relationship between the renin-angiotensin system genes and diabetic nephropathy in the Chinese.

OBJECTIVE: To clarify whether genetic variants of the renin-angiotensin system (RAS) contribute to the development of diabetic nephropathy (DN) in the Chinese. METHODS: Totally 173 Chinese subjects of Han nationality from Shanghai were classified into! control, DN (-) and DN (+) groups. The latter was subdivided according to diabetic duration at the onset of DN and the stage of DN. Genotyping of five polymorphic sites in four key genes of the RAS: the AGT-T174M, AGT-M235T and AGTR1 genotypes were determined by PCR/restriction enzyme digestion. The insertion/deletion (I/D) and [ACAC] n-STR microsatellite polymorphic markers were used for ACE and REN genotyping, respectively. Statistical analysis showed comparisons of gene frequencies between any two groups were made with Fisher's exact test or Chi-square test. Logistic regression analysis was performed to identify predictors of DN. RESULTS: The frequencies of ACE-DD genotype and ACE-D allele were much higher in DN(+) group than in DN (-) group (0.25 vs 0.05, 0.47 vs 0.29, respectively), so were the frequencies of TT genotype and T allele in AGT-M235T (0.73 vs 0.54, 0.85 vs 0.68, respectively). DN (+) DUR < 5 years group had greatly increased frequencies of AGT-M235T allele and ACE-DD genotype in comparison with DN(-) group (0.92 vs 0.68 and 0.28 vs 0.05, respectively). Logistic regression analysis further identified these two genes as contributing factors to DN. Although AGTR1 and AGT-T174M genotyping analysis revealed differences in frequency distribution between DN (+) and DN (-) or control groups, logistic regression analysis failed to implicate them in the development of DN. CONCLUSIONS: Our study revealed RAS genes, ACE and AGT-M235T but not AGT-T174M, AGTR1 or REN genotypes, as contributing factors for DN in type 2 diabetes mellitus in Chinese.

Aged↗
PubMed1999

The impact of codon 54 variation in intestinal fatty acid binding protein gene on the pathogenesis of diabetes mellitus in Chinese.

OBJECTIVE: To investigate whether or not the intestinal fatty acid binding protein gene (FABP2)-Ala54Thr variation is related to non-insulin dependent diabetes mellitus (NIDDM), obesity, dyslipidemia and glucose stimulated insulin secretion (GSIS) in Chinese. METHODS: The FABP2-Ala54Thr variation was detected by PCR/Hhal digestion in 231 Chinese subjects (116 with normal glucose tolerance (NGT), 54 with impaired glucose tolerance (IGT) and 61 with NIDDM). Plasma glucose, insulin and C-peptide levels before and after 75 g glucose load as well as fasting lipid profile were determined. RESULTS: (1) The Ala54 and Thr54 allele frequencies in Chinese were 0.71 and 0.29 respectively; (2) The FABP2-Ala54Thr variation was neither associated with fasting and post-challenged plasma glucose levels nor with NIDDM; (3) This variation was neither associated with fasting lipid profile nor with obesity; (4) The IGT subjects with genotype Thr54(+) (Thr54 homozygotes and heterozygotes) had lower fasting, 2-hour and total C-peptide levels and smaller AUC representing lesser C-peptide secretion after glucose challenge than those with genotype Thr54(-) (Ala54 homozygotes) (P = 0.04, 0.03, 0.01 and 0.01 respectively). The serum insulin levels changed in the same tendency. CONCLUSIONS: The glucose stimulated insulin secretion (GSIS) reserve of islet beta-cells is more limited in subjects with FABP2-Thr54(+) genotype than in those with FABP2-Thr54(-) genotype. It suggests that FABP2-codon 54 variation might contribute to the insufficient insulin secretion in the development of NIDDM in Chinese.

Alanine↗
PubMed1999

[The mechanism of tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance by variation in promoter region of TNF-alpha gene].

OBJECTIVE: To investigate the relationship between the G to A variant at the--308 bp of the promoter region of tumor necrosis factor-alpha gene (TNF-alpha-P) and the body adiposity, the insulin secretion and action, and the glucose and lipid levels in Chinese population. METHOD: 359 Chinese were genotyped for the TNF-alpha-P by using PCR/Nco I digestion. Fasting blood lipid profile and the levels of plasma glucose (PG), insulin (INS), c-peptide (CP) and the free fatty acids (FFA) at 0, 1/2, 1, 2 and 3 hours after glucose challenge were measured. RESULTS: Genotype frequencies of TNF-alpha-P were not associated with diabetes and obesity. The genotype frequency of the G/A heterozygotes was significantly increased in non-diabetic subgroups with less decreased levels of 2 h-FFA and AUC-FFA after glucose challenge (Fisher exact P = 0.002 and 0.041 respectively). The FFA levels in non-diabetics with G/A heterozygotes were higher than those with G/G homozygotes, especially in the comparisons of the 2 h and 3 h FFA levels after glucose challenge (P = 0.029 and 0.030 respectively). Similar tendency was also observed in diabetics. CONCLUSION: Circulation FFA level reflects the degree of lipolysis in adipose tissue. The difference in the degree of lipolysis led by the variant of the promoter region of TNF-alpha may be one of the mechanisms for the variation in the degree of insulin resistance in general population.

Adult↗
PubMed1999

[Association of Gln223Arg variant in leptin receptor gene with metabolic abnormalities and hypertension in type II diabetes mellitus in Shanghai "Han" population].

OBJECTIVE: To investigate the association of Gln223Arg variant in leptin receptor gene with metabolic abnormalities and hypertension in type II diabetes mellitus. METHODS: The genotypes of Gln223Arg variant in leptin receptor gene were determined by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) assay in 359 unrelated subjects of Shanghai "Han" population (including 193 subjects with normal glucose tolerance and 166 type II diabetic patients). The clinical data were also analyzed. The parameters for regional adipose tissue distribution were measured by magnetic resonance imaging (MRI). RESULTS: Significant difference of genotype frequency of Gln223Arg variant in leptin receptor gene was observed between hypertensive and normotensive type II diabetic male patients (P = 0.008). "A" allele was associated with increased systolic blood pressure (P = 0.0026) and diastolic blood pressure (P = 0.0084) in type II diabetic male patients. Logistic regression analysis showed that this gene variant was an independent risk factor of type II diabetic male patients accompanied with hypertension (P = 0.0031), and it was associated with elevation of systolic blood pressure (P = 0.0054). The odds ratio of hypertension in type II diabetic male patients with "A" allele was 2.825 (95% CI 1.418, 5.627). CONCLUSION: Gln223Arg variant in leptin receptor gene is associated with hypertension in type II diabetic male patients, especially with elevation of systolic blood pressure.

Adult↗
PubMed1998

[Effects of Trp64Arg mutation in the beta 3-adrenergic receptor gene on body fat, plasma glucose level, lipid profile, insulin secretion and action in Chinese].

OBJECTIVE: To ascertain the association of the Trp64Arg mutation in the beta 3-adrenergic receptor (ADRB3) gene with the total body fat and fat distribution, plasma glucose level, lipid profile, insulin secretion and action in Chinese. METHODS: Genotyping of the Trp64Arg mutation in the ADRB3 gene as well as measurment of clinical variables body mass index(BMI), percent of desirable weight(PDW), area of regional adipose tissue depots, fasting lipid profile, and also, plasma glucose, insulin, C-peptide, free fatty acids levels before and after glucose challenge and blood pressure were performed in 308 Chinese, of whom, 161 were nondiabetics and 147, type 2 diabetic subjects. RESULTS: (1) The frequency of Arg64 allele of ADRB3 gene in Chinese was similar to that in Japanese but slightly higher than that in Caucasians. (2) No association of any of the clinical varaibles with Trp64Arg mutation was observed in nondiabetics. (3) The Trp64Arg mutation in the ADRB3 gene was associated with BMI(P=0.019), PDW(P=0.001) and waist circumference (P=0.045) in type 2 diabetic subjects. In female diabetic subjects, more significant association with BMI(P=0.001), PDW(P=0.001), waist circumference(P=0.023), and also, association with abdominal and femoral subcutaneous fat area(P=0.032 and P=0.023) were observed. The frequencies of Arg64 allele were 21%, 14% and 4% in female diabetics with obesity, over-weight and normal-weight respectively (P=0.026). Logistic regression analysis showed that BMI was the only independent clinical variable related to the Trp64Arg mutation in the ADRB3 gene (P=0.0027). CONCLUSION: The Trp64Arg mutation in ADRB3 gene contributes to the variation of total body fat in Chinese type 2 diabetic subjects.

Adipose Tissue↗
PubMed1998

[The relationship between angiotensin II type 1 receptor gene and coronary heart disease, hypertension and diabetes mellitus in Chinese].

OBJECTIVE: To ascertain whether the angiotensin II type 1 receptor (AGTR1) gene is associated with coronary heart disease (CHD), hypertension (HTN) and non-insulin-dependent diabetes mellitus (NIDDM) in Chinese and to observe the interaction of AGTR1 gene and angiotensin I converting enzyme(ACE) gene to the development of the associated disease in Chinese. METHODS: 270 cases of Chinese with CHD, HTN or NIDDM in single or in different combinations were genotyped for the A1166C variation at the 3'-untranslated region of AGTR1 gene by using PCR/Dde I restriction endonuclease digestion. And also, the insertion/deletion polymorphism at the intron 16 of ACE gene was typed by PCR. RESULTS: (1) AGTR1 gene was associated with CHD (logistic regression analysis, P=0.02), but not with HTN and NIDDM; (2) The attributable risk of AGTR1 gene for CHD was 12.5% and the odds ratio was 4.55. Both AGTR1 gene and ACE gene were independent variation factors for CHD (P=0.032 and P=0.002 respectively); (3) The contribution of AGTR1 gene to the development of CHD was independent of total body adiposity, blood lipid profile and blood pressure; (4) The analysis of individual combined genotypes of AGTR1 gene and ACE gene showed significant difference in frequency distribution between patients with CHD and controls. CONCLUSION: AGTR1 gene contributes to the development of CHD and is an independent risk factor for CHD in Chinese.

Adult↗
PubMed1998

[The impact of the missense mutation-ser20gly in islet amyloid polypeptide gene on NIDDM in Chinese].

OBJECTIVES: To ascertain the presence of the Ser 20Gly mutation of islet amyloid polypeptide (IAPP) gene and its impact on NIDDM in Chinese. METHODS: In 896 Chinese, 825 were unrelated subjects (NIDDM in 609 and non-diabetics, 216) and 71 were family members of the pedigrees with IAPP gene-Ser 20Gly carrier probands detected from population screening. The mutation was examined by PCR-RFLP MspI digestion in population screening and the results was randomly checked by direct DNA sequencing. Data were analyzed through association as well as linkage approaches. RESULTS: The Ser20Gly mutation of the IAPP gene was observed in Chinese. It was more prevalent in NIDDM (17 cases, 2.8%) than in non-diabetics (1 cases, 0.5%) (Fisher two-tailed exact P = 0.05). The mutation carrier detected by PCR-RFLP was confirmed to be the A to G point mutation in nucleotide 582 of IAPP gene cDNA encoding the amino acid codon 20. All the mutation carriers detected in population screening were heterozygotes. Analysis of the family members of the 12 NIDDM pedigrees with the IAPP gene Ser20Gly mutation showed that in two families, the mutation was not cosegregated with the affection status. The older was the age of Ser20Gly mutant carrier, the more prevalent was the diabetes in families (P = 0.0001). The highest total lod score of this 12 pedigree was 0.021(theta = 0) in parametric linkage analysis with the model of autosomal dominance with incomplete penetrance. CONCLUSION: The Ser20Gly mutation of IAPP gene was present in Chinese. This mutation does not cause monogenic inheritance diabetes, but may be a pathogenetic factor for the development of NIDDM, the complex genetic disease.

Adult↗
PubMed1997

Mitochondrial tRNA(Leu(UUR)) gene mutation diabetes mellitus in Chinese.

OBJECTIVE: To ascertain the prevalence and clinical features of mitochondrial tRNALeu(UUR) gene nucleotide (nt) 3243 A-->G mutation diabetes mellitus in Chinese and to establish the approaches for genetic diagnosis of this subtype of diabetes during routine daily clinical practice. METHODS: Mitochondrial nt 3243 A-->G mutation was screened among 207 unrelated non-insulin-dependent diabetes mellitus (NIDDM) patients by using polymerase chain reaction (PCR)/Apa I restriction endonuclease digestion. Samples with positive result were confirmed by DNA sequence analysis. Genetic and clinical analysis were carried out in family members of the proband with positive genetic diagnosis. RESULTS: Positive results were found in two subjects during screening of unrelated NIDDM patients, which account for 2.4%-11.1% of NIDDM subjects with uncommon clinical features (with early age-of-onset, with low body-mass-index and on insulin therapy) or with positive family history of diabetes consistent with or unable to exclude from maternal inheritance. Genetic diagnosis was positive in 10 out of 25 family members in the pedigrees of these two probands. CONCLUSIONS: Mitochondrial tRNALeu(UUR) gene nt 3242 A-->G mutation should be considered in diabetic patients with the above-mentioned clinical features. The genetic diagnosis in daily clinical practice can be performed with allele specific priming amplification, or PCR/Hae III or Apa I digestion which are technically simple to perform and diagnostically easy to define.

Adolescent↗
PubMed1997

[Relationship between angiotensin 1 converting enzyme gene polymorphism and diabetic nephropathy].

OBJECTIVE: To clarify if ACE gene I/D polymorphism attributes to the development of non-insulin dependent diabetes mellitus (NIDDM) and renal complication. METHODS: A fragment of 287 bp Alu sequence in inron 16 of ACE gene was used as I/D polymorphic marker. After PCR amplification of DNA fragment, 12% non-denatured polyacrylamide gel electrophoresis was undertaken to analyze the PCR products. RESULTS: Allele D was the prominent one (frequency 0.75) in the subgroup of DN which was complicated in the earliest stage of NIDDM without HTN, CHD and diabetic retinopathy. However, the frequency of allele D was low (0.39) in the subgroup of NIDDM without DN, HTN, CHD and diabetic retinopathy, in which the duration of each subject was over 5 years. It was significant to compare these two mentioned subgroups (P < 0.02, continuity-adjusted X2test, P < 0.05). The distribution of genotype in the whole NIDDM group without HTN and CHD (69 cases) was very similar to the normal control (110 subjects) (I 0.60 to 0.59, D 0.40 to 0.41). CONCLUSION: The I/D polymorphism of ACE gene may be the factor of genetic predisposition of early-onset diabetic nephropathy in Chinese NIDDM.

Adult↗
PubMed1996

A genome-wide search for human non-insulin-dependent (type 2) diabetes genes reveals a major susceptibility locus on chromosome 2.

Non-insulin-dependent (type 2) diabetes mellitus (NIDDM) is a common disorder of middle-aged individuals characterized by high blood glucose levels which, if untreated, can cause serious medical complications and lead to early death. Genetic factors play an important role in determining susceptibility to this disorder. However, the number of genes involved, their chromosomal location and the magnitude of their effect on NIDDM susceptibility are unknown. We have screened the human genome for susceptibility genes for NIDDM using non-and quasi-parametric linkage analysis methods in a group of Mexican American affected sib pairs. One marker, D2S125, showed significant evidence of linkage to NIDDM and appears to be a major factor affecting the development of diabetes mellitus in Mexican Americans. We propose that this locus be designated NIDDM1.

Chromosomes, Human, Pair 2↗