Distribution of blood and serum protein group characteristics in patients with diabetes

Scholz, W.; Knussmann, Rainer; Daweke, H.

doi:10.1007/bf00422822

Cited by 12 publications

(12 citation statements)

References 10 publications

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“…First, a dose effect is often taken as evidence that an observed association is causal. In our data, An association between RH blood group and diabetes has been reported from Oslo, Norway, by Berg et al 17 and from Germany by Scholz et al 18 Berg et al noted a deficiency of phenotypes containing the R, (CDe) haplotype and an excess of phenotypes containing the R 2 (cDE) haplotype among diabetic subjects whereas Scholz et al observed the opposite pattern. In a population-based study of the type described here, it is not possible to assign specific haplotypes based on individual phenotypes.…”

Section: Discussionsupporting

confidence: 58%

Association Between NIDDM, RH Blood Group, and Haptoglobin Phenotype: Results from the San Antonio Heart Study

et al. 1986

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We examined seven red cell antigen and 10 polymorphic protein phenotypes in 1237 Mexican Americans randomly selected from three San Antonio neighborhoods. Statistically significant associations were found between non-insulin-dependent diabetes mellitus (NIDDM) and RH blood type (X2 = 32.87, df = 10, P = 0.0003) and haptoglobin phenotype (X2 = 9.15, df = 2, P = 0.010). The haptoglobin association showed a dose effect with a single dose of the haptoglobin-1 allele associated with an approximately 50% increase and a double dose of the haptoglobin-1 allele associated with an approximately 100% increase in NIDDM prevalence. Multivariate analysis indicated statistically significant associations between NIDDM and age, sex, adiposity, and neighborhood of residence. However, even after taking these potential confounding variables into account, there was still a significant, independent association between NIDDM and haptoglobin phenotype. The results suggest that the haptoglobin gene may be in linkage disequilibrium with a major susceptibility gene for NIDDM.

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Section: Discussionsupporting

confidence: 58%

Association Between NIDDM, RH Blood Group, and Haptoglobin Phenotype: Results from the San Antonio Heart Study

et al. 1986

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“…Moreover, it is in the same chromosomal region as, and therefore in possible linkage disequilibrium with, the Rh blood group locus (1p35-31.3 for GLUT1 and 1p36.2-34 for Rh). This close proximity combined with the fact that population associations between Rh phenotype and diabetes have been reported in several populations (59,60), including Mexican Americans from San Antonio (61), suggest that GLUT1 also merits consideration as a candidate gene for type II diabetes.…”

Section: Finding the Diabetes Gene(s): Relationship To Primary-prevenmentioning

confidence: 87%

Kelly West Lecture: Primary Prevention of Type II Diabetes Mellitus

Stern

1991

Diabetes Care

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A useful paradigm for developing a public health strategy for combating chronic diseases consists of three phases: observational epidemiological studies, first cross-sectional and then prospective; intervention trials; and, finally, public health action. Although the field of cardiovascular epidemiology is well advanced into the third phase, i.e., public health action, the field of diabetes epidemiology is at least a generation behind and has only recently entered the phase of prospective observational studies. Part of the reason for this lag may be that, unlike cardiovascular disease, non-insulin-dependent (type II) diabetes has not been traditionally viewed as an epidemic, thereby detracting from a sense of urgency about the disease. Although this perspective may be appropriate for white populations, data from around the world make it increasingly apparent that type II diabetes has indeed reached epidemic proportions in non-white populations. Prospective studies are needed to firmly establish risk factors on which public health actions can be confidently based. Although anthropometric and metabolic risk factors such as obesity, body fat distribution, and circulating glucose and insulin concentrations are becoming well established as risk factors for type II diabetes, much less is known about behavioral risk factors. These latter risk factors are especially important because they are often amenable to public health action. There are preliminary data suggesting that decreased physical activity and increased fat consumption may be behavioral risk factors for diabetes. Decreased total energy intake, reflecting either low levels of physical activity or an intrinsically low metabolic rate, perhaps genetic in origin, may also be a diabetes risk factor. Unlike the field of cardiovascular epidemiology, in which there is already a critical mass of intervention trials on primary prevention, such trials are essentially nonexistent in the field of diabetes epidemiology; they are urgently needed. Although the notion of a single gene causing diabetes is clearly simplistic, there is a reasonable expectation that genetic markers can be identified that would be useful in screening for genetic susceptibles, at least in selected predisposed populations. Such markers could then be used to identify target populations for primary-prevention trials and public health action. Although primary-prevention trials should not be deferred until genetic markers are available, these two research paths may someday converge and genetic markers may come to play an important role in screening individuals as part of a comprehensive public health strategy. Numerous trial designs should be considered for testing hypotheses about the primary prevention of type II diabetes. These include single risk factor, multiple risk factor, and factorial designs.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…A polymorphism at the LPL locus has been associated recently with hyperinsulinemia, hypertriglyceridemia, and reduced levels of highdensity lipoprotein cholesterol, three components of the so-called insulin resistance syndrome, which is thought to be an antecedent of NIDDM (13). The Rh locus was typed because polymorphisms at this locus have been associated previously with diabetes in at least three different population studies (14)(15)(16). The Rh locus is also near TNFR2, a receptor for tumor necrosis factor-a, a cytokine having important metabolic effects on adipocyte metabolism (17).…”

Section: Methodsmentioning

confidence: 99%

Evidence for Linkage of Postchallenge Insulin Levels With Intestinal Fatty Acid-Binding Protein (FABP2) in Mexican-Americans

et al. 1995

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Single genes with large effects may contribute to insulin resistance or influence susceptibility to non-insulin-dependent diabetes mellitus (NIDDM). In the Pima Indians, results from sib-pair analysis have suggested that a gene on chromosome 4q influences both fasting insulin levels and maximal insulin action. We conducted sib-pair and logarithm of odds (LOD)-score linkage analysis to seek evidence for linkage between genes influencing insulin levels and chromosome 4q loci. Analyses were conducted on nondiabetic individuals from 28 different families participating in the San Antonio Family Diabetes Study. All subjects received a 2-h oral glucose tolerance test. Fasting insulin levels were measured in 382 nondiabetic individuals, and 2-h insulin levels were measured in 366 individuals. Initial sib-pair linkage analysis revealed a possible association between 2-h post-glucose challenge insulin levels and the intestinal fatty acid-binding protein (FABP2) locus located in the region of chromosome 4q28-31 (P = 0.006). Subsequent sib-pair linkage analysis of 11 additional chromosome 4q markers supported this hypothesis. We next conducted segregation analyses to estimate allele frequencies and other model parameters for the putative locus influencing 2-h insulin levels. Results of LOD-score linkage analysis indicated possible linkage between the major gene described by the segregation model and FABP2. Using combined segregation and linkage analysis, we obtained a LOD-score of 2.80 at recombination frequency of 0.0 between FABP2 and the putative locus influencing 2-h insulin levels. The maximum likelihood estimate of the allele associated with low insulin levels was 0.21.(ABSTRACT TRUNCATED AT 250 WORDS)

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Distribution of blood and serum protein group characteristics in patients with diabetes

Cited by 12 publications

References 10 publications

Association Between NIDDM, RH Blood Group, and Haptoglobin Phenotype: Results from the San Antonio Heart Study

Association Between NIDDM, RH Blood Group, and Haptoglobin Phenotype: Results from the San Antonio Heart Study

Kelly West Lecture: Primary Prevention of Type II Diabetes Mellitus

Evidence for Linkage of Postchallenge Insulin Levels With Intestinal Fatty Acid-Binding Protein (FABP2) in Mexican-Americans

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