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Results for “Prediabetic State”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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PubMed1979

Long-term treatment of subjects with borderline glucose tolerance.

Subjects with borderline glucose tolerance are at a higher risk of suffering and dying from cardiovascular disease than subjects with normal glucose tolerance. Our data on the progression to overt diabetes and our data on cardiovascular morbidity and mortality suggests that tolbutamide treatment reduces these risks. In any case, we have no data supporting the theory that tolbutamide promotes cardiovascular damage.

Blood Pressure↗
PubMed1988

Genetic relationships between type I and type II diabetes mellitus.

We propose that at least certain subsets of Type I and Type II diabetes share factor(s) responsible for genetic susceptibility. The data presented here to support this contention include: 1. A significantly increased cumulative risk (CR40) to age 40 for Type I diabetes in sibs of probands in families with a Type II diabetic parent (Type II diabetic parent: CR40-24.7 +/- 10.7%; normal parent: CR40 = 7.5 +/- 2.0%, x2 = 12.8, p less than 0.0005). 2. The relative risk (RR) for HLA DR4 in Type I diabetic probands with a Type II diabetic parent is higher than in probands with normal parents (RR = 2.4). 3. The haptoglobin genotype 2-2 is increased in Type I diabetics with Type II parents and the sharing of both HLA and haptoglobin haplotypes in affected sib pairs is distorted with an excess sharing of both haplotypes.

Age Factors↗
PubMed1988

Hereditary diabetes in the KK mouse: an overview.

Table III compares metabolic and morphologic characteristics of different species of control and KK mice. The C57BL/6J demonstrates no significant metabolic, clinical or histologic abnormalities. Our two highly inbred Swiss albino groups I and II also do not show significant glomerular lesions, although we found striking intolerance to glucose, hyperinsulinism, and obesity among them. Thus a genetic predisposition may be necessary in addition to various environmental factors to produce microangiopathy in KK mice. The yellow AY mouse is included in this table, since it is strikingly hyperinsulinemic and obese without concomitant vasculopathy such as the other mentioned control strains have. In conclusion, the KK mice develop chemical diabetes preceded by a stage of prediabetes and also demonstrate renal, retinal and neurologic complications similar to those seen in human diabetes. Of particular interest is the development of mild to moderate glomerulosclerosis in the prediabetic stage; with progression to severe glomerulosclerosis and attendant proteinuria later in life. With proper back-crossing, both hyperglycemia and glomerulosclerosis can be transmitted to normal control mice, suggesting that a specific genetic background is necessary for the development of diabetes and diabetic-like microangiopathy. We therefore suggest that the KK mouse serves as an ideal genetic animal for the study of non-insulin-dependent diabetes mellitus and its complications for rational prevention and therapy.

Animals↗