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Results for “Prediabetic State”

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At least 505 records · Page 28Linked to original sources
PubMed1991

Insulin autoantibodies as determined by competitive radiobinding assay are positively correlated with impaired beta-cell function--the Ulm-Frankfurt Population Study.

Out of a random population of 4208 non-diabetic pupils without a family history of Type I diabetes 44 (1.05%) individuals had islet cell antibody (ICA) levels greater or equal to 5 Juvenile Diabetes Foundation (JDF) units. 39 of these ICA-positives could be repeatedly tested for circulating insulin autoantibodies (CIAA) using a competitive radiobinding assay. The results were compared with the insulin responses in the intravenous glucose tolerance tests (IVGTT) and with HLA types. Six pupils were positive for CIAA. All of them had complement-fixing ICA, and 5 of them were HLA-DR4 positive. Three of the 6 showed a first-phase insulin response below the first percentile of normal controls. Our data indicate that in population-based studies CIAA can be considered as a high risk marker for impaired beta-cell function in non-diabetic ICA-positive individuals.

Adolescent↗
PubMed1976

[Fatty acid patterns and glucose tolerance in Huntington's chorea (author's transl)].

Fatty acid patterns of plasma lipids and glucose-tolerance in Huntington's chorea. 25 patients with Huntington's chorea of various manifestation (9 predisposed symptomefree, 5 with light and 11 with severe manifestation) had studies of carbohydrate and lipid metabolism. These studies measured glucose-tolerance tests, insulin-, HGH-secretion, serum lipids and plasma fatty acid conposition of the cholesterylesters, triglycerides and phospholipids. The reactive insulin- but not HGH-levels were significantly raised, 32 % of the patients with Huntington's chorea had abnormal glucose-tolerance tests, compared with 3.2 % in a control group. Duration of symptoms correlated with higher cholesterol levels. Minor deviations were found in the fatty acid patterns in various lipid clases.

Cholesterol↗
PubMed1976

Elevated kidney glucosyltransferase activity in genetic prediabetic mice.

Glucosyltransferase activity in the renal cortex of genetic diabetic KK mice was significantly increased at 40 days of age when compared to that of Swiss albino and F1 hybrid mice. This increase in enzyme activity in the absence of glucose intolerance can be regarded as an earlier genetic marker for the diagnosis of diabetic microangiopathy.

Age Factors↗
PubMed1992

Influence of the development of diabetes mellitus on clinical status in patients with cystic fibrosis.

The impact of pre-diabetes on clinical status was retrospectively studied in 38 cystic fibrosis (CF) patients with diabetes mellitus (DM) and 38 non-diabetic CF patients (control patients), matched in pairs for age, sex, and chronic Pseudomonas aeruginosa lung infection. Quarterly parameters of CF clinical status were collected for 6 years prior to the diagnosis of DM in the index case. Compared to the control patients, decreases in body weight, body mass index (BMI), forced expiratory volume in 1s (FEV1), and forced vital capacity (FVC) and an increase in the daily intake of pancreatic enzyme capsules were found in the pre-diabetic patients. Statistically significant differences in body weight, BMI, FEV1, FVC, and intake of pancreatic enzyme capsules between pre-diabetic and control patients emerged 4, 4, 1.25, 3 and 4.5 years prior to the diagnosis of DM, respectively. The number of lung infections did not differ between the two groups of patients. Thus, when DM develops in CF patients, an insidious decline in overall clinical status is observed for years prior to its diagnosis. Whether clinical deterioration in CF leads to DM, or pre-diabetes results in declining CF clinical status is presently unknown. Accumulating evidence suggests that the latter may be the case since insulin therapy seems to improve lung function in CF.

Adolescent↗
PubMed1993

The preventive effect of aldose reductase inhibition on diabetic optic neuropathy in the BB/W-rat.

A polyol-pathway-related mechanism has been invoked in the pathogenesis of murine and human diabetic peripheral neuropathy in which progressive axonal atrophy and axo-glial dysjunction constitute the cardinal structural abnormalities. We have previously reported similar neuroanatomical changes in the optic nerve of 6-month diabetic BB/W-rats. In the present study we demonstrate progression of axonal atrophy and axo-glial dysjunction in the optic nerve in 12-month diabetic BB/W-rats. These structural lesions showed highly significant correlations with the associated prolongation of the latencies of the visual evoked potentials, suggesting that axo-glial dysjunction and axonal atrophy are major determinants for impaired optic nerve function. As in peripheral nerve, the polyol-pathway is present in the optic nerve and is activated by hyperglycaemia and galactosaemia. In this study we further examined the treatment effect of the aldose reductase inhibitor ponalrestat, given from 3 weeks of diabetes and continued throughout the study protocol. This regimen resulted in complete prevention of axo-glial dysjunction, and had a significant ameliorating effect on visual evoked potential latencies, but had no effect on optic nerve axonal atrophy. This latter finding differs from the effect of aldose reductase inhibition on diabetic peripheral nerve and suggests that axonal atrophy of central nerve tracts in diabetes may be the consequence of other metabolic abnormalities or alternatively the present regimen was insufficient to protect central axons from the effects of an increased activity of the polyol pathway.

Aldehyde Reductase↗
PubMed1993

Pre-diabetic blood pressure predicts urinary albumin excretion after the onset of type 2 (non-insulin-dependent) diabetes mellitus in Pima Indians.

Blood pressure was measured in 490 non-proteinuric Pima Indians from the Gila River Indian Community in Arizona at least 1 year before the diagnosis of Type 2 (non-insulin-dependent) diabetes mellitus. Urine albumin concentration was measured in the same subjects 0-24 years (mean 5 years) after diabetes was diagnosed. Prevalence rates of abnormal albumin excretion (albumin-to-creatinine ratio > or = 100 mg/g) after the onset of Type 2 diabetes were 9%, 16%, and 23%, respectively, for the lowest to highest tertiles of pre-diabetic mean blood pressure. When controlled for age, sex, duration of diabetes and pre-diabetic 2-h post-load plasma glucose concentration, higher pre-diabetic mean blood pressure predicted abnormal urinary excretion of albumin after the onset of diabetes. This finding suggests that the higher blood pressure seen in diabetic nephropathy is not entirely a result of the renal disease, but may precede and contribute to it.

Adolescent↗
PubMedDate not supplied

Glucagon and insulin secretion in potential diabetes.

Insulin and glucagon have been studied in 20 subjects (both of the subjects' parents were diabetic or in case of only one diabetic parent, the other showed a first degree familiarity of diabetes): 10 showed normal glucose tolerance ('true prediabetics') and 10 impaired glucose tolerance ('genetic chemical diabetes'). Mean insulin response to oral (100 g) and i.v. glucose load (200 mg/kg followed by 20 mg/kg/min for 60 min) and to arginine infusion (25 g in 30 min) was normal in the prediabetics and delayed and higher in the subjects with chemical diabetes as compared to the control group. Glucagon response to arginine was higher, but not significantly, in prediabetics and in subjects with chemical diabetes. In both of these groups glucagon suppression by glucose was not observed. The insulin/glucagon molar ratio was significantly reduced after glucose infusion in these two groups. No correlation was found between insulin and glucagon secretion after arginine or glucose. A possible alteration in the mechanism controlling glucagon secretion even in the earliest phases of diabetes is suggested.

Adult↗
PubMedDate not supplied

Relationship between carbohydrate tolerance, insulin secretion, and insulin sensitivity of isolated fat cells from obese protodiabetics.

Six normal weight subjects without any heredity of diabetes (group 1), 3 obese subjects with normal (group 2) and 9 with pathological carbohydrate tolerance (group 3) were characterized by a 2-h glucose infusion test. Adipose tissue fragments were obtained from the abdominal wall by surgical biopsy under intracutaneous anesthesia. Adipocytes were isolated by collagenase digestion and incubated in buffer containing [1-14C] glucose and different concentrations of insulin. The metabolic effect of insulin was expressed as percent increase above control 14CO2 production. Maximal CO2 raised to 207 +/- 25% and 154 +/- 9% in groups 1 and 2, respectively. These values were significantly higher than in obese subjects displaying a pathological carbohydrate tolerance (group 3; 119 +/- 6%). A negative correlation was found between blood glucose levels and biological activity of insulin on adipocytes. The results suggest that insulin sensitivity of target tissue seems to play an important role in development of carbohydrate intolerance.

Adipose Tissue↗