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Results for “DIABETES MELLITUS”

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At least 19 recordsLinked to original sources
PubMed1977

Diabetes mellitus, diabetes insipidus, and optic atrophy. An autosomal recessive syndrome?

Twenty-one families were selected from the published reports in which the propositus had the triad of juvenile diabetes mellitus, diabetes insipidus, and optic atrophy. The data were consistent with the hypothesis of an autosomal gene which, in the homozygote, causes juvenile diabetes mellitus and one or more of diabetes insipidus, optic atrophy, and nerve deafness. Heterozygotes appear to have an increased probability of developing juvenile diabetes mellitus.

Child↗
PubMed2000

[The effect of non-surgical periodontal therapy on blood sugar level of non-insulin dependent diabetes mellitus diabetics with periodontitis].

OBJECTIVE: To investigate the effect of periodontal therapy on blood sugar level of non-insulin dependent diabetes mellitus(NIDDM) diabetics with periodontitis. METHODS: Patients with unfavorable control of diabetes were selected from out patients of the first affiliated hospital of Sun Yat-sen University of Medical Science. The percentage of bleeding on probing, probing depth and glycosylated hemoglobin level were studied at baseline, four weeks and eight weeks after non-surgical treatment. RESULTS: The percentage of bleeding on probing and probing depth were significantly reduced in all the patients after treatment. The mean glycosylated hemoglobin level were significantly decreased in patients with advanced periodontitis while patients with moderate periodontitis showed no changes following therapy. CONCLUSIONS: The control of periodontal inflammation can improve metabolism to some extent in patients with diabetes mellitus, but the effect may relate to blood sugar level and periodontal conditions at baseline.

Aged↗
PubMed1995

An assessment of cochlear hair-cell loss in insulin-dependent diabetes mellitus diabetic and noise-exposed rats.

OBJECTIVE: The purpose of this study was to investigate if insulin-dependent diabetes mellitus causes degenerative changes in the inner ear and whether these changes are exacerbated by noise exposure. METHODS: Insulin-dependent diabetes mellitus was induced in male rats using streptozotocin (65 mg/kg of body weight, intravenously). Half the animals were exposed to 95 dB of random noise for 12 hours per day over a period of 6 months. The cochleae were removed, fixed, decalcified, dissected, and the hair cells counted. RESULTS: A significant loss of outer hair cells was exhibited in both noise-exposed groups; however, although there was no significant difference between these two groups, the noise-exposed diabetic animals had significant loss in more turns than did the noise-exposed control animals. The diabetic animals were not statistically different from the control animals. CONCLUSION: These results suggest that insulin-dependent diabetes mellitus may increase the hair-cell loss caused by noise overstimulation.

Animals↗
PubMed1997

The beta cell glucokinase promoter variant is an unlikely risk factor for diabetes mellitus. Diabetes Incidence Study in Sweden (DISS).

Glucokinase plays an important role in the regulation of insulin secretion and is therefore an attractive candidate gene for both insulin dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. A single G-A nucleotide polymorphism at the -30 position of the beta-cell specific promoter region of the glucokinase gene was previously associated with reduced beta-cell function. In the present study we analysed 268 consecutive newly diagnosed Swedish patients classified with either IDDM (n = 205), NIDDM (n = 31) or unclassifiable (n = 32) diabetes between the ages of 15 and 35 years along with a group of 158 age- and sex-matched control subjects. The beta-cell promoter region was amplified by the polymerase chain reaction and the G-A variant identified by single strand conformational polymorphism. There was no significant difference in allele frequencies of G and A between any of the subject groups and likewise, no significant difference in the frequencies of the G/G, G/A, or A/A genotypes. Eight subjects were homozygous for the less common A allele, five had IDDM and three were control subjects. Our results suggest that the -30 beta-cell glucokinase promoter variant is not associated with IDDM.

Adolescent↗
PubMed1994

Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin-dependent diabetes mellitus: Diabetes Control and Complications Trial. Diabetes Control and Complications Trial Research Group.

The Diabetes Control and Complications Trial has demonstrated that intensive diabetes treatment delays the onset and slows the progression of diabetic complications in subjects with insulin-dependent diabetes mellitus from 13 to 39 years of age. We examined whether the effects of such treatment also occurred in the subset of young diabetic subjects (13 to 17 years of age at entry) in the Diabetes Control and Complications Trial. One hundred twenty-five adolescent subjects with insulin-dependent diabetes mellitus but with no retinopathy at baseline (primary prevention cohort) and 70 adolescent subjects with mild retinopathy (secondary intervention cohort) were randomly assigned to receive either (1) intensive therapy with an external insulin pump or at least three daily insulin injections, together with frequent daily blood-glucose monitoring, or (2) conventional therapy with one or two daily insulin injections and once-daily monitoring. Subjects were followed for a mean of 7.4 years (4 to 9 years). In the primary prevention cohort, intensive therapy decreased the risk of having retinopathy by 53% (95% confidence interval: 1% to 78%; p = 0.048) in comparison with conventional therapy. In the secondary intervention cohort, intensive therapy decreased the risk of retinopathy progression by 70% (95% confidence interval: 25% to 88%; p = 0.010) and the occurrence of microalbuminuria by 55% (95% confidence interval: 3% to 79%; p = 0.042). Motor and sensory nerve conduction velocities were faster in intensively treated subjects. The major adverse event with intensive therapy was a nearly threefold increase of severe hypoglycemia. We conclude that intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy and nephropathy when initiated in adolescent subjects; the benefits outweigh the increased risk of hypoglycemia that accompanies such treatment.

Adolescent↗
PubMed1984

Exercise-induced left ventricular dysfunction in young men with asymptomatic diabetes mellitus (diabetic cardiomyopathy).

Radionuclide ventriculographic studies were performed at rest and during exercise on 30 consecutive men, aged 21 to 35 years with diabetes mellitus without evidence of coronary artery or any other cardiovascular disease, and in 20 normal age-matched subjects. Sixteen (53%) were treated with insulin and 14 (47%) were treated with either diet (6 patients) or oral antidiabetic therapy (8 patients). All patients from both groups had normal left ventricular (LV) ejection fraction (EF) at rest. In 5 of the 30 diabetic patients (17%), LVEF decreased after exercise, in 8 (27%) it remained unchanged and in 17 it increased normally. Mean LVEF at rest and after exercise in this group was 66 +/- 7% and 72 +/- 7% (+/- standard deviation), respectively. In all normal subjects, LVEF increased after exercise. Mean LVEF at rest and after exercise in the normal group was 66 +/- 7% and 76 +/- 9%, respectively. No patient had evidence of regional dysfunction at rest or after exercise. LV function was not related to serum glucose levels during the test, modality of treatment, insulin dependency or duration of the disease. Three of 4 patients with diabetic microvascular complications showed LV dysfunction. In 4 of 5 patients in whom LVEF decreased after exercise, thallium studies showed normal perfusion. Thus, diabetes mellitus may cause exercise-induced global LV dysfunction in young men with no evidence of cardiovascular disease. This phenomenon apparently does not seem to follow the known course of diabetic microvascular complications.

Adolescent↗
PubMed2003

[Bone loss in type 2 diabetes mellitus--diabetic osteopenia].

Loss of bone mineral content has been recognized as one of the chronic complications of type 2 diabetes mellitus, although its mechanism is not fully documented. A negative calcium balance due to both enhanced urinary calcium excretion and decreased intestinal calcium absorption has been occurred because of alteration of vitamin D metabolism and/or decreased parathyroid function. From the view point of bone cell metabolism, osteoblastic bone formation is suppressed by alternation of vitamin D metabolism, hypoparathyroidism, chronic hyperglycemia and insufficient insulin action. On the other hand, osteoclastic bone resorption is rather enhanced. The functional bone uncoupling system between osteoblast and osteoclast in type 2 diabetes mellitus could result in loss of bone density.

Bone Diseases, Metabolic↗
PubMedDate not supplied

Diabetes mellitus, diabetes insipidus, optic atrophy and deafness (DIDMOAD syndrome).

Two patients with diabetes mellitus (DM), diabetes insipidus (DI), optic atrophy (OA), deafness (D) and dilatation of the urinary tract-the so-called DIDMOAD syndrome are presented. In one of the patients, the presenting components were DI and OA. In the second case, DM was the first manifestation to be diagnosed, and in this patient the course of the syndrome was complicated by associated epileptical activity disorders, and later septicemia. The admission of these patients led us to review the literature describing this syndrome.

Adolescent↗
PubMed1996

Development and progression of renal disease in Pima Indians with non-insulin-dependent diabetes mellitus. Diabetic Renal Disease Study Group.

BACKGROUND: Non-insulin-dependent diabetes mellitus (NIDDM) is a major cause of end-stage renal disease. However, the course and determinants of renal failure in this type of diabetes have not been clearly defined. METHODS: We studied glomerular function at intervals of 6 to 12 months for 4 years in 194 Pima Indians selected to represent different stages in the development and progression of diabetic renal disease. Initially, 31 subjects had normal glucose tolerance, 29 had impaired glucose tolerance, 30 had newly diagnosed diabetes, and 104 had had diabetes for five years or more; of these 104, 20 had normal albumin excretion, 50 had microalbuminuria, and 34 had macroalbuminuria. The glomerular filtration rate, renal plasma flow, urinary albumin excretion, and blood pressure were measured at each examination. RESULTS: Initially, the mean (+/-SE) glomerular filtration rate was 143+/-7 ml per minute in subjects with newly diagnosed diabetes, 155+/-7 ml per minute in those with microalbuminuria, and 124+/-7 ml per minute in those with macroalbuminuria; these values were 16 percent, 26 percent, and 1 percent higher, respectively, than in the subjects with normal glucose tolerance (123+/-4 ml per minute). During four years of follow-up, the glomerular filtration rate increased by 18 percent in the subjects who initially had newly diagnosed diabetes (P=0.008); the rate declined by 3 percent in those with microalbuminuria at base line (P=0.29) and by 35 percent in those with macroalbuminuria (P<0.001). Higher base-line blood pressure predicted increasing urinary albumin excretion (P=0.006), and higher base-line urinary albumin excretion predicted a decline in the glomerular filtration rate (P<0.001). The initial glomerular filtration rate did not predict worsening albuminuria. CONCLUSIONS: The glomerular filtration rate is elevated at the onset of NIDDM and remains so while normal albumin excretion or microalbuminuria persists. It declines progressively after the development of macroalbuminuria.

Adolescent↗
PubMed1977

Simultaneous occurrence of diabetes mellitus, diabetes insipidus, and optic atrophy in a brother and sister.

We report the cases of two siblings who died at age 21 and 15 years respectively. Both had optic atrophy, pitressinsensitive diabetes insipidus, and insulin-dependent diabetes mellitus, with onset occurring in early childhood. Although there are now 21 patients from 15 families with this syndrome, this is the first time that necropsy findings have become available. They include the expected atrophy of hypothalamic nuclei and degeneration of the optic nerves, chiasm and tract, as well as a totally unexpected degeneration of the pons and cerebellum.

Adolescent↗
PubMedDate not supplied

Treatment of patients with non-insulin-dependent diabetes mellitus: diabetic control and insulin secretion and action after different treatment modalities.

In order to define the relationship between treatment-induced changes in diabetic control and improvement in in vivo insulin-stimulated glucose utilization (insulin clamp technique) 30 patients with non-insulin-dependent diabetes mellitus (NIDDM) were treated with either insulin, glipizide or diet alone, depending on their initial weight. Fasting plasma glucose concentrations fell from 16.3 +/- 1.2, 15.9 +/- 1.0, and 16.3 +/- 1.0 mmol/l, (mean +/- SE) to 6.3 +/- 0.5, 11.6 +/- 0.6, and 13.4 +/- 1.6 mmol/l, after insulin, glipizide and weight reduction, respectively. These changes in fasting plasma glucose concentration were associated with an improvement in insulin-stimulated glucose uptake, which increased by 69% after insulin, 45% after glipizide, and 72% after weight reduction. Thus, the improvement in insulin action was comparable in the three different groups of patients following each therapeutic intervention, and appeared to be unrelated to the fall in plasma glucose concentration. These results appear to suggest that the ability of any specific treatment to improve diabetic control can vary independently of its effect on in vivo insulin-stimulated glucose utilization.

Adult↗
PubMed1988

Geographic patterns of childhood insulin-dependent diabetes mellitus. Diabetes Epidemiology Research International Group.

Population-based registries of insulin-dependent diabetes mellitus (IDDM) worldwide have reached the critical mass needed to investigate global patterns of the disease. International collaboration of 24 registries from 15 countries resulted in the first set of standardized incidence measures among divergent areas and ethnic groups. The average annual age-adjusted incidence under age 15 yr ranged from 1.7/100,000 person-yr in Hokkaido, Japan, to 29.5/100,000 person-yr in Finland during the years 1978-1980. The geographic differences in IDDM in childhood are rarely seen among chronic diseases. It appears that the risk for IDDM is determined by factor(s) correlated to the average yearly temperature of environment and to the ethnicity of the population at risk.

Adolescent↗
PubMed1995

Ocular manifestations of diabetes mellitus: diabetic cataracts in dogs.

Cataracts form in diabetic dogs because of the disruption of normal lens metabolism. The pathophysiology seems to be a combination of increased lens cell membrane permeability, reduced cell membrane function, damage from accumulating osmotic products (polyols), glycosylation of lens proteins, and oxidative injury. Lens-induced uveitis must be recognized and managed in presurgical preparation of dogs with diabetes cataracts. Phacoemulsification is the current treatment of choice for diabetic cataracts in dogs and can be performed at an earlier time than traditional extracapsular lens extraction. This may allow for greater success rates after surgery.

Animals↗