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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↗
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↗
PubMed1978

[New viewpoints on the pathogenesis of diabetes mellitus].

Diabetes mellitus is a syndrome characterised primarily by an increase in blood glucose and an absolute or relative deficiency of insulin. Etiologically, it is a complex disorder because many different genetic, environmental, immunological, metabolic and hormonal influences interact to produce the clinical picture diabetes. By introducing HLA typing in diabetes research in the last four years, it became possible to clearly distinguish between the juvenile-onset, insulin-dependent type and the non-insulin-dependent, maturity-onset type of diabetes mellitus. On the basis of this and other evidence, at least five nosologically distinct types of diabetes can be identified.

Autoimmune Diseases↗
PubMed1978

The genetics of diabetes mellitus.

Diabetes mellitus is a geneticist's nightmare. We examine herein what causes the nightmare, how bad it is and how it is being alleviated by modern advances. Diabetes is more than one disease, it is indefinable, probably genetically multifactorial, and presents several facets with varying degrees of heredity and environment in their constitution.

Animals↗
PubMed1977

Genetic, acquired, and related factors in the etiology of diabetes mellitus.

Diabetes mellitus is not a single disease entity, but a heterogenous group of disorders with a striking diversity of etiopathogenetic mechanisms as well as clinical manifestations. Lack of a known genetic marker for the disease(s) and variable influences of environmental factors on the expression of a putative diabetic genome have resulted in considerable debate over its etiology. Over the past few years, systematic epidemiologic studies, along with knowledge gained from a close association of certain human-leukocyte-antigens with the diabetic diathesis and possible role of host-immune factors, and gene-virus interaction have led to considerable advancement in the understanding of the disease-complex. Pending the availability of definite genetic marker(s), we propose a new, tentative classification based on the etiologic mechanisms. We also suggest that the term "prediabetes" be abandoned as a prospective entity, since as presently employed, this connotation carries a risk probability no different than the terms like prehypertension or precoronary thrombosis.

Adolescent↗
PubMed1979

The development, enhancement, and reversal of the secondary complications of diabetes mellitus.

Diabetic glomerulopathy continues as a major problem in the management of the patient with diabetes mellitus; however, evidence in man and in animals underlines the fact that good control of diabetes favorably alters the course of this complication. Islet transplantation in the diabetic rat returns plasma glucose and insulin levels to normal. In parallel mesangial matrix thickening, mesangial deposition of immunoglobulin and urinary excretion of albumin markedly improve following islet transplantation. Although amelioration of diabetes affects the course of glomerulopathy, other factors (most notably measures that increase glomerular capillary pressure) enhance the development of the diabetic renal lesions. Following uninephrectomy or clipping of a renal artery, the remaining (in the case of uninephrectomy) or unclipped diabetic kidney develops the morphologic and functional changes of diabetic nephropathy at a rate greater than in kidneys in an intact diabetic rat. The clipped kidney demonstrates diminished diabetic changes, suggesting a protective effect with decreased glomerular capillary pressures. In addition to measures improving the control of diabetes, procedures reducing factors accelerating diabetic complications may improve the prognosis in diabetic glomerulopathy.

Albuminuria↗
PubMedDate not supplied

[Blood serum euglobulins in diabetes mellitus and diabetic microangiopathies].

A study of serum euglobulins carried out in 26 patients with diabetes mellitus and in 14 healthy persons permitted to detect definite differences between sick and healthy individuals. In the patients with diabetes mellitus (most distinctly in those with microangiopathies) the level of soluble and insoluble in the phosphate buffer euglobulins was greater than in the healthy persons. The microprecipitation reaction and immunoelectrophoresis with the monospecific immunoglobulins (IgA, IgM and IgG) more frequent and higher titers demonstrated IgA and IgG in diabetic patients. More pronounced heterogeneity (particularly distinct in the subfraction of euglobulins insoluble in the phosphate buffer) than in healthy individuals was revealed in the patients with diabetic microangiopathies by disc electrophoresis in polyacrylamide gel. The data obtained served as the basis for the search in the serum euglobulins of the patients with diabetes of compounds possibly possessing the antigenic properties, capable of producing antibodies and immune complexes, i.e. the immunological factors taking part in the vascular wall injury.

Antibody Formation↗
PubMed1976

Uroradiology of diabetes mellitus.

Diabetes mellitus is a prevalent disorder, well controlled in many persons with prolongation of life. Several radiologic manifestations are sufficiently specific to suggest a diagnosis in the unidentified patient, but even more important is an awareness of the sometimes life-threatening complications of diabetes which can be diagnosed from uroradiologic studies. We review the following urinary tract manifestations and complications of diabetes: pyelonephritis, perinephric abscess, renal papillary necrosis, emphysematous pyelonephritis, emphysematous cystitis, fungus infections, calcification of the vas deferens, seminal vesicle, and intrarenal branches of the renal artery, neuropathic bladder, and renal failure.

Abscess↗
PubMed2026

Protective association of the ELMO1 rs741301 variant against diabetes mellitus and diabetic nephropathy: a systematic meta-analysis of case-control studies.

CONTEXT: Diabetes mellitus (DM), an endocrine disorder, is characterised by persistently elevated blood glucose levels due to inadequate insulin production. Diabetic nephropathy (DN), is a critical complication associated with DM, often leading to end-stage renal failure and increased mortality. OBJECTIVE: This meta-analysis aimed to evaluate the association between the ELMO1 rs741301 polymorphism and susceptibility to DN among individuals with diabetes. METHOD: A systematic literature search was conducted for studies published between 2014 and 2024 using Embase, Google Scholar, and PubMed. Eligible case-control studies investigating the association between ELMO1 rs741301 and DN among individuals with DM were selected according to predefined inclusion criteria. Nine case-control studies comprising 880 individuals with DM and 1008 individuals with DN were included in the meta-analysis. RESULTS: The pooled analysis demonstrated a significant protective association between the ELMO1 rs741301 polymorphism and DN under the allelic model (OR = 0.77, 95% CI: 0.67-0.88), recessive model (OR = 0.74, 95% CI: 0.61-0.90), and dominant model (OR = 0.68, 95% CI: 0.53-0.88). In contrast, no statistically significant association was observed under the over-dominant model. CONCLUSION: The findings suggest that the ELMO1 rs741301 polymorphism may be associated with a reduced susceptibility to DN among individuals with DM. These findings provide evidence for a potential genetic contribution of ELMO1 to DN susceptibility and may help improve understanding of the genetic factors underlying diabetic complications. Further well-designed studies in diverse populations are warranted to validate this association.

Humans↗
PubMed1979

Diabetic nephropathy as the mode of presentation of diabetes mellitus.

Diabetic nephropathy have only rarely been described in patients who have minimal or no glucose intolerance. We herein report the case of a 59-yr-old man who presented with nephrotic syndrome and minimal glucose intolerance whose renal biopsy showed the nodular (Kimmelsteil-Wilson) and diffuse glomerulosclerosis lesions characteristic of diabetes. We critically review the literature on this subject, pointing out the pitfalls in diagnosis and establishing strict criteria for the diagnosis of diabetic nephropathy in patients wihout overt clinical diabetes.

Basement Membrane↗
PubMed1977

Monozygotic triplets with discordance for diabetes mellitus and diabetic microangiopathy.

A set of monozygotic triplets (PE.K., P.K., S.K.) has been studied. There is no diabetes in first-degree relatives. PE.K. developed insulin-requiring (60 U. NPH) diabetes at the age of 13 years. Over a period of 11 years since that time, numerous studies of insulin and growth-hormone secretion were performed on P.K. and S.K., including multiple oral glucose tolerance tests (OGTTs), cortisone-primed oral glucose tolerance tests (C-OGTTs), intravenous glucose tolerance tests (IVGTTs), and intravenous tolbutamide tests (IVTTs). The results of each test were compared with age- and sex-matched control subjects. P. K. developed insulin-requiring (56 U. NPH) diabetes after remaining discordant for eight years. Glucose, insilin, and growth-hormone responses during all tests were normal except during the IVGTT performed four months prior to the onset of diabetes. This last IVGTT revealed a glucose disappearance rate of 0.98 per cent per minute, and the slope of the regression line of serum-insulin response (IRI) on blood glucose (BG) was markedly decreased to 0.005 micronU./ml. IRI/mg./dl. BG (controls 0.340 +/- 0.04; mean +/- S.E.M.). The insulin responses in P.K. and S.K. were similar during all OGTTs, C-OGTTs, and IVTTs. S.K. has continued to maintain normal glucose tolerance and normal insulin and growth-hormone responses during all tests. The histocompability antigen studies have revealed HLA-A2, AW24, BW15, and BW40 phenotype in these monozygotic triplets. Muscle capillary basement membranes of the nondiabetic triplet were normal, whereas both diabetic triplets manifested evidence of capillary basement membrane thickening. The clinical and biochemical profiles in these triplets and the capillary basement membrane data lend strong credence to the role of "nongenetic" determinants in the development of "genetic" diabetes as well as diabetic microangiopathy in juvenile-onset-type diabetes.

Adolescent↗