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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proposition that lifestyle is a major determinant of community health is explored by contrasting the features of a rural subsistence community in the highlands of Papua New Guinea and the features of the community in urbanized, industrialized Australia. Reference is made to differences in physical environment, housing, work, social situation, human relationships, patterns of disease, population statistics, diet, growth, obesity, physical fitness, blood lipid concentrations, blood pressure, salt intake and the occurrence of hypertension, diabetes, cardiovascular disease and signs of degenerative changes in various tissues. The Papua New Guinea community is seen as a self-reliant, self-contained, socially cohesive subsistence society whose members are well adapted to their physical and social environment, free from major degenerative cardiovascular diseases, with little overt psychiatric illness, but with a heavy burden of infectious disease, with marginal nutritional levels of degenerative disease and disease from psychological stress. It is clear that health, in its fullest sense, is not the prerogative of any one type of society.
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PMID:Lifestyle, health and disease: a comparison between Papua New Guinea and Australia. 73 10

Two per cent of "diabetic" children actually exhibit a specific condition which is not a disease in the conventional acceptance of the term. Characteristics of this biologic anomaly, whose pathophysiology is as yet incompletely understood, include the absence of clinical manifestations, with the diagnosis being established upon routine tests (e.g., as part of a school health check-up or during screening tests in family members of diabetics); blood glucose levels or glucose tolerance test results consistently above the 97th percentile of reference values, with some degree of variation over time; normal serum insulin levels; glycosylated hemoglobin levels usually near the upper limit of normal; dominant autosomal inheritance; lack of association with either HLA markers or insulin-dependent diabetes mellitus; lack of microvascular degenerative disease, at least in this study group, even after more than 30 years follow-up; lack of progression towards insulin-dependent diabetes mellitus.
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PMID:[Chronic non-insulin deficient hyperglycemia in children]. 206 61

Diabetes mellitus is characterized by recurrent metabolic abnormalities which postmortem studies suggest might be associated with degenerative changes in the central nervous system. Acute hypoglycemia does indeed lead to cognitive impairment, whereas acute hyperglycemia in the absence of ketoacidosis or hyperosmolarity does not. Insulin-dependent diabetes mellitus is associated with cognitive deficits that tend to be relatively slight, inconsistent between different studies, and unrelated to clinical indicators; they can be ascribed as plausibly to psychogenic factors as to degenerative disease. In contrast, cognitive impairment in noninsulin-dependent diabetes mellitus is more conspicuous in tests of learning and memory, consistently associated with a patient's level of glycemic control, and more plausibly to be ascribed to structural neuropathology. Nevertheless, in both cases the deficits in question are unlikely to interfere significantly with patients' everyday functioning.
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PMID:Cognitive function in diabetes mellitus. 228 78

The clinical, pathological, and epidemiological relationships between fasting plasma glucose (FPG) concentrations and the sites of lesion in osteoarthritis (OA) were evaluated in 1026 patients. The mean FPG (99 +/- 22.2 mg/dL) was significantly higher in OA (p less than 0.01) than in the normal controls (88 +/- 19.9 mg/dL). In addition, the mean FPG (97.9 +/- 23 mg/dL) was significantly higher in female patients with OA (p less than 0.01) than in an osteoporotic sex-matched control group (92.8 +/- 24.5). FPG concentrations did not vary significantly according to the sites of the OA lesions. Fifty-six (5.5%) OA patients had long-term diabetes mellitus (FPG greater than 140 mg/dl). Few significant differences in the pathological and clinical findings were seen between normoglycemic and hyperglycemic OA patients, only the ESR (p less than 0.01) and pain at rest (p less than 0.02) being higher in the second group. These epidemiological data support the observation that hyperglycemia, which acts on matrix macromolecules, may be related to the development of bone degenerative disease.
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PMID:Plasma glucose concentration in symptomatic osteoarthritis: a clinical and epidemiological survey. 237 41

Spinal neuroarthropathy is a little-known complication of traumatic paraplegia. Four cases of this syndrome are described, with emphasis on the characteristic radiographic findings of severe juxta-articular bone destruction, dense appositional new bone formation, large osteophytosis, and soft-tissue bony debris. The factors predisposing patients to develop a neuropathic joint are diminished pain and proprioceptive sensations with maintained mobility. When a paraplegic patient transfers in or out of a wheelchair or moves his upper torso, he exerts force on an insensate spine. Repeated trauma increases joint mobility beyond the normal limits, and this leads to further damage, with the process culminating in severe instability and bone destruction. The other causes of neuropathic joints in the spine--tertiary syphilis, syringomyelia, and diabetes--must be ruled out on clinical grounds. Neuropathic changes in the spine are often silent, delaying treatment, or may be mistaken for infection or degenerative disease. Their true prevalence is difficult to determine, but the possibility should be considered in paraplegic patients with the characteristic radiographic findings.
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PMID:Spinal neuroarthropathy after traumatic paraplegia. 312 83

Analysis of 109 well documented cases of permanent total atrial paralysis reported in the literature illustrated the features of this arrhythmia which is a well defined entity consisting of suppression of all electrical and mechanical activity of both atria lasting for more than 6 months. Standard electrocardiogram reveals junctional bradycardia of about 40 bpm without any visible P waves and narrow supraventricular QRS complexes in 80% of cases. This diagnosis can only be confirmed by meticulous bipolar endocavitary recordings exploring all atrial walls without recording an auriculogram and by right intra-atrial and coronary sinus stimulation which proves to be ineffective. This disease has a male predominance in two-thirds of cases and a familial nature in 18% of cases. Seventy one per cent of affected subjects are under the age of 50 years. In 33% of cases, it is associated with Emery-Dreifuss muscular dystrophy, in which it constitutes a specific sign allowing this dystrophy to be differentiated from all other forms, especially facio-scapulo-humeral myopathy, and in 30% of cases, it is associated with a degenerative disease such as diabetes, amyloidosis or primary cardiomyopathy. Idiopathic dilatation of the right atrium is revealed in 15% of cases. The arrhythmia is responsible for syncope or faintness in 31% of cases, cerebral vascular accidents in 21% of cases and heart failure in 35% of cases. Cardiac activation is dependent on a junctional escape rhythm. The mechanism of the lesion responsible is atrial fibrosis which may extend to the sinoatrial node. The treatment of choice consists of implantation of a VVI or VVIR mode cardiac pacemaker in combination with anticoagulant therapy.
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PMID:[Total permanent auricular paralysis. Review of the literature apropos of 109 cases]. 779 52

The case of a 45-year-old woman with gyrate atrophy of the choroid and retina is documented. Additional features in this case, to the authors' knowledge not previously described in gyrate atrophy, are massive cystinuria, massive lysinuria, axial hypermetropia and diabetes. Gyrate atrophy is a rare autosomal recessive degenerative disease of the choroid and retina and is accompanied by defective ornithine metabolism. Simell and Takki demonstrated the association with hyperornithinaemia in 1973. The main metabolic features are those of hyperornithinaemia and ornithuria caused by a deficiency of the mitochondrial matrix enzyme, ornithine aminotransferase (OAT). The responsible human gene has been localised to chromosome 10. Despite the generalised deficiency of OAT, the literature indicates significant pathological involvement of the eye only. Ophthalmological features of the disease are myopia (up to 10-20 dioptres), night blindness, constricted visual fields and complicated cataracts. The clinical picture has been detailed previously by various authors. The case of a 45-year-old woman with gyrate atrophy and hyperornithinaemia is documented here. She has been followed up for 12 years and fully investigated. Additional features in this case, to our knowledge not previously described in gyrate atrophy, are massive cystinuria, massive lysinuria, axial hypermetropia and diabetes.
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PMID:Gyrate atrophy of the choroid and retina with hyperornithinaemia, cystinuria and lysinuria. 795 31

A variety of degenerative diseases involving deficiencies in mitochondrial bioenergetics have been associated with mitochondrial DNA (mtDNA) mutations. Maternally inherited mtDNA nucleotide substitutions range from neutral polymorphisms to lethal mutations. Neutral polymorphisms are ancient, having accumulated along mtDNA lineages, and thus correlate with ethnic and geographic origin. Mildly deleterious base substitutions have also occurred along mtDNA lineages and have been associated with familial deafness and some cases of Alzheimer's Disease and Parkinson's Disease. Moderately deleterious nucleotide substitutions are more recent and cause maternally-inherited diseases such as Leber's Hereditary Optic Neuropathy (LHON) and Myoclonic Epilepsy and Ragged-Red Fiber Disease (MERRF). Severe nucleotide substitutions are generally new mutations that cause pediatric diseases such as Leigh's Syndrome and dystonia. MtDNA rearrangements also cause a variety of phenotypes. The milder rearrangements generally involve duplications and can cause maternally-inherited adult-onset diabetes and deafness. More severe rearrangements frequently involving detections have been associated with adult-onset Chronic Progressive External Ophthalmoplegia (CPEO) and Kearns-Sayre Syndrome (KSS) or the lethal childhood disorder, Pearson's Marrow/Pancreas Syndrome. Defects in nuclear-cytoplasmic interaction have also been observed, and include an autosomal dominant mutation causing multiple muscle mtDNA deletions and a genetically complex disease resulting in the tissue depletion of mtDNAs. MtDNA nucleotide substitution and rearrangement mutations also accumulate with age in quiescent tissues. These somatic mutations appear to degrade cellular bioenergetic capacity, exacerbate inherited mitochondrial defects and contribute to tissue senescence. Thus, bioenergetic defects resulting from mtDNA mutations may be a common cause of human degenerative disease.
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PMID:Mitochondrial DNA mutations in diseases of energy metabolism. 807 79

Insulin-like growth factor-I (IGF-I) is a pleiotropic protein that acts on many tissues and organs. As it is one of the major trophic factors in the circulation, its actions in peripheral tissues are well established. It has been used for the treatment of several diseases, including growth deficiency, osteoporosis, catabolic disorders and diabetes. Recent evidence supports the significance of IGF-I in the maintenance of the integrity and homeostasis of the nervous system. The widespread distribution of its receptor allows IGF-I to affect the survival of numerous populations of neurones and glial cells in both the CNS and the PNS. Most recently, a clinical trial has revealed the beneficial effects of IGF-I in amyotrophic lateral-sclerosis (ALS), a degenerative disease of the motoneurones. We review briefly here experimental and clinical information that suggests the potential usefulness of IGF-I in the treatment of certain neurodegenerative diseases, including ALS, Alzheimer's disease, various neuropathies and brain trauma. The rather unique propensity of IGF-I to act on a variety of neuronal cells might provide a general means of reducing or slowing down neuronal losses that occur following various brain insults.
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PMID:Rediscovering an old friend, IGF-I: potential use in the treatment of neurodegenerative diseases. 924 19

Experimental investigations in animals have highlighted the role of early reduced calorie and protein nutrition on fetal cardiovascular development, and the occurrence of a transition from a low fetal arterial blood pressure in late gestation to a high arterial blood pressure postnatally. These observations may explain the correlation between health, including appropriate nutrition, in pregnant women and the outcome of their pregnancies. Emphasis has been placed on low birth weight infants who have an increased risk of developing cardiovascular diseases, including hypertension, coronary heart disease and stroke in adulthood. Vascular pathology in adults is not always associated with low birth weight and animal experiments indicate that substantial changes in cardiovascular and endocrine function can result from maternal or fetal undernutrition without impairing fetal growth. Experimental investigation on organogenesis shows the pivotal role of adequate protein availability as well as total caloric intake. Amino acid metabolism in the feto-maternal unit appears to have a key influence on the development of organs involved in chronic degenerative disease in the adult. Experimental investigation has also highlighted the role of carbohydrate metabolism and its effect on the fetus in this respect. Either restriction of protein intake or diabetes in pregnant rats has intergenerational effects at least on the endocrine pancreas and the brain. Further investigation is needed to clarify the mechanisms involved and lead to a new understanding of the importance of nutrition during pregnancy. This will provide an important approach to the primary prevention of diabetes and chronic degenerative diseases.
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PMID:Intrauterine nutrition: its importance during critical periods for cardiovascular and endocrine development. 988 34


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