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

Collagen undergoes progressive browning with age and diabetes characterized by yellowing, fluorescence, and cross-linking. The present research was undertaken in order to investigate the nature of the collagen-linked fluorescence. Human collagen was exhaustively cleaved into peptides by enzymatic digestion. Upon purification, a highly fluorescent chromophore was identified and purified from old human collagen. Structure elucidation revealed the presence of an imidazo [4,5-b] pyridinium-type structure acting as a cross-link between arginine, lysine, and a pentose. This advanced glycosylation end-product and protein cross-link results from the reaction of pentoses with proteins and was named pentosidine. Further work indicated that long-term glycosylation of proteins with hexoses also leads to pentosidine formation through sugar fragmentation. The proposed mechanism of pentosidine formation involves the dehydration of the pentose-derived Amadori compound to form an intermediate which is attacked under base catalysis by the guanido group of arginine. The strict requirement for the Amadori rearrangement is uncertain. However, oxidation is definitely involved since pentosidine is not formed in the absence of oxygen. Five-carbon sugars contributing to pentosidine formation could be formed from larger sugars by oxidative fragmentation or from trioses, tetroses, and ketoses by condensation and/or reverse aldol reactions. Pentosidine increases exponentially in human skin at autopsy. Mean age-adjusted skin levels were significantly increased in subjects with uremia and especially in type 1 diabetics with uremia vs. controls. In skin biopsy, levels were significantly elevated in all diabetic (type 1) vs. control subjects. The highest degree of association was with the cumulative grade of diabetic complication (retinopathy, nephropathy, arterial stiffness, and joint stiffness). Pentosidine also forms in various proteins other than collagen, although to a much lesser extent. In blood, pentosidine is mainly associated with plasma proteins and is highly elevated during uremia. In the lens, it is associated with both water-soluble and -insoluble protein fractions and is especially elevated during brunescent cataract formation. The origin of pentosidine in vivo is uncertain. Evidence suggests that the pentoses are the most reactive sugars in pentosidine formation in vitro; however, the origin and importance of free pentoses in vivo, especially during the diabetic state, are not certain. Possible origins include hemolysis and/or a defect in the primary pentose metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)
Diabetes Metab Rev 1991 Dec
PMID:Pentosidine: a molecular marker for the cumulative damage to proteins in diabetes, aging, and uremia. 181 79

The phases of wound healing--inflammatory, fibroblastic, and maturation--are continuous, though they overlap and do not always occur in an orderly fashion. Wound healing may be retarded by age, diabetes, smoking, immunosuppression, poor nutrition, cell hypoxia, dehydration, bacteria, and other factors. Bacteria and pus may be so great at the inflammatory phase that the wound remains at that phase. It is important that the nurse recognize when pus is a major factor in an unhealed wound and initiate local care to assist in cleaning the wound bed. It is also important to recognize a clean wound and to initiate appropriate local care that facilitates wound healing. New information about wound healing at the cellular level continues to become available. Epidermal growth factors, platelet-derived growth factors, and the growth hormone somatomedin are being studied, and new methods based on these studies may change local wound care measures. It is essential to understand the phases of wound healing to determine appropriate wound care measures for individual patients.
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PMID:Phases of wound healing. 182 67

Atrial natriuretic hormone (ANH) levels in plasma and the right atrium of non-obese diabetic mice in the decompensated diabetic state were investigated by radioimmunoassay and histological examination. Severely diabetic mice, with blood glucose levels over 33.6 mmol/l showed significantly higher hematocrit, plasma sodium and calculated plasma osmolarity than the age-matched normoglycemic mice. The plasma ANH levels in diabetic mice were significantly lower (17.5 pmol/l) than those in normoglycemic mice (43.6 pmol/l). The ANH concentrations in the right atrium were 26.6 mg/g protein in the diabetic and 11.2 mg/g protein in the normoglycemic mice. The right atrium in the diabetic mice showed much wider immunohistochemical staining by anti-human ANH antiserum compared with the normoglycemic mice. An increase in the number of atrial specific granules in the diabetic mice was observed by transmission and scanning electron microscopy. Morphometrical analysis indicated that the number of granules increased to more than twice that in the normoglycemic mice. These findings indicate that plasma ANH decreases in diabetic mice. The store of right atrial ANH may be increased to compensate for the marked dehydration in severe diabetes.
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PMID:Effect of diabetes mellitus on levels of atrial natriuretic hormone in plasma and the right atrium in the non-obese diabetic mouse. 182 62

Dehydration, in childhood as in adulthood, may origin from an inadequate water ingestion or an excessive water elimination. Causes may be found in fever, vomiting, scalds, pulmonary hyperventilation, diabetes. Water loss during acute diarrhea in children can be even 6-7 times higher in comparison with an healthy child. Together with water, electrolytes are lost. We differentiate dehydration in isonatremic d. (70% of cases), hyponatremic d. (10%) and hypernatremic d. (20%) basing on Sodium loss. Important dehydration causes severe clinical symptoms as shock, renal and cardiocirculatory failure, convulsion, coma. Symptoms at the central nervous system level derivate both from hyperosmolarity in brain cells and from thrombosis or hemorrhages in subdural sites. Dehydration, following acute diarrhea, is slight when weight loss is lower than 5%. The child health conditions still remain good. Dehydration become moderate if weight loss reaches 5% and the child starts suffering. When the weight loss reaches 10%, dehydration is now severe and circulatory deficiency becomes evident. When it is higher than 10%, prognosis is very severe and shock and coma may be observed. In the present work, we illustrate the different ways of rehydration after acute diarrhea. Initially, oral rehydration must be established with one of the oral solutions, differing each other for amount of electrolytes and glucose. Recently, a new solution, "supersolution", has been presented differing from the other ones for electrolytes concentration and for the presence of rice starch instead of glucose. In most cases of diarrhea, oral rehydration appears adequate but sometimes an intravenous rehydration becomes necessary, e.g. in case of vomiting, CNS depression and in any case of severe gastroenteric symptomatology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dehydrated child]. 189 82

This article reviews diagnosis and management of infants with diabetes. These infants present with signs and symptoms confused with other more common illnesses in this age group. A physician examining an ill-appearing dehydrated infant, without any obvious cause for the dehydration, should quickly screen the urine for glucose and ketones. Diagnosis of diabetes is a problem when an infant has only hyperglycemia or ketonuria. Febrile illnesses, convulsions, and dehydration can cause these laboratory abnormalities. Once the diagnosis of diabetes is made in the infant, management is complicated by the difficulty in administering small doses of insulin, monitoring blood glucose, complementing insulin administration with feedings, and hypoglycemia. The potential for brain damage with unrecognized episodes of hypoglycemia is always a concern in infants. This article offers suggestions for treating hypoglycemia as well as guidelines for making insulin adjustments when the infant is ill. The physician should be aware of the psychosocial issues involving the family of an infant with diabetes. Optimism and ongoing support should be provided to the family, so that the infant can grow up healthy and possibly benefit from research on the cure of diabetes.
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PMID:Diabetes in infancy: diagnosis and current management. 192 May 10

Contrast-induced nephropathy is a potentially serious untoward reaction to radiologic contrast media. The incidence of this nephropathy and the predisposing conditions are not well established, possibly because of methodologic differences between studies. We evaluated the incidence of contrast-induced nephropathy after femoral arteriography in 394 patients by using multiple definitions (different increases in serum creatinine or blood urea nitrogen levels at various times). When an increase in the level of serum creatinine of greater than 0.3 mg/dl and greater than 20% on day 1, 2, or 3 and on day 5, 6, or 7 was used to define the disorder, the incidence in our group of patients was 10% for nonazotemic patients vs 30% for azotemic patients (p less than .001); 2% for nondiabetic, nonazotemic patients vs 16% for diabetic, nonazotemic patients (p = .003); and 38% for patients who were both diabetic and azotemic vs 16% for diabetic, nonazotemic patients (p = .022). Baseline renal insufficiency and diabetes mellitus (especially when insulin dependent) were significant predisposing factors. The effects of dehydration and increased volume of contrast medium on the incidence of contrast-induced nephropathy were not clear; the age and sex of the patient were not important risk factors. The incidence of contrast-induced nephropathy depends on the definition used. Although contrast-induced nephropathy may develop in any patient, diabetes, renal insufficiency, and, possibly, dehydration and dose of contrast medium are risk factors.
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PMID:Radiocontrast-associated renal dysfunction: incidence and risk factors. 204 41

We have described a case of hyperosmolar nonketotic hyperglycemia atypically manifested as an ascending progressive predominantly motor neuropathy with sensory involvement. Although the patient noticed polydipsia, the lack of endogenous renal function prevented the expected polyuria and dehydration. Treatment with insulin produced such marked clinical improvement that 15 days after admission he was discharged home, fully mobile and self-sufficient. Because hyperosmolar nonketotic decompensation is uncommon and patients may initially have neurologic signs without a previous history of diabetes mellitus, the diagnosis may be overlooked.
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PMID:Hyperosmolar nonketotic hyperglycemia manifested as ascending polyneuropathy. 210 69

Fluid therapy is practical and beneficial when properly administered to cattle. Mature cattle are more frequently alkalotic than acidotic, so nonalkalizing solutions are usually indicated. Exceptions include cattle with choke, carbohydrate engorgement, diabetes mellitus, and, occasionally, renal disease, diarrhea, and fatty liver/ketosis. Most dehydrated cattle need supplemental potassium and calcium as well as sodium, chloride, and water. Intravenous administration is indicated in patients with obstructive gastrointestinal disease and those with severe dehydration. Oral or intraruminal administration is less expensive and often very effective.
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PMID:Fluid therapy in mature cattle. 217 37

Age-related cataract is a condition characterized by multiple mechanisms and multiple risk factors. The mechanisms that bring about a loss in transparency include oxidation, osmotic stress, and chemical adduct formation. Risk factors for cataract include diabetes, radiation (ultraviolet B, x-ray), certain pharmaceutical substances, certain nutritional states, and possibly acute episodes of dehydration. Interaction occurs between and among mechanistic factors and risk factors. Thus nutrition must be considered as one part of a tapestry of intertwined events and responses. Certain experimental models for nutritional cataract have been useful for study of the cataractogenic process but are probably not important factors in the human disease. Little current evidence supports significant roles in human senile cataract for imbalances of tryptophan or other amino acids, deficiencies of calcium or selenium, or excessive intake of selenium. Overconsumption of galactose is likely to be hazardous only in subjects with genetic inability to metabolize this sugar. Vitamins with antioxidant potential (riboflavin, vitamin E, vitamin C, carotenoids) deserve further research scrutiny to ascertain their significance in cataract etiology. Excessive caloric intake needs to receive added emphasis as a factor contributing to cataract. Diabetes increases the likelihood of cataract three- to four-fold. Obesity, defined as more than 20% overweight, is considered a major risk factor for non-insulin-dependent, or type II, diabetes (69, 73). Weight control can be recommended as a prudent, safe, economic, and effective means of lowering risk probability for diabetes and the associated complication of cataract.
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PMID:Nutritional factors in cataract. 220 Apr 64

A method is described in which the viability of isolated adult human islets of Langerhans can be assessed in vivo. The Rowett nude rat, made diabetic with streptozocin (STZ), has been used as the islet recipient in these studies. Although these animals are athymic and are able to accept xenogeneic grafts for prolonged periods, they are very susceptible to dehydration and infection once made diabetic. Therefore, a considerably shortened diabetes induction period was used. The basis of the study was to prepare pure adult human pancreatic islets that were cultured for 48 h. Nude rats were given 80 mg/kg i.v. STZ during islet isolation and were transplanted with 800-1000 islets under the renal capsule at 48 h. To monitor islet function, animals were bled regularly for random blood glucose measurements and were given a glucose tolerance test at day 20. The kidney containing the graft was removed on day 21 to allow histological assessment of the graft and to confirm that glucose control was due to the transplanted islets and was not secondary to reversion of the animal's own islets. Seven rats were transplanted, and five were deemed to have received viable human islets. Two rats that received islets from the same donor did not reverse their diabetes and were found by histology to have vacuolated islet structures with scant insulin-staining tissue under the kidney capsule. This method allows a definitive judgment of the ability of isolated adult human islets to reverse diabetes.
Diabetes 1989 Feb
PMID:Successful reversal of diabetes in nude rats by transplantation of isolated adult human islets of Langerhans. 249 76


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