Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.
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PMID:Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria. 206 52

Malnutrition is a common problem of patients undergoing liver transplantation. To treat malnutrition, it must first be identified through a nutritional assessment. Because many objective nutritional assessment parameters have limitations in end-stage liver disease, subjective nutritional indicators may be used as an alternative. Nutritional needs following transplantation are categorized as short and long term. The short-term nutritional goal, anabolism, can be complicated by the nutritional status of the patient, surgical procedures, and necessary medications. The increased nutrient needs during the early posttransplant phase require particular nutritional support. Nutrition-related problems following transplantation may include obesity, hyperlipidemia, hypertension, diabetes mellitus, hyperkalemia, edema, or osteoporosis. Dietetic advice relative to the nutritional needs of the liver transplant recipient can improve both the short- and long-term outcomes.
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PMID:Nutritional implications of liver transplantation. 208 51

Fifty-eight insulin-dependent diabetic (IDDM) patients with a disease duration of more than three years were evaluated and divided in three groups depending on the mean sugar blood levels in a three month follow-up. In the first group sugar blood level was lower than 7.7 mmol/l, in the second group it was between 7.7 and 11.1 mmol/l, and in the third group it was higher than 11.1 mmol/l. The nutritional status was evaluated. Protein malnutrition was found in 50% of the evaluated subjects, with a significant relation between the degree of metabolic control and the prevalence of protein malnutrition. In group I (sugar blood level less than 7.7 mmol/l) the prevalence of malnutrition was 31%, whereas in groups II and III (greater than 7.7 mmol/l) it was 54% and 61%, respectively. We discuss the importance to evaluate the nutritional status in diabetic patients, as protein malnutrition is a significant cause of general morbidity and mortality, which can be added to those attributable to diabetes itself.
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PMID:[Protein malnutrition in insulin-dependent or type I diabetes mellitus. Relationship with the degree of metabolic control]. 209 Aug 93

Thirty three patients, 24 male and 9 female, aged from 19 to 90 with an average of 58.8, were admitted to the medical intensive care unit (ICU) from 1988 December to 1989 December. Their host defenses were evaluated. Cell-mediated immunity (CMI) included delayed type skin test (MULTITEST CMI), total lymphocyte count and lymphocyte subpopulations (CD3, CD4 and CD8) were determined. Investigation of humoral immunity (HI) included use of serum levels of immunoglobulins (IgG, IgA and IgM) and complements (C3 and C4). Episodes of nosocomial infection were documented by patients' clinical and laboratory data, including positive culture. The CMI, especially for total lymphocyte count, T lymphocyte count and skin test, was impaired by underlying diabetes mellitus and such associated conditions as malnutrition, steroid administration and surgical procedures. The longer the admission period, the lower was the CMI including total lymphocyte count, CD3 percentage, CD4 percentage and skin test response. The HI was less impaired by underlying conditions and not influenced by admission duration. More infection episodes were found in patients with longer admission duration. In conclusion, the host defense was impaired in patients hospitalized longer in medical ICU, and the combination of compromised immunity and impaired mucocutaneous barriers made them more susceptible to infections.
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PMID:Evaluation of host defense in critically ill patients in medical intensive care unit. 209 3

Cases of malnutrition-related diabetes mellitus conforming to the description of the protein deficient pancreatic diabetes type in Ethiopian patients were compared with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic. Fourteen of 39 malnutrition-related diabetes mellitus patients had fat malabsorption compared with only two of ten Type 1 diabetic patients and one of nine control subjects. Xylose absorption was normal favouring a pancreatic cause for the malabsorption. Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucagon secretion patterns were similar in malnutrition-related and Type 1 diabetic patients. Of 23 new malnutrition-related diabetic patients treated with glibenclamide after nutritional rehabilitation and insulin treatment, only three responded, 14 were unresponsive but remained ketosis free for over eight days while another six developed ketoacidosis or significant ketonuria within two to six days during the trial. Sixteen unselected Type 1 diabetic patients who discontinued their insulin therapy all developed frank ketoacidosis after a mean of 5.5 days. The similarity of the malnutrition-related and Type 1 diabetes mellitus in age of onset, insulin requirement for diabetic control and appearance of ketosis-proneness in some cases, together with the similarity of C-peptide and glucagon secretion patterns suggest that the protein deficient pancreatic diabetes variant of malnutrition-related diabetes mellitus may be Type 1 diabetes mellitus modified by the background of malnutrition rather than an aetiologically separate entity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical and hormonal (C-peptide and glucagon) profile and liability to ketoacidosis during nutritional rehabilitation in Ethiopian patients with malnutrition-related diabetes mellitus. 211

We investigated the cellular mechanisms responsible for growth hormone (GH) resistance in diabetes and malnutrition in the rat. In insulin-dependent diabetes, a post-receptor defect participates in GH resistance. During fasting, there is a loss of liver GH binding sites. Dietary protein restriction causes a post-receptor defect. This defect can be attributed to the combined effects of decreased liver IGF-I mRNA content and impaired message translation.
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PMID:[Diabetes, malnutrition and growth retardation]. 211 33

Sixty-one diabetic patients, followed for two years, were divided in two groups for evaluation. One group consisted of the patients who had a bacterial or fungal infection, and the other those in whom no infection had been recorded. The association of the infection with the degree of metabolic control and with the presence or absence of protein malnutrition were assessed. The group of patients with infection was positively correlated with malnutrition and poor metabolic control. In the group with infections, the prevalence of protein malnutrition was 77% while in the patients without infection it was 36%. 11% of patients with sugar blood level lower than 140 mg/dl (7.7 mmol/l) had infections, whereas 79% of those with sugar blood levels higher than 200 mg/dl (11.1 mmol/l) had infections. We emphasize the relevance of hyperglycemia and protein malnutrition as predisposing factors of infection in diabetes and the need to assess the nutritional status in those patients.
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PMID:[Infection in diabetes: the relation to the degree of metabolic control and protein malnutrition]. 212 57

The Insulin-like Growth Factors (IGFs) or Somatomedins are polypeptide growth factors which are similar to insulin in respect to their aminoacid sequence, structure and biologic activities. The IGFs bind to high affinity receptors which are present on many cells and in many tissues. In the circulation the IGFs are bound to transport (binding) proteins (IGF-BPs). In this review the physiologic role, the basic chemistry and the gene expression of this family of growth factors is summarized systematically. The pathophysiology of growth disorders, diabetes mellitus, malnutrition, liver and kidney disease in relation to the IGFs as well as the therapeutic and diagnostic potentials of these peptides are discussed in detail.
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PMID:[Principles and clinical significance of insulin-like growth factors/somatomedins]. 217 3

Reports of an increased incidence of wound complications in surgical patients with diabetes mellitus may actually reflect the increased incidence of general surgical risks or metabolic abnormalities associated with diabetes mellitus. Factors such as age, obesity, malnutrition, and macrovascular and microvascular disease may contribute to wound infection and delayed wound healing especially in the type II diabetic patient. In addition, hyperglycemia caused by decreased insulin availability and increased resistance to insulin can affect the cellular response to tissue injury. Studies of the immune cells necessary for wound healing, such as PMN leukocytes and fibroblasts, as well as studies of injured tissue suggest that there is a delayed response to injury and impaired functioning of immune cells in diabetes mellitus. There is evidence that these impairments may be the result of both an inherent (genetic) defect as well as decreased insulin availability and increased blood glucose concentration. At the time of hospital admission, little can be done to affect most of the risk factors or inherent cellular defects. However, blood glucose levels can be controlled with the use of bedside blood glucose monitoring and frequent adjustment of insulin dosing. Nurses have traditionally played an important role in monitoring recovery from surgery and watching for signs of infection and wound complications. These nursing functions are especially important in the diabetic patient. In addition, frequent evaluation of the effectiveness of insulin therapy is an important nursing function throughout the perioperative period. Through improving management of blood glucose levels in surgical patients, nurses can have a major impact on the incidence of wound complications in diabetes mellitus.
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PMID:Wound healing in the patient with diabetes mellitus. 217 91

The aging process alters body composition so that nutritional status changes as we get older. The aging process shows interindividual variability in its rate of development. Determinants of the rates of aging of systems and tissues are largely genetic. Premature aging of cells and tissues is due to genetic factors and to long-term exposure to physical or chemical environments that cause irreversible tissue damage. Whereas maximal lifespan is fixed for us all, individuals vary in life expectancy both because of variability in the risk of genetic disease which shortens life and because of variable capability for avoidance of those factors in our environment which cause early aging. Early aging as well as geriatric disease foreshorten life, but both can be prevented to some extent by diet or by diet and exercise. Diseases that can be nutritionally prevented, giving us a greater chance of achieving our genetically determined lifespans, include nutritional deficiency states and chronic diet-related diseases such as non-insulin-dependent diabetes, hypertension, coronary artery disease, and cancer. Disabilities resulting from these diseases and from degenerative arthritis are also subject to modulation by diet. The nutritional requirements of the elderly are mostly similar to those of younger people. Elderly usually need fewer calories and similar nutrient intakes compared with those of younger people. Elderly with higher needs for specific nutrients include homebound or institutionalized people who lack sunlight exposure and therefore require more vitamin D. Nutritional requirements to promote longer life expectancy and freedom from disabilities that result from chronic disease include restriction of food energy and fat. Nutritional assessment of the elderly is aimed at identifying not only the presence of deficiency states but also states of nutrient excess and chronic diet-related diseases. There are certain problems in carrying out nutritional assessment in the elderly, but techniques are now available which make valid assessment possible even in the oldest old. Those who live longest have less genetic risk of premature aging, but as a result of native intelligence, education, coping skills, and higher socioeconomic status, they also have a greater likelihood of eating a diet that best meets their long-term nutritional needs. Those most at risk for developing malnutrition as they get older are those who lack food access because of poverty, because of disability resulting from chronic geriatric disease, or because of a combination of these factors. Malnutrition is found in elderly in our society who live in their own homes if they are indigent, isolated, and homebound because of disability.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Geriatric nutrition. 218 27


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