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

To evaluate the risk factors for diabetes mellitus, I examined 2573 people (1851 males and 722 females) who received medical checkups more than twice at a health examination center in Tokyo during the period from 1976 through 1991. Diabetic patients were excluded at the beginning. The mean follow up duration was 5.2 years. A self-registering questionnaire was administered at the time of the health checkup. The standard of this study was the onset of diabetes mellitus or glucose intolerance (fasting blood sugar over 110 mg/dl). I compared two prognosis groups (a normal group and a diabetic group) in terms of age, examination findings and prevalence of health risks (lifestyle, stress and working form). I also assessed family history of diabetes and past history including hypertension, hepercholesterolemia and hyperuricemia. After assessing each variable, I employed Cox's proportional hazards model analysis. 1) Among the subjects, 296 persons (243/1851 [13.1%] males, and 53/722 [7.3%] females) were newly diagnosed with diabetes during the observation period. 2) The diabetic group had significant differences compared to the normal group in age, BMI (Body Mass Index), FBS (fasting blood sugar), smoking, drinking, eating no breakfast, dairy intake, hypertension, hypercholesterolemia, hyperuricemia, and family history by t-test and chi 2 test. 3) According to proportional hazards model analysis, FBS, age, family history, hypertension, smoking and BMI were selected as significant risk factors for diabetes in males. For females, breakfast, FBS, age, drinking and hypertension were selected. 4) Diabetes seemed to be related to fixed factors such as age, or genetic factors such as family history and FBS in males. For females, lifestyle, such as eating no breakfast and drinking habit played an important role.
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PMID:[Risk factors for diabetes mellitus evaluated by long-term observation]. 858 85

A decision support system for the management of oral hypoglycaemic therapy in type II diabetes was evaluated. The ruleset contained therein forms the basis of a prototype computer programme, but in order to assess the robustness of the individual rules, it was decided it was necessary to use a paper-based form of the ruleset. A nurse with no previous experience of managing type II diabetes was trained to use the system and then undertook the exclusive management of half of all new type II diabetics, from a district population of 300,000, over a 16-month period. General practices within this area were divided into two groups, study and control, matching for size, geographical area and standards of existing diabetes care. Patients (n = 102) from the study group practices were then assigned to her care. Those patients (n = 116) in the control group of practices were treated according to their normal procedures. The decision support system for oral hypoglycaemic therapy was based on the following criteria: the current type of treatment (six levels); current glycaemic control (HbA1 and FBS)-whether improving, steady or worsening; and weight-%IBW, whether rising, steady or falling. Each of these parameters was carefully defined on the basis of established practice and clinical experience. Patients after initial education were seen at their usual clinic by the nurse only, on a monthly basis, until satisfactory glycaemic control was established and thereafter reviewed 3 monthly. She was also responsible for ensuring the organisation of Diabetes Annual Review procedures. The medical records of the control group patients were examined at the end of the study and data on glycaemic control and Annual Reviews extracted. In the study group 98% patients achieved HbA1 levels within the normal range and all patients had full annual reviews performed. The control practices achieved much poorer degrees of metabolic control (P < 0.01) and completed fewer annual reviews. The study group did not demonstrate a significantly increased frequency of clinical hypoglycaemia consequent upon better blood sugar control. No exceptions to the ruleset, as initially defined, were detected. In conclusion, this decision support system was successful at achieving standards of diabetes control and care equal to or better than conventional structures of diabetes care. Implementation of such a system, on a simple computer platform, could greatly assist and possibly improve diabetes management in general practice.
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PMID:Implementation and evaluation of a decision support system for type II diabetes. 889 84

To investigate the possible implication of non-enzymatic glycosylation in the etiopathogenesis of the diabetic retinopathy, we studied the effect of early and advanced glycation products on the growth of retinal microvascular cells. Glucose modified products were obtained by incubating bovine serum albumin or fetal bovine serum with 0.5 M glucose for 10 (early glycation products: EG-BSA and EG-FBS, respectively) or 60 days (advanced glycation end products: AGE-BSA and AGE-FBS, respectively). Cell growth was assessed by cell counting and DNA content determination. EG-BSA or AGE-BSA significantly decreased pericyte proliferation after 8 days of culture (33 and 13% inhibition, respectively). Concerning endothelial cells, EG-BSA reduced proliferation to 40% whereas AGE-BSA increased it to 156% after 4 days of culture. The glucose-treated sera didn't exhibit the same growth effects, neither the EG-FBS nor the AGE-FBS significantly affected endothelial cell proliferation. Only the AGE-FBS showed a significant inhibitory effect on pericyte proliferation (40% inhibition). We conclude that retinal microvascular cell growth in vitro could be differently modulated by early and advanced glycation products. The inhibitory effect of AGEs observed on pericyte growth, suggests that glycoxidation could be implicated in the pericyte loss observed in diabetic retinopathy.
Diabetes Res Clin Pract 1997 Jan
PMID:Growth modulation of retinal microvascular cells by early and advanced glycation products. 906 64

We student basal, glucose- and glucagon-induced insulin secretion in non-insulin diabetes mellitus (NIDDM) patients in relation to body mass index (BMI) and fasting serum glucose (FBS) level. A total of 46 NIDDM patients and 22 control subjects with varying degrees of BMI and FBS were given 100 g of oral glucose and 1 mg of intravenous glucagon on separate days. C-peptide response to glucose, but not basal serum C-peptide and C-peptide response to glucagon, was significantly lower in NIDDM than in controls (P < 0.001). FBS was inversely correlated with C-peptide response to glucose in NIDDM patients (r = -0.67, P < 0.001), but not with basal C-peptide level and C-peptide response to glucagon. On the other hand, BMI was positively correlated with basal serum C-peptide level both in NIDDM (r = 0.60, P < 0.001) and in control subjects (r = 0.74, P < 0.001). In 15 poorly controlled NIDDM patients, the tests were repeated after insulin treatment for 10-14 days. C-peptide response to glucose significantly increase, but not to a level in control subjects, after glycemic control. Basal serum C-peptide level and the C-peptide response to glucagon decreased after glycemic control to significantly lower levels than those in the baseline and those in control subjects. These results suggest that beta cell secretory reserve is reduced in moderate to severe NIDDM patients.
Diabetes Res Clin Pract 1997 Sep
PMID:Differential effects of ambient blood glucose level and degree of obesity on basal serum C-peptide level and the C-peptide response to glucose and glucagon in non-insulin-dependent diabetes mellitus. 930 37

Leptin is the protein product of the ob gene, an adipocyte-specific gene, recently discovered in mice. Plasma leptin levels were determined in six normals, twenty-one subjects with impaired glucose tolerance, and forty-nine untreated NIDDM subjects. They increased with the augmentation of obesity (body mass index, BMI kg/m2) and were higher in females than in males: in BMI less than 25 kg/m2 the values of plasma leptin were 2.24 +/- 0.25 ng/ml (n=29) in males and 3.01 +/- 0.39 ng/ml (n=13) in females (P<0.054), respectively, in BMI between 25 kg/m2 and 30 kg/m2 they were 3.14 +/- 0.31 ng/ml (n=10) in males and 10.66 +/- 2.86 ng/ml (n=7) in females (P<0.0018) and in BMI higher than 30 kg/m2 their levels were 8.98 +/- 1.5 ng/ml (n=11) and 11.74 +/- 2.2 ng/ml (n=6) (P<0.23), respectively. The severity of diabetes mellitus judged from the fasting plasma glucose level had no influence on the plasma leptin levels during OGTT, but the leptin levels decreased significantly during a tolerance test (P<0.001), and similar results were also seen during a breakfast test. The fasting plasma leptin in the male with FBS less than 140 mg/dl had a significant correlation with the fasting plasma IRI level, but this correlation disappeared after taking obesity into consideration. Thus the plasma leptin was chiefly dependent on the body weight and gender and had no special relation to diabetic severity.
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PMID:Human plasma leptin in obese subjects and diabetics. 946 22

Cancer has the potential to provoke worries which should be assessed in order to adequately respond to patients' problems. We highlight in this paper the problems that concerned 30 women with cervical cancer (mean age 51.2) and 76 with breast cancer (mean age 44.9), how these concerns affected their emotional lives, and the factors associated with these worries. They were interviewed with the 33-item modified version of a German questionnaire rating psychosocial concerns (FBS) by Sullwold, and Goldberg's General Health Questionnaire (GHQ-12) for psychopathological symptoms. Cervical cancer patients had significantly higher FBS and GHQ-12 scores than breast cancer. Breast cancer cases had FBS scores similar to those of women with sickle cell disease and insulin-dependent diabetes mellitus. The commonest recurrent worries in both groups were depression about their condition (45%), thoughts of death (37%), insomnia (33.3%), bodily odour (30%), impairment of work efficiency (30%) terrifying dreams (27%) and fear of illness being life-long (25%). Over 90% denied experience of worries indicating social stigma. FBS scores were significantly correlated with GHQ scores and both were negatively associated with adequacy of social contacts. These data suggest the need for psychosocial intervention in such cases in Nigeria.
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PMID:Psychosocial concerns of Nigerian women with breast and cervical cancer. 988 90

A 30-year-old female complained of lancinating pain in the bilateral thighs for 10 days. The patient had a 22-year history of insulin-dependent diabetes mellitus. Physical examination revealed swelling of the bilateral lower extremities. There was exquisite tenderness on palpation over the medial thighs, with marked increase in pain on hip and knee flexion. Muscle strength of quadriceps, hamstrings, and hip adductor was decreased due to muscle pain. Pedal pulses were palpable bilaterally. Roentogenograms of the left femur revealed calcification of the left femoral arterial wall. Venogram revealed no obstruction with normal drainage. Complete blood cell count showed left shift of the neutrophils, markedly accelerated erythrocyte sedimentation rate, prolonged prothorombin time of 9 sec (normal 11.7 sec), C-reactive protein of 7.3 mg/dl and serum creatine kinase level of 175 IU/L. FBS was 225 mg/dl and Hb A 1 c was 16.4%. An MR imaging of the thighs revealed high signal intensities in the bilateral adductor muscles on T 2-weighted images. The symptoms resolved spontaneously over a three week period. From the course of the illness and MR imaging, the patient was diagnosed having diabetic muscle infarction (DMI), a rare complication of diabetes mellitus. To our knowledge, this is the first reported case of DMI in Japan. Diabetic microangiopathy and hypercoagulability are thought to be responsible for inducing DMI. Because the diagnosis can be made from the characteristic clinical and the typical MR imaging findings, muscle biopsy is not always necessary to obtain the diagnosis of DMI.
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PMID:[Bilateral diabetic infarction of the thigh adductor muscles in a diabetic female patient-- A case report and review of the literature]. 1039 Oct 74

Skin fibroblasts from patients with diabetes mellitus display abnormalities in cell proliferation. The use of exogenous growth factors on diabetic wounds has been found to stimulate fibroblast proliferation and facilitate wound healing. However, the results of application of FGF-2 alone to diabetic wounds in clinical trials have been disappointing. The objective of this experiment was to study the effects of FGF-2 and media supplements on in vitro proliferation of skin fibroblasts from patients with type II diabetes and nondiabetic controls, and to evaluate the association between fibroblast proliferation and cAMP production. Fibroblast cell lines (n = 5 from diabetic and n = 5 from control individuals) were cultured in DMEM + 20% FBS for 7 days. Cells were then counted, plated into 24-well plates at a concentration of 2 x 10(4) cells/well and incubated for 24 h in DMEM with serum. The next day, medium was changed to serum-free DMEM alone or DMEM with supplements (albumin, transferrin, insulin and hydrocortisone). Cells were cultured in the presence or absence of varying doses of FGF-2 (0, 0.3, 1, 3, 10 and 30 ng/ml) for 72 hrs then counted and medium was collected for cAMP radioimmunoassay. The doubling time for cell number tended to be greater (p < 0.2) for diabetic fibroblasts than for control fibroblasts. The addition of supplements to the medium reduced (p < 0.05) the doubling time for both fibroblast types. FGF-2 stimulated (p < 0.05) proliferation of diabetic fibroblasts only in medium containing supplements. In contrast, FGF-2 stimulated proliferation of control fibroblasts in medium with or without supplements. The maximal effects of FGF-2 on fibroblast proliferation were greater (p < 0.02) in medium with supplements than in medium without supplements. The K(D) of FGF-2 for fibroblast proliferation was greater (p < 0.06) for diabetic than for control fibroblasts, and lower (p < 0.02) for medium with supplements than for medium without supplements. Fibroblasts from patients with diabetes mellitus produced more (p < 0.05) cAMP than control fibroblasts. These results demonstrate that FGF-2 requires the presence of supplements to enhance proliferation of fibroblasts from patients with type II diabetes mellitus. In addition, fibroblasts from diabetic patients showed a greater K(D) for FGF-2 in terms of cell proliferation. These data suggest a defective FGF receptor or down-regulation of the FGF receptor-mediated cascade that leads to cell proliferation. Identifying methods of reducing the K(D) of FGF-2 in stimulating the proliferation of diabetic fibroblasts may improve the clinical response of diabetic wounds to FGF-2.
Exp Clin Endocrinol Diabetes 2002 Jun
PMID:Effects of basic fibroblast growth factor (FGF-2) on proliferation of human skin fibroblasts in type II diabetes mellitus. 1205 41

Embryonic stem (ES) cells are pluripotent cells isolated from the inner cell mass of blastocysts. ES cells are able to differentiate into the three primitive layers (endoderm, mesoderm, and ectoderm) of the organism, including the germline. In recent reports mouse ES cells have been successfully applied in the treatment of spinal cord injury, hereditary myelin disorder of the central nervous system, and diabetes mellitus. In this study, we investigated the induction of mouse ES cell differentiation, using culture of embryoid bodies (EBs) into the diverse tissues. EBs were formed by culturing ES cells (129/SV strain) in DMEM supplemented with 10% FBS, in the absence of feeder cells and leukemia inhibitory factor (LF). EBs were induced to differentiate by treatment with retinoic acid (RA). In control medium (non-RA medium) beating muscles, blood vessels, hemocytes, and cartilages were frequently observed in EBs. Moreover, when EBs were cultured in medium including RA (5 x 10(-8) M, and 5 x 10(-9) M), differentiation of the optic vesicle, lens, retina, and neural groove was observed. In this study we demonstrated that an efficient system for inducing the differentiation of ES cells using EBs.
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PMID:In vitro differentiation of mouse embryonic stem cells after activation by retinoic acid. 1270 48

Macrophages from nonobese diabetic (NOD) mice, which spontaneously develop type I diabetes, share a defect in elicited cytokine production with macrophages from multiple diverse strains of systemic lupus erythematosus (SLE)-prone mice. We have previously shown that, in SLE-prone mice, this defect is triggered by exposure to apoptotic cells. We report in this work that macrophages from prediseased NOD mice also respond abnormally to apoptotic cells, mimicking closely the apoptotic cell-dependent abnormality that we have observed in multiple SLE-prone strains. This defect is characterized by the underexpression of IL-1 beta and multiple other cytokines. In the presence of apoptotic cells or FBS, elicited expression of IL-1 beta by NOD macrophages is markedly reduced compared with that by macrophages from control mice, including three strains of mice that develop type II (nonautoimmune) diabetes. Given the increasing role of apoptotic cells in tolerance and autoimmunity, a macrophage defect triggered by apoptotic cells has broad potential to upset the balance between tolerance and immunity. The concordance of this defect among so many diverse autoimmune-prone strains suggests that the genetic basis for this abnormality may constitute a permissive background for autoimmunity.
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PMID:Cytokine dysregulation induced by apoptotic cells is a shared characteristic of macrophages from nonobese diabetic and systemic lupus erythematosus-prone mice. 1506 61


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