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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

Concentrative and facilitative glucose transporters are responsible for the movement of glucose across the plasma membrane of human cells. Defects in concentrative glucose transporters cause renal glycosuria and glucose-galactose malabsorption. Alterations in facilitative glucose transporters explain the newly discovered syndrome of low CNS glucose in the presence of normal blood sugar, causing seizures and developmental delay. Defects in other facilitate glucose transporters also help explain Fanconi-Bickel syndrome, glycogen storage disease type, Id, and non-insulin-dependent diabetes mellitus.
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PMID:Human glucose transporters. 974 6

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

Maturity-onset diabetes of the young (MODY), an autosomal dominant, early-onset form of type-2 diabetes, is caused by mutations in five different genes all leading to defect(s) in the pancreatic beta cell. However, some patients with this form of diabetes do not bear a mutation in any of the known (MODY1-MODY5) loci, a notion prompting the search for new MODY genes. Clinical and genetic data point toward a defect in beta cell function in the majority of patients with MODY, and partners of the glucose-sensing device are reasonable functional candidates. The high-capacity glucose transporter GLUT2 has the ideal kinetic features for performing this task. However, complete GLUT2 deficiency in humans leads to hepato-renal glycogenosis (Fanconi-Bickel syndrome), and heterozygous GLUT2 mutations apparently behave in a recessive manner. Furthermore, in the human beta cell GLUT1 mRNA is predominant when compared to GLUT2 and glucose influx appears to be largely mediated by this low-Km transporter. Thus, we looked for the presence of sequence variants by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP) within the GLUT1 gene in 90 Italian pedigrees negative at the search for mutations in glucokinase (MODY2) and hepatocyte nuclear factor-1alpha (MODY3), the two genes responsible for about 60% of MODY cases in Italian children. We found three already described silent mutations and a new single base deletion in position -173 of the 5' regulatory region. The -173de1A variant, which was detected in the heterozygous or homozygous state in 30.8% of MODY patients examined and is located in a Nuclear Factor Y binding sequence, is not associated with hyperglycemia in affected relatives of MODY probands. In conclusion, it appears from these results that the glucose transporter gene GLUT1 is unlikely to play a major role in the etiology of MODY diabetes.
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PMID:Single-strand conformation polymorphism analysis of the glucose transporter gene GLUT1 in maturity-onset diabetes of the young. 1148 13

We describe a patient with Fanconi-Bickel syndrome diagnosed by clinical manifestations and the identification of a novel mutation in the GLUT 2 gene. She was initially diagnosed with neonatal diabetes mellitus due to hyperglycaemia and glycosuria at 3 days of life. In addition, newborn screening for galactosaemia revealed hypergalactosaemia. Thereafter, she was managed with lactose-free milk and insulin therapy. However, she failed to grow and her liver became progressively enlarged. Her liver function deteriorated with increased prothrombin time. A liver biopsy done at age 9 months showed micronodular cirrhosis with marked fatty changes and she succumbed to hepatic failure with pneumonia at 10 months of age. DNA sequencing analysis of the GLUT 2 gene using her genomic DNA revealed a novel mutation in codon 5, lysine5 stop(K5X).
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PMID:Identification of a novel mutation in the GLUT2 gene in a patient with Fanconi-Bickel syndrome presenting with neonatal diabetes mellitus and galactosaemia. 1202 58


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