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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the immunological characteristics of human peripheral T lymphocytes and behavior of PHA-stimulated lymphocytes in Type II diabetes mellitus, investigated two-color flow cytometry. The subsets of Leu11+Leu7+, Leu11-Leu7+ and Leu7+Leu2+ were decreased significantly in peripheral Natural Killer cells. After PHA stimulation the T-cell subsets demonstrated a decrease in the inducer subset and in the cytotoxic subset. The helper cell subset showed a negative regression with HbA1. The cytotoxic cell subset showed a positive regression with HbA1 and also FBS. The CD4/CD8 ratio, and the IL2+Leu2+ subset, showed a negative regressions with HbA1, and the diabetic duration, respectively. Thus, these results are a further demonstration of changes in lymphocytes in NIDDM.
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PMID:T-lymphocyte subsets in human non-insulin-dependent diabetes mellitus (type II) studied by two-color flow cytometry. 183 23

In this study, in vitro B-cell models are described, which may be applicable for studying the reported B-cell desensitization produced by hyperglycemia in IDDM and NIDDM. Using a programmable perifusion/perfusion system, insulin secretion from perifused islets was measured at 10-30-min intervals for 24-50 h. After 3-4 h continuous glucose (11 mM), a new phase of insulin release occurs in which secretion declines to, and remains at, approximately 25% maximal release. Results were similar when using: perifused islets embedded in Cytodex 3, or Bio-Gel P-2, 100-200 mesh; batchincubated islets with hourly changes of medium; and the isolated pancreas perfused for 8 h. Three different media, Hana HB 104 (fortified, fully defined medium), RPMI-1640 + 10% FBS, and perfusion bufferalbumin, were used. Despite reduced secretion to continuous glucose, each system responded vigorously to an acute stimulation with glucose-forskolin. Decreased secretion was primarily caused by decreased secretagogue efficiency (reduced fractional secretion). Prolonged stimulation with glucose or glucose-IBMX produced a similar waning of secretion regardless of the amount of insulin released. It is concluded that the third phase of insulin secretion may represent a secret-agogue-induced, signal desensitization of the B-cell, rather than exhaustion of a B-cell compartment of stored insulin.
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PMID:The third phase of in vitro insulin secretion. Evidence for glucose insensitivity. 351 47

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.
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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

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.
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PMID:Effects of basic fibroblast growth factor (FGF-2) on proliferation of human skin fibroblasts in type II diabetes mellitus. 1205 41

This study was designed to develop and validate a computerized exercise intervention program using the transtheoretical model (TTM) for Korean patients with type 2 diabetes mellitus (DM). This computerized program was web-based and developed by designing a flow chart. An expert group (n=24), who validated the content of the computerized program, produced a mean score for the evaluation scale of 4.25 (SD.56). Of the patients (n=28) with type 2 DM who participated in clinical validity testing of the program, the mean score for the satisfaction scale was 4.82 (SD.12). In the validation of the program, significant differences between baseline and after-intervention were observed in the stage of readiness for exercise (Z=-3.78, p < 0.001), physical activity (Z=-2.33, p < 0.05), blood glucose profiles [FBS (Z=-2.84, p < 0.01), pc 2 hr. glucose (Z=-2.33, p < 0.05), HbA1c (Z=-2.77, p < 0.01)], and VO2max (Z=-2.52, p < 0.01). The study confirmed that the computerized program could be used to construct a database and continue to provide follow-up intervention for patients in all stages.
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PMID:Development and validation of a computerized exercise intervention program for patients with type 2 diabetes mellitus in Korea. 1458 8

This study investigated levels of fasting plasma glucose (FBS), homeostasis model of the assessment of the insulin resistance (HOMA), lipid profile, insulin, and resistin hormones in 202 individuals, divided into four groups. Two groups had type II diabetes mellitus (DM): one group had been overnourished (DM/OB) (body mass index: BMI equal or above 25) and the other had not (DM/nOB). Two additional groups not suffering from diabetes were either overnourished (nDM/OB) or of normal nutritional status (nDM/nOB). Only the DM/OB group had insulin levels elevated above the other three groups. Resistin levels had been lowest in the nDM/nOB group. When participants of the two nOB groups were pooled into one group and the subjects of the two OB groups were combined into another group, the median plasma resistin levels of the OB groups were significantly higher compared with the nOB groups. Likewise the DM groups had higher resistin levels than the nDM groups. A significant correlation of plasma resistin with BMI, waist circumference, waist-to-hip ratio, FBS, and HOMA score had been observed. The result suggests that plasma resistin has a role in linking central obesity and obesity-related insulin resistance to type II diabetes mellitus.
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PMID:Plasma resistin, insulin concentration in non-diabetic and diabetic, overweight/obese Thai. 1704 91

In 2004, the human islet amyloid polypeptide (HIP) rat model was created by transfecting the Sprague-Dawley rat with the human islet amyloid polypeptide (hIAPP)-amylin gene. The objective of this study is to utilize the transmission electron microscope to study the longitudinal cellular and extracellular morphological changes within the islets of this model at 4, 8, and 14 months of age. It has been previously demonstrated that the 2-, 5-, and 10-month HIP models have no diabetes, impaired fasting glucose, and diabetes, respectively. The 4-month HIP model (FBS 123 mg/dl) demonstrated an abundance of beta-cells and insulin secretory granules with significant pericapillary and inter-beta-cell islet amyloid deposition. The 8-month model (FBS 187 mg/dl) demonstrated extensive islet amyloid deposition and marked changes of beta-cell apoptosis. The 14-month-old model (FBS 244 mg/dl) demonstrated islet and beta-cell atrophy with even greater amounts of extracellular islet amyloid compared to the 4-month-old and 8-month-old models. Functional beta cells were sparse and were associated with intra islet adipose deposition. These findings of ultrastructure cellular and extracellular morphological longitudinal remodeling changes in this novel animal model of type 2 diabetes may provide investigators with a better understanding regarding the role of islet amyloid in human islet.
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PMID:Longitudinal ultrastructure study of islet amyloid in the HIP rat model of type 2 diabetes mellitus. 1752 69

The purposes of this study were to determine the incidence rates and predictors of type 2 diabetes and impaired fasting plasma glucose (IFG) among the employees of a university hospital in Bangkok, Thailand. Totally 2370 and 1619 workers without diabetes and IFG at baseline, respectively, who were +35 years old were followed up during 2001-2005. Type 2 diabetes incidence rates (95% CI) were 13.6 (8.4-22.3) and 6.4 (4.5-9.1) per 1000 PYs, respectively, for men and women, while those of the IFG were 37.8 (26.3-54.4) and 23.6 (19.3-29.0) per 1000 PYs, respectively, for both genders. Baseline FBS predicted future IFG risk even at the levels as low as 63-70 mg/dl. The OR (95% CI) of IFG for those with baseline FPG of 63-70, 71-80, and >80 mg/dl-compared to those with baseline FPG < or =62 mg/dl-were 2.51 (1.12-5.64), 5.39 (2.51-11.56), and 8.30 (3.67-18.75), respectively. Future diabetes risk was observed only in those with baseline FPG of 96 mg/dl or higher, with the OR (95% CI) of 6.0 (2.29-15.75). In conclusion, baseline FPG even at the level as low as 63-70 mg/dl predicts future IFG risk among a hospital employee group in Thailand, while increased diabetes risk was found only in those at the FBS level of > or =96 mg/dl.
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PMID:Incidence and predictors of abnormal fasting plasma glucose among the university hospital employees in Thailand. 1795 98

This study investigated the association of apolipoprotein A5 (apoA5) gene polymorphism at position -1131T>C with cerebral infarction in patients with type 2 diabetes. A total of 256 type 2 diabetic patients without cerebral infarction (T2DM), 220 type 2 diabetic patients with cerebral infarction (T2DMCI) and 340 healthy subjects were recruited from the same region (Hubei province, China). The genotype of apoA5 -1131T[Symbol: see text]C was analyzed by polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP). Total cholesterol, HDL cholesterol, LDL-cholesterol and triglycerides were quantitatively detected by using standard enzymatic techniques. The results showed that the prevalence of the apoA5 -1131C allele was significantly higher in T2DMCI group than that in control group (42.7% versus 31.2%, P<0.01). The carriers of rare C allele had higher TG levels as compared with carriers of common allele in the three groups (P<0.01). Logistic regression models, which were adjusted for age, gender, blood pressure, BMI, FBS, smoking, LDL-C and HDL-C, revealed that patients carrying the apoA5 -1131C allele and CC homozygotes were at high risk for T2DMCI. It was concluded that the apoA5 -1131C allele variant is an independent genetic risk factor for T2DMCI.
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PMID:Polymorphism of apolipoprotein A5 is a risk factor for cerebral infarction in type 2 diabetes. 1910 59


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