Gene/Protein Disease Symptom Drug Enzyme Compound
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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

The serum zinc level and immune functions were analyzed in 34 patients with NIDDM before and after the treatment with zinc gluconate supplement during conventional therapy (after the blood glucose level stabilization). The results showed that before treatment the level of serum zinc and red cell C3b receptor rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR) were increased. After treatment with zinc gluconate for 1 month the serum zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also approached to normal. All the above figures were significantly different before and after zinc therapy. The data showed that various degrees of lowering of serum zinc and abnormal immune functions were present during the conventional antidiabetic therapy. Thus, zinc supplement should be used as an important adjunctive therapy for NIDDM patients.
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PMID:[Influence of insufficient zinc on immune functions in NIDDM patients]. 1080 82

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor transcription factor that regulates cell growth, differentiation, and homeostasis. PPARgamma agonists are potent therapeutic agents for type 2 diabetes, obesity, and inflammation. Experimental allergic encephalomyelitis (EAE) is a Th1 cell-mediated inflammatory demyelinating autoimmune disease model of multiple sclerosis. We have shown recently that PPARgamma agonists inhibit EAE by blocking IL-12 production, IL-12 signaling, and neural Ag-induced Th1 differentiation. In this study, we show that the PPARgamma-deficient heterozygous mice develop an exacerbated EAE with prolonged clinical symptoms than the wild-type littermates, following immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 peptide. The exacerbation of EAE in PPARgamma(+/-) mice associates with an increased expansion of CD4(+) and CD8(+) T cells and expression of CD40 and MHC class II molecules in response to MOGp35-55 Ag. The PPARgamma(+/-) mice also showed an increase in T cell proliferation and Th1 response to MOGp35-55 Ag than the wild-type littermates. These findings suggest that PPARgamma be a critical physiological regulator of CNS inflammation and demyelination in EAE and perhaps multiple sclerosis and other Th1 cell-mediated autoimmune diseases.
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PMID:Peroxisome proliferator-activated receptor-gamma-deficient heterozygous mice develop an exacerbated neural antigen-induced Th1 response and experimental allergic encephalomyelitis. 1463 82

We have compared the concentrations of intracellular glutathione (GSH), glutathione-dependent antioxidative enzymes, the cell death rate and immunophenotype profile of peripheral blood mononuclear cells (PBMC) from healthy donors and from patients with insulin-dependent type II (NIDDM) diabetes mellitus. The IDDM and NIDDM patients had above-normal absolute lymphocyte counts, whereas the percentages of CD3, CD4 adn CD8 T lymphocytes were significantly reduced. In contrast, the absolute number and percentage of B lymphocytes was higher in diabetic patients than in healthy donors. The low intracellular reduced glutathione(GSH) and the unbalanced profile of key enzymes involved in GSH metabolism, gamma-glutamyltransferase (gamma-GT) and glutathione-S-transferase (GST), account for the increased oxidative status of PBMC from diabetic patients. The plasma membranes of PBMC for diabetic patients were less permeable to propidium iodide than those of PBMC from healthy donors, indicating that the apoptotic cell death rate was lower in the cells from diabetic patients. These differences are potentially useful markers of pathogenic metabolic changes which occur during clinical diabetes and if they are confirmed could be use dot identify the onset of diabetes.
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PMID:Apoptosis and oxidative status in peripheral blood mononuclear cells of diabetic patients. 1469 96

Recently, we identified in normally type 1 diabetes-prone NOD/LtJ mice a spontaneous new leptin receptor (LEPR) mutation (designated Lepr(db-5J)) producing juvenile obesity, hyperglycemia, hyperinsulinemia, and hyperleptinemia. This early type 2 diabetes syndrome suppressed intra-islet insulitis and permitted spontaneous diabetes remission. No significant differences in plasma corticosterone, splenic CD4(+) or CD8(+) T-cell percentages, or functions of CD3(+) T-cells in vitro distinguished NOD wild-type from mutant mice. Yet splenocytes from hyperglycemic mutant donors failed to transfer type 1 diabetes into NOD.Rag1(-/-) recipients over a 13-week period, whereas wild-type donor cells did so. This correlated with significantly reduced (P < 0.01) frequencies of insulin and islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD8(+) T-effector clonotypes in mutant mice. Intra-islet insulitis was also significantly suppressed in lethally irradiated NOD-Lepr(db-5J)/Lt recipients reconstituted with wild-type bone marrow (P < 0.001). In contrast, type 1 diabetes eventually developed when mutant marrow was transplanted into irradiated wild-type recipients. Mitogen-induced T-cell blastogenesis was significantly suppressed when splenic T-cells from both NOD/Lt and NOD-Lepr(db-5J)/Lt donors were incubated with irradiated mutant peritoneal exudate cells (P < 0.005). In conclusion, metabolic disturbances elicited by a type 2 diabetes syndrome (insulin and/or leptin resistance, but not hypercorticism) appear to suppress type 1 diabetes development in NOD-Lepr(db-5J)/Lt by inhibiting activation of T-effector cells.
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PMID:Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysis. 1638 Apr 90

The latent autoimmune diabetes in adults (LADA) is a subgroup of type 1 diabetes, which procession of autoimmune destruction of beta-cells was slower than classic type 1 diabetes. To investigate the pathogenesis of LADA, we examined the lymphocyte subsets including the CD4(+)CD25(+) T-cells in 60 LADA patients and 30 patients of type 2 diabetes and 30 healthy individuals by FACS. And we compared the expression of FOXP3 mRNA in CD4(+) T-cell between 10 patients of LADA and 10 matched healthy individuals by real time PCR. The percent of CD4(+)CD25(+) T-cells were higher (11.89+/-4.96% versus 8.16+/-3.65%, P<0.01), and the percent CD8(+) T-cells elevated (24.58+/-6.80% versus 19.39+/-7.12, P<0.01) in LADA patients than healthy individuals. While the expression of FOXP3 mRNA in CD4(+) T-cell was markedly decreased in LADA patients (0.52-fold, n=10, P=0.004) compared with normal subjects. In addition, the percent of CD8(+) T-cells related with GAD-Ab titers in LADA patients (r=0.292, P=0.03). Our results showed that there were cellular immune disorder and decreased CD4(+) regulatory T-cells in LADA patients. The adoptive transfer regulatory T-cells seem to be a potential therapeutics for LADA.
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PMID:The CD4(+) regulatory T-cells is decreased in adults with latent autoimmune diabetes. 1700 88

With the emerging obesity pandemic, identifying those who appear to be protected from adverse consequences such as type 2 diabetes and certain malignancies will become important. We propose that the circulating immune system plays a role in the development of these comorbidities. Clinical data and blood samples were collected from 52 patients with severe obesity attending a hospital weight-management clinic and 11 lean healthy controls. Patients were classified into metabolically "healthy obese" (n = 26; mean age 42.6 years, mean BMI 46.8 kg/m(2)) or "unhealthy obese" (n = 26; mean age 45 years, mean BMI 47.5 kg/m(2)) groups, based upon standard cutoff points for blood pressure, lipid profile, and fasting glucose. Circulating lymphoid populations and phenotypes were assessed by flow cytometry. Obese patients had significantly less circulating natural killer (NK) and cytotoxic T lymphocytes (CTL) compared to lean controls. There were significantly higher levels of NK cells and CTLs in the healthy obese group compared to the unhealthy obese group (NK: 11.7% vs. 6.5%, P < 0.0001, CD8 13.4% vs. 9.3%, P = 0.04), independent of age and BMI and these NK cells were also less activated in the healthy compared to the unhealthy group (CD69, 4.1% vs. 11.8%, P = 0.03). This is the first time that quantitative differences in the circulating immune system of obese patients with similar BMI but different metabolic profiles have been described. The significantly higher levels of CTLs and NK cells, which express fewer inhibitory molecules, could protect against malignancy, infection, and metabolic disease seen in obesity.
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PMID:Are natural killer cells protecting the metabolically healthy obese patient? 1923 45

The frequency and functionality of peripheral blood invariant (iNKT) cells and their subsets, as well as other regulatory T-cell subsets, were evaluated in patients with type 1A diabetes mellitus (DM1), Hashimoto's disease, and Graves' disease. In addition to healthy individuals (HC), patients with type 2 diabetes mellitus (DM2) were included as controls because this disease has a different physiopathology. A similar frequency of total iNKT cells, as well as their subsets, existed among HC and the different study groups. Similar results were reported when we compared the frequency of CD4(+)/CD25(high) T cells, CD8(+)/CD28(negative) T cells, and gamma-delta T cells among HC and study groups, whereas patients with DM2 exhibited a higher frequency of CD8(+)/CD28(negative) T cells compared with HC and DM1. Also, patients with DM2 exhibited a lower frequency of CD4(negative) and CD4(+) iNKT cells expressing tumor necrosis factor-alpha (TNF-alpha) than HC. We did not observe significant differences in the frequency of iNKT cells expressing interleukin-4 or interferon-gamma among study groups and controls. Our findings support a normal frequency and function of peripheral blood iNKT cells in different endocrine autoimmune diseases, but an abnormal expression of TNF-alpha by circulating iNKT cells from patients with DM2.
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PMID:Frequency and function of circulating invariant NKT cells in autoimmune diabetes mellitus and thyroid diseases in Colombian patients. 1948 Aug 56

Doxazosin, an alpha(1)-adrenergic receptor inhibitor, is commonly administered to patients with type 2 diabetes, hypertension and nephropathy. The impact of 3 months' doxazosin therapy on the prevalence of activated and regulatory T lymphocytes was analysed in this pilot study of men with type 2 diabetes (n = 10) who received doxazosin 4 mg/day in addition to their ongoing therapy. The prevalence of CD4(+), CD8(+), CD25(+) and CD69(+) cells at baseline and after 3 months of add-on therapy was determined. The prevalence of regulatory T-cells was detected by two different approaches: forkhead box P3 (FoxP3) positivity; and the number of CD4(+)CD25(+high) cells. During 3 months of doxazosin therapy, patients' blood pressure, blood glucose control and lipid profiles all significantly improved. Simultaneously, the prevalence of activated T-cells (CD4(+)CD69(+) and CD8(+)CD69(+) cells) decreased, whereas that of regulatory T-cells increased. These results indicate an immunomodulatory action of doxazosin in type 2 diabetic patients.
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PMID:Effect of 3 months of doxazosin therapy on T-cell subsets in type 2 diabetic patients. 2014 98

Obesity has been associated with increasing the risk for type 2 diabetes and heart disease, but its influence on the immune response to viral infection is understudied. Memory T cells generated during a primary influenza infection are important for protection against subsequent influenza exposures. Previously, we have demonstrated that diet-induced obese (DIO) mice have increased morbidity and mortality following secondary influenza infection compared with lean mice. To determine whether the problem resided in a failure to maintain functional, influenza-specific CD8(+) memory T cells, male DIO and lean mice were infected with influenza X-31. At 84 d postinfection, DIO mice had a 10% reduction in memory T cell numbers. This reduction may have resulted from significantly reduced memory T cell expression of interleukin 2 receptor beta (IL-2R beta, CD122), but not IL-7 receptor alpha (CD127), which are both required for memory cell maintenance. Peripheral leptin resistance in the DIO mice may be a contributing factor to the impairment. Indeed, leptin receptor mRNA expression was significantly reduced in the lungs of obese mice, whereas suppressor of cytokine signaling (Socs)1 and Socs3 mRNA expression were increased. It is imperative to understand how the obese state alters memory T cells, because impairment in maintenance of functional memory responses has important implications for vaccine efficacy in an obese population.
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PMID:Diet-induced obesity in mice reduces the maintenance of influenza-specific CD8+ memory T cells. 2059 5


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