Zeitschriftenartikel: „Type-2 development“

1

Jarvis, Blair, and Shelley Elkinson. "Agents in Development for Type 2 Diabetes." Drugs in R & D 2, no. 2 (1999): 95–99. http://dx.doi.org/10.2165/00126839-199902020-00002.

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2

Marott, Sarah C. W., Børge G. Nordestgaard, Anne Tybjærg-Hansen, and Marianne Benn. "Causal Associations in Type 2 Diabetes Development." Journal of Clinical Endocrinology & Metabolism 104, no. 4 (2018): 1313–24. http://dx.doi.org/10.1210/jc.2018-01648.

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Abstract Context Obesity, glucose, insulin resistance [homeostatic model assessment, version 2, for insulin resistance (HOMA2-IR)], and insulin secretion (HOMA2-β) have been associated with type 2 diabetes (T2D) observationally. However, the causal, genetic contribution of each parameter to this risk is largely unknown and important to study because observational data are prone to confounding but genetic, causal data are free of confounding and reverse causation. Objective We examined the causal, genetic contribution of body mass index (BMI), glucose level, C-peptide level, HOMA2-IR, and HOMA2-β to the risk of T2D in 95,540 individuals from the Copenhagen General Population Study and estimated the absolute 10-year risks. Methods Cox regression analysis, instrumental variable analysis, and Poisson regression analysis were performed to estimate the observational hazard ratios, causal, genetic ORs, and absolute 10-year risks of T2D. Results For 1-SD greater level, BMI was associated with an observational 66% (95% CI, 62% to 72%) and causal, genetic 121% (95% CI, 25% to 291%) greater risk of T2D; glucose with an observational 44% (95% CI, 41% to 46%) and causal, genetic 183% (95% CI, 56% to 416%) greater risk of T2D; and HOMA2-IR with an observational 30% (95% CI, 18% to 44%) and causal, genetic 12% (95% CI, 2% to 22%) greater risk of T2D. In contrast, for 1-SD greater level, HOMA2-β was associated with an observational 14% (95% CI, 11% to 16%) and causal, genetic 21% (95% CI, 8% to 32%) lower risk of T2D. The upper tertiles of HOMA2-IR were associated with absolute 10-year diabetes risks of 31% and 37% in obese women and men, age &gt;60 years, and a glucose level of 6.1 to 11.0 mmol/L. Conclusions BMI, glucose level, HOMA2-IR, and HOMA2-β are causally associated with T2D.

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Bhartia, Mithun, Abd A. Tahrani, and Anthony H. Barnett. "SGLT-2 Inhibitors in Development for Type 2 Diabetes Treatment." Review of Diabetic Studies 8, no. 3 (2011): 348–54. http://dx.doi.org/10.1900/rds.2011.8.348.

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4

Elizabeth, Miranda-Perez, Bentham Science Publisher Alarcon-Aguilar, Francisco J., Ortega-Camarillo Clara, Bentham Science Publisher Escobar-Villanueva та Maria Carmen. "Pancreatic β-Cells and Type 2 Diabetes Development". Current Diabetes Reviews 13, № 2 (2017): 108–21. http://dx.doi.org/10.2174/1573399812666151020101222.

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5

MacKinnon, Neil J., Nicole R. Hartnell, Emily K. Black, et al. "Development of clinical indicators for type 2 diabetes." Canadian Pharmacists Journal 141, no. 2 (2008): 120–28. http://dx.doi.org/10.3821/1913-701x(2008)141[120:docift]2.0.co;2.

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6

Lu, Da-Yong, Jin-Yu Che, Nagendra Sastry Yarla, et al. "Type 2 Diabetes Treatment and Drug Development Study." Open Diabetes Journal 8, no. 1 (2018): 22–33. http://dx.doi.org/10.2174/1876524601808010022.

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The causality and etio-pathologic risks for patients with Type 2 Diabetes (T2DM) are important areas in modern medicine. Disease complications are largely unpredictable in patients with T2DM. In the future, we welcome therapeutics of both cutting-edge and traditional for anti-diabetic treatments and management with higher efficiency and less cost. Expanding medical knowledge, behavior/life-style notification in healthcare, modern genetic/bioinformatics diagnostic promotion, clinical developments (Traditional Chinese Medicine and personalized medicine) and new drug developments - including candidate drug targets should be implemented in the future. These efforts might be useful avenues for updating anti-diabetic therapeutics globally. This article aims at introducing this information for T2DM treatment boosts.

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Li, Kejia, Xin Liao, Kuan Wang, et al. "Myonectin Predicts the Development of Type 2 Diabetes." Journal of Clinical Endocrinology & Metabolism 103, no. 1 (2017): 139–47. http://dx.doi.org/10.1210/jc.2017-01604.

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8

GOTOU, Naofumi, Shunsuke MIYAKE, and Toshiaki KANEMOTO. "506 Development of Yawing Type Hydroelectric Unit(2)." Proceedings of the Fluids engineering conference 2006 (2006): _506–1_—_506–4_. http://dx.doi.org/10.1299/jsmefed.2006._506-1_.

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9

ISHIHARA, Hiroaki, Naofumi GOTO, and Toshiaki KANEMOTO. "806 Development of Yawing Type Hydroelectric Unit(2)." Proceedings of the Fluids engineering conference 2007 (2007): _806–1_—_806–4_. http://dx.doi.org/10.1299/jsmefed.2007._806-1_.

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10

Fernandes, P., C. Peixoto, V. M. Santiago, E. J. Kremer, A. S. Coroadinha, and P. M. Alves. "Bioprocess development for canine adenovirus type 2 vectors." Gene Therapy 20, no. 4 (2012): 353–60. http://dx.doi.org/10.1038/gt.2012.52.

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11

Brooks-Worrell, Barbara, Heba Ismail, Michael Wotring, et al. "Autoimmune Development in Phenotypic Type 2 Diabetes Patients." Clinical Immunology 123 (2007): S66—S67. http://dx.doi.org/10.1016/j.clim.2007.03.367.

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12

Meier, Juris J., and Michael A. Nauck. "Incretins and the development of type 2 diabetes." Current Diabetes Reports 6, no. 3 (2006): 194–201. http://dx.doi.org/10.1007/s11892-006-0034-7.

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13

Marshall, J. A., and D. H. Bessesen. "Dietary Fat and the Development of Type 2 Diabetes." Diabetes Care 25, no. 3 (2002): 620–22. http://dx.doi.org/10.2337/diacare.25.3.620.

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14

Pinney, Sara E., and Rebecca A. Simmons. "Epigenetic mechanisms in the development of type 2 diabetes." Trends in Endocrinology & Metabolism 21, no. 4 (2010): 223–29. http://dx.doi.org/10.1016/j.tem.2009.10.002.

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15

Reagan, L. P., M. Theveniau, X. D. Yang, et al. "Development of polyclonal antibodies against angiotensin type 2 receptors." Proceedings of the National Academy of Sciences 90, no. 17 (1993): 7956–60. http://dx.doi.org/10.1073/pnas.90.17.7956.

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16

Quinn, Laurie. "Mechanisms in the Development of Type 2 Diabetes Mellitus." Journal of Cardiovascular Nursing 16, no. 2 (2002): 1–16. http://dx.doi.org/10.1097/00005082-200201000-00002.

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17

Hoshino, Kazumi, Steven H. Zarit, and Makoto Nakayama. "Development of the Gerotranscendence Scale Type 2: Japanese Version." International Journal of Aging and Human Development 75, no. 3 (2012): 217–37. http://dx.doi.org/10.2190/ag.75.3.b.

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18

Hampton, Tracy. "Cilia Dysfunction May Promote Development of Type 2 Diabetes." JAMA 313, no. 1 (2015): 20. http://dx.doi.org/10.1001/jama.2014.17620.

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19

Loering, Svenja, Guy J. M. Cameron, Malcolm R. Starkey, and Philip M. Hansbro. "Lung development and emerging roles for type 2 immunity." Journal of Pathology 247, no. 5 (2019): 686–96. http://dx.doi.org/10.1002/path.5211.

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20

Verma, Subodh, Abhinav Sharma, Naresh Kanumilli, and Javed Butler. "Predictors of heart failure development in type 2 diabetes." Current Opinion in Cardiology 34, no. 5 (2019): 578–83. http://dx.doi.org/10.1097/hco.0000000000000647.

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21

Xie, Xi-tao, Qiang Liu, Jie Wu, and Makoto Wakui. "Impact of cigarette smoking in type 2 diabetes development." Acta Pharmacologica Sinica 30, no. 6 (2009): 784–87. http://dx.doi.org/10.1038/aps.2009.49.

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22

Antonijevic, Zoran, Martin Kimber, David Manner, Carl-Fredrik Burman, José Pinheiro, and Klas Bergenheim. "Optimizing Drug Development Programs: Type 2 Diabetes Case Study." Therapeutic Innovation & Regulatory Science 47, no. 3 (2013): 363–74. http://dx.doi.org/10.1177/2168479013480501.

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23

Tachibana, Kimiyasu. "Development of Tubular Type SOFC by Wet Process (2)." ECS Proceedings Volumes 1995-1, no. 1 (1995): 208–15. http://dx.doi.org/10.1149/199501.0208pv.

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24

Weiss, Ram, Sara E. Taksali, and Sonia Caprio. "Development of type 2 diabetes in children and adolescents." Current Diabetes Reports 6, no. 3 (2006): 182–87. http://dx.doi.org/10.1007/s11892-006-0032-9.

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25

Hardman, Timothy Colin, and Simon William Dubrey. "Development and potential role of type-2 sodium-glucose transporter inhibitors for management of type 2 diabetes." Diabetes Therapy 2, no. 3 (2011): 133–45. http://dx.doi.org/10.1007/s13300-011-0004-1.

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26

Browne, Jessica L., Adriana D. Ventura, Kylie Mosely, and Jane Speight. "Measuring the Stigma Surrounding Type 2 Diabetes: Development and Validation of the Type 2 Diabetes Stigma Assessment Scale (DSAS-2)." Diabetes Care 39, no. 12 (2016): 2141–48. http://dx.doi.org/10.2337/dc16-0117.

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27

Lu, Da-Yong, Jin-Yu Che, Nagendra Sastry Yarla, et al. "Type 2 Diabetes Study, Introduction and Perspective." Open Diabetes Journal 8, no. 1 (2018): 13–21. http://dx.doi.org/10.2174/1876524601808010013.

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Background:The prevalence of Type 2 Diabetes Mellitus (T2DM) continues to rise globally. The T2DM prevalence is not only in developing countries, but also in developed countries now. Correspondingly, the therapeutics of T2DM calls for a change (higher efficiency) due to growing number of patients and increasing economic burdens globally. Entering into this millennium, both piecemeal pathways (idea driven) and exponential growth of human genomic study are developing quickly. Genetypic-phenotypic translation, modern diagnostics, pharmacology, drug developments, traditional Chinese medicine, personalized medicine and so on are promising disciplines for this change. The clinical anti-diabetic therapeutics, pathogenesis, drug development pipelines are especially highlighted.Conclusion:In summary, a general landscape and principle of T2DM is provided.

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Langin, D. "The role of uncoupling protein 2 in the development of type 2 diabetes." Drugs of Today 39, no. 4 (2003): 287. http://dx.doi.org/10.1358/dot.2003.39.4.737960.

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29

Tahrani, Abd A., and Anthony H. Barnett. "Dapagliflozin: a sodium glucose cotransporter 2 inhibitor in development for type 2 diabetes." Diabetes Therapy 1, no. 2 (2010): 45–56. http://dx.doi.org/10.1007/s13300-010-0007-3.

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30

Kelly, Shona J., and Mubarak Ismail. "Stress and Type 2 Diabetes: A Review of How Stress Contributes to the Development of Type 2 Diabetes." Annual Review of Public Health 36, no. 1 (2015): 441–62. http://dx.doi.org/10.1146/annurev-publhealth-031914-122921.

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31

Wareham, N. J., C. D. Byrne, R. Williams, N. E. Day, and C. N. Hales. "Fasting proinsulin concentrations predict the development of type 2 diabetes." Diabetes Care 22, no. 2 (1999): 262–70. http://dx.doi.org/10.2337/diacare.22.2.262.

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32

M.Ahmed, Ibrahim, and Abeer M. Mahmoud. "Development of an Expert System for Diabetic Type-2 Diet." International Journal of Computer Applications 107, no. 1 (2014): 13–21. http://dx.doi.org/10.5120/18714-9932.

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33

Hong, Eun-Gyoung. "The Association between Development of Cancer and Type 2 Diabetes." Korean Clinical Diabetes 10, no. 1 (2009): 11. http://dx.doi.org/10.4093/kcd.2009.10.1.11.

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34

Simka, Marian. "Liposuction and diabetes type 2 development risk reduction – A commentary." Medical Hypotheses 69, no. 4 (2007): 958–59. http://dx.doi.org/10.1016/j.mehy.2007.01.056.

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35

Gilbert, Elizabeth R., Zhuo Fu, and Dongmin Liu. "Development of a Nongenetic Mouse Model of Type 2 Diabetes." Experimental Diabetes Research 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/416254.

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Insulin resistance and loss of β-cell mass cause Type 2 diabetes (T2D). The objective of this study was to generate a nongenetic mouse model of T2D. Ninety-six 6-month-old C57BL/6N males were assigned to 1 of 12 groups including (1) low-fat diet (LFD; low-fat control; LFC), (2) LFD with 1 i.p. 40 mg/kg BW streptozotocin (STZ) injection, (3), (4), (5), (6) LFD with 2, 3, 4, or 5 STZ injections on consecutive days, respectively, (7) high-fat diet (HFD), (8) HFD with 1 STZ injection, (9), (10), (11), (12) HFD with 2, 3, 4, or 5 STZ injections on consecutive days, respectively. After 4 weeks, serum insulin levels were reduced in HFD mice administered at least 2 STZ injections as compared with HFC. Glucose tolerance was impaired in mice that consumed HFD and received 2, 3, or 4 injections of STZ. Insulin sensitivity in HFD mice was lower than that of LFD mice, regardless of STZ treatment. Islet mass was not affected by diet but was reduced by 50% in mice that received 3 STZ injections. The combination of HFD and three 40 mg/kg STZ injections induced a model with metabolic characteristics of T2D, including peripheral insulin resistance and reduced β-cell mass.

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36

Jayapaul, Muthu K., and Mark Walker. "Review: Mechanisms contributing to the development of type 2 diabetes." British Journal of Diabetes & Vascular Disease 4, no. 4 (2004): 227–31. http://dx.doi.org/10.1177/14746514040040040201.

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37

Won, S. H., S. B. Lim, D. H. Koo, and J. Lee. "Development of 2-Phase/4-Phase Flat-Type Vibration Motor." IEEE Transactions on Magnetics 42, no. 10 (2006): 3482–84. http://dx.doi.org/10.1109/tmag.2006.879076.

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38

Zhu, Junfang, Toshiyuki Hayashi, Atsuhiro Nishino, and Koji Ogushi. "Development of 2 N dead-weight type force standard machine." Measurement 154 (March 2020): 107463. http://dx.doi.org/10.1016/j.measurement.2019.107463.

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39

Skapenko, Alla, Jan Leipe, Uwe Niesner, et al. "GATA-3 in Human T Cell Helper Type 2 Development." Journal of Experimental Medicine 199, no. 3 (2004): 423–28. http://dx.doi.org/10.1084/jem.20031323.

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The delineation of the in vivo role of GATA-3 in human T cell differentiation is a critical step in the understanding of molecular mechanisms directing human immune responses. We examined T cell differentiation and T cell–mediated effector functions in individuals lacking one functional GATA-3 allele. CD4 T cells from GATA-3+/− individuals expressed significantly reduced levels of GATA-3, associated with markedly decreased T helper cell (Th)2 frequencies in vivo and in vitro. Moreover, Th2 cell–mediated effector functions, as assessed by serum levels of Th2-dependent immunoglobulins (Igs; IgG4, IgE), were dramatically decreased, whereas the Th1-dependent IgG1 was elevated compared with GATA-3+/+ controls. Concordant with these data, silencing of GATA-3 in GATA-3+/+ CD4 T cells with small interfering RNA significantly reduced Th2 cell differentiation. Moreover, GATA-3 mRNA levels increased under Th2-inducing conditions and decreased under Th1-inducing conditions. Taken together, the data strongly suggest that GATA-3 is an important transcription factor in regulating human Th2 cell differentiation in vivo.

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40

Chen, Desu, and Ming-Wei Wang. "Development and application of rodent models for type 2 diabetes." Diabetes, Obesity and Metabolism 7, no. 4 (2005): 307–17. http://dx.doi.org/10.1111/j.1463-1326.2004.00392.x.

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41

Ivannikova, Е. V., and O. M. Smirnova. "The Patients at High Risk of Type 2 Diabetes Development." Effective Pharmacotherapy 16, no. 26 (2020): 50–55. http://dx.doi.org/10.33978/2307-3586-2020-16-26-50-55.

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Prediabetes is defined as a state of abnormal glucose homeostasis where blood glucose levels are elevated above those considered normal, but not as high as those required for a diagnosis of diabetes. Prediabetes is associated with high risks of developing serious diseases and poor quality of life of the patient. Globally, there are about 352.1 million people with prediabetes. By 2045, the number of able-bodied patients with a similar diagnosis is expected to double to 587 million. In this connection, timely diagnosis and identification of risk groups for the correction of carbohydrate metabolism is of great importance. The article provides data from numerous studies, a description of tactics and methods of treatment for patients with prediabetes.

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42

Huang, Yu-Min, Yassir Hussien, Dmitry Yarilin, Bao-Guo Xiao, Yong-Jun Liu, and Hans Link. "INTERFERON-BETA INDUCES THE DEVELOPMENT OF TYPE 2 DENDRITIC CELLS." Cytokine 13, no. 5 (2001): 264–71. http://dx.doi.org/10.1006/cyto.2000.0835.

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43

Christensen, Michael L., Brandi E. Franklin, Jeremiah D. Momper, and Michael D. Reed. "Pediatric drug development programs for type 2 diabetes: A review." Journal of Clinical Pharmacology 55, no. 7 (2015): 731–38. http://dx.doi.org/10.1002/jcph.497.

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44

Nagao, Mototsugu, Akira Asai, Hitoshi Sugihara, and Shinichi Oikawa. "Fat intake and the development of type 2 diabetes [Review]." Endocrine Journal 62, no. 7 (2015): 561–72. http://dx.doi.org/10.1507/endocrj.ej15-0055.

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45

Camargo García, Antonio, Sonia García-Carpintero, Javier Lopez-Moreno, et al. "Postprandial endotoxemia may influence the type 2 diabetes mellitus development." Atherosclerosis 263 (August 2017): e98. http://dx.doi.org/10.1016/j.atherosclerosis.2017.06.319.

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46

Loza, Matthew J., and Bice Perussia. "Peripheral Immature CD2−/lowT Cell Development from Type 2 to Type 1 Cytokine Production." Journal of Immunology 169, no. 6 (2002): 3061–68. http://dx.doi.org/10.4049/jimmunol.169.6.3061.

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47

Bekkering, Pjotr, Ismael Jafri, Frans J. van Overveld, and Ger T. Rijkers. "The intricate association between gut microbiota and development of Type 1, Type 2 and Type 3 diabetes." Expert Review of Clinical Immunology 9, no. 11 (2013): 1031–41. http://dx.doi.org/10.1586/1744666x.2013.848793.

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48

Mamillapalli, Chaitanya, Ramesh Tentu, Nitesh Kumar Jain, and Ramanath Bhandari. "COPD and Type 2 Diabetes." Current Respiratory Medicine Reviews 15, no. 2 (2019): 112–19. http://dx.doi.org/10.2174/1573398x15666190211155640.

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COPD and Type 2 diabetes are two highly prevalent global health conditions associated with high mortality and morbidity. The connection between these two common diseases is complex, and more research is required for further understanding of these conditions. COPD is being increasingly recognized as a risk factor for the development of type2 diabetes through different mechanisms including systemic inflammation, obesity, hypoxia and use of corticosteroids. Also, hyperglycemia in diabetes patients is linked to the adverse impact on lung physiology, and a possible increase in the risk of COPD. In this review article, we discuss the studies demonstrating the associations between COPD and Type 2 Diabetes, underlying pathophysiology and recommended therapeutic approach in the management of patients with coexisting COPD and diabetes.

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Galicia-Garcia, Unai, Asier Benito-Vicente, Shifa Jebari, et al. "Pathophysiology of Type 2 Diabetes Mellitus." International Journal of Molecular Sciences 21, no. 17 (2020): 6275. http://dx.doi.org/10.3390/ijms21176275.

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Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM.

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Moghissi, Etie. "Insulin Therapy in Type 2 Diabetes." US Endocrinology 09, no. 01 (2013): 6. http://dx.doi.org/10.17925/use.2013.09.01.6.

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Due to the progressive nature of Type 2 diabetes, insulin therapy is often required to achieve glycemic control. When lifestyle modifications and treatment with metformin with or without other oral antidiabetic drugs (OADs) have failed to achieve normoglycemia, timely initiation of singledose basal insulin treatment is a convenient, effective, and recommended strategy. The development of the long-acting basal insulin analogs, insulin detemir (IDet) and insulin glargine (IGlar), has resulted in significant improvements in the management of Type 2 diabetes, and specifically, in reducing rates of hypoglycemia. However, hypoglycemia still remains a limiting factor in the intensification of insulin therapy. Combination regimens involving insulin and incretin-based therapies have resulted in improved glycemic control with a similar rate of hypoglycemia compared with insulin alone. Novel basal insulin analogs may also help address the unmet needs associated with basal insulin therapy. Insulin degludec (IDeg) is a basal insulin analog that offers an ultra-long duration of action of more than 42 hours in adults, more flexibility compared with other long-acting insulin analogs in terms of daily dosing times, and reduced rates of hypoglycemia. Pegylated (PEG) lispro, an agent that is currently in clinical development, also offers an extended duration of action. The potential for fewer hypoglycemic episodes offered by combined regimens and new agents may improve adherence to insulin regimens.

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Zeitschriftenartikel zum Thema „Type-2 development“

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