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Thematische Bibliographien / Diabetes resistance / Zeitschriftenartikel

Zeitschriftenartikel zum Thema „Diabetes resistance“

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Autor: Grafiati

Veröffentlicht am 6. Juli 2024

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1

Gokalp, Deniz, Alpaslan Tuzcu, Ster Irmak, Mithat Bahceci und Ozlem Demirpence. „FREQUENCY OF ASPIRIN RESISTANCE IN PATIENTS WITH TYPE 1 AND 2 DIABETES MELLITUS AND ITS ASSOCIATION WITH METABOLIC PARAMETERS“. International Journal of Surgery and Medicine 2, Nr. 3 (2016): 122. http://dx.doi.org/10.5455/ijsm.aspirin-resistance-diabetes.

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2

McClain, D. A., und E. D. Crook. „Hexosamines and insulin resistance“. Diabetes 45, Nr. 8 (01.08.1996): 1003–9. http://dx.doi.org/10.2337/diabetes.45.8.1003.

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3

Sceppa, Carmen Castaneda. „Resistance Training and Diabetes“. Medicine & Science in Sports & Exercise 36, Supplement (Mai 2004): S93—S94. http://dx.doi.org/10.1249/00005768-200405001-00442.

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4

Sceppa, Carmen Castaneda. „Resistance Training and Diabetes“. Medicine & Science in Sports & Exercise 36, Supplement (Mai 2004): S93???S94. http://dx.doi.org/10.1097/00005768-200405001-00442.

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5

Kraegen, E. W., P. W. Clark, A. B. Jenkins, E. A. Daley, D. J. Chisholm und L. H. Storlien. „Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats“. Diabetes 40, Nr. 11 (01.11.1991): 1397–403. http://dx.doi.org/10.2337/diabetes.40.11.1397.

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6

Mykkanen, L., D. J. Zaccaro, L. E. Wagenknecht, D. C. Robbins, M. Gabriel und S. M. Haffner. „Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the insulin resistance atherosclerosis study“. Diabetes 47, Nr. 5 (01.05.1998): 793–800. http://dx.doi.org/10.2337/diabetes.47.5.793.

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7

Goran, M. I., und B. A. Gower. „Longitudinal Study on Pubertal Insulin Resistance“. Diabetes 50, Nr. 11 (01.11.2001): 2444–50. http://dx.doi.org/10.2337/diabetes.50.11.2444.

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8

Zhan, Yiqiang, Zheng Tang und Jinming Yu. „Serum ferritin, diabetes, diabetes control, and insulin resistance“. Acta Diabetologica 51, Nr. 6 (22.10.2014): 991–98. http://dx.doi.org/10.1007/s00592-014-0656-1.

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9

Wang, J., S. Obici, K. Morgan, N. Barzilai, Z. Feng und L. Rossetti. „Overfeeding Rapidly Induces Leptin and Insulin Resistance“. Diabetes 50, Nr. 12 (01.12.2001): 2786–91. http://dx.doi.org/10.2337/diabetes.50.12.2786.

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10

Massarelli, Laura, Giuseppe Musumeci, Carlo Bussolino und Valerio Tomaselli. „Diabetes mellitus and clopidogrel “resistance”“. Clinical Management Issues 5, Nr. 2S (13.10.2015): 55–58. http://dx.doi.org/10.7175/cmi.v5i2s.1112.

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In our Department arrives a 75-year-old patient with hypertension, diabetes mellitus (DM) treated with hypoglycaemic drugs, dyslipidaemia and ischaemic heart disease post-acute myocardial infarction treated with triple coronary artery bypass surgery and subsequent percutaneous transluminal coronary angioplasty (PTCA). After a new PTCA and positioning of medical stent he is discharged with a double antiplatelet therapy. But after one month two thrombotic events occur in this patients almost simultaneously. Antiplatelet therapy such as clopidogrel and aspirin in combination, is the current gold standard for reducing cardiovascular events in patients with DM, providing a synergistic platelet inhibition through different platelet activation pathways, but platelets of DM patients are characterised by disregulation of several signalling pathways which may play a role not only in the higher risk of developing cardiovascular events and the worse outcome, but also in the larger proportion of DM patients with inadequate response to antiplatelet drugs compared to non DM subjects.

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11

Ozsahin, Akatli, Suheyl Asma, Aydana Aksoyek, Cigdem Gereklioglu und Asli Korur. „Obesity- Insulin Resistance and Diabetes“. Turkish Journal of Family Medicine & Primary Care 9, Nr. 2 (2015): 36. http://dx.doi.org/10.5455/tjfmpc.172673.

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12

Livingstone, C., und G. W. Gould. „Insulin Resistance in Diabetes Mellitus“. Scottish Medical Journal 40, Nr. 2 (April 1995): 37–39. http://dx.doi.org/10.1177/003693309504000202.

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13

DeFronzo, Ralph A., und Stefano Del Prato. „Insulin resistance and diabetes mellitus“. Journal of Diabetes and its Complications 10, Nr. 5 (September 1996): 243–45. http://dx.doi.org/10.1016/1056-8727(96)00046-3.

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14

Hadigan, Colleen. „Diabetes, insulin resistance, and HIV“. Current Infectious Disease Reports 8, Nr. 1 (Februar 2006): 69–75. http://dx.doi.org/10.1007/s11908-006-0037-1.

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15

Laville, M., und J. A. Nazare. „Diabetes, insulin resistance and sugars“. Obesity Reviews 10 (März 2009): 24–33. http://dx.doi.org/10.1111/j.1467-789x.2008.00562.x.

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16

Takano, Chika, Erika Ogawa und Satoshi Hayakawa. „Insulin Resistance in Mitochondrial Diabetes“. Biomolecules 13, Nr. 1 (07.01.2023): 126. http://dx.doi.org/10.3390/biom13010126.

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Mitochondrial diabetes (MD) is generally classified as a genetic defect of β-cells. The main pathophysiology is insulin secretion failure in pancreatic β-cells due to impaired mitochondrial ATP production. However, several reports have mentioned the presence of insulin resistance (IR) as a clinical feature of MD. As mitochondrial dysfunction is one of the important factors causing IR, we need to focus on IR as another pathophysiology of MD. In this special issue, we first briefly summarized the insulin signaling and molecular mechanisms of IR. Second, we overviewed currently confirmed pathogenic mitochondrial DNA (mtDNA) mutations from the MITOMAP database. The variants causing diabetes were mostly point mutations in the transfer RNA (tRNA) of the mitochondrial genome. Third, we focused on these variants leading to the recently described “tRNA modopathies” and reviewed the clinical features of patients with diabetes. Finally, we discussed the pathophysiology of MD caused by mtDNA mutations and explored the possible mechanism underlying the development of IR. This review should be beneficial to all clinicians involved in diagnostics and therapeutics related to diabetes and mitochondrial diseases.

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17

Ajjan, R., R. F. Storey und P. J. Grant. „Aspirin resistance and diabetes mellitus“. Diabetologia 51, Nr. 3 (16.01.2008): 385–90. http://dx.doi.org/10.1007/s00125-007-0898-3.

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18

Maqbool, Mudasir. „Role of Insulin Resistance in Gestational Diabetes Mellitus: A Literature Review“. Chettinad Health City Medical Journal 11, Nr. 02 (30.06.2022): 69–74. http://dx.doi.org/10.24321/2278.2044.202218.

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Several physiologic, hormonal, and molecular processes contribute to the emergence of hyperglycaemia during pregnancy. Increased insulin resistance is seen during the course of a healthy pregnancy. During the early stages of normal pregnancies, the pancreatic β-cells secrete more insulin, which slows the rise in plasma glucose levels. This regulation explains the abnormally modest increases in plasma glucose levels brought on by elevated insulin resistance. The aim of this review was to evaluate the role of insulin resistance in gestational diabetes mellitus (GDM). The authors extensively searched various electronic databases like PubMed, Scopus, and Google Scholar for the collection of material regarding the role of insulin resistance in GDM. It was seen that hyperglycaemia results from the combination of the pregnancy’s increased insulin tolerance and pancreatic beta-cell insufficiency. Scientific studies have revealed that individuals who present with GDM are more likely to acquire chronic insulin resistance because of the superimposition of lower insulin production by the cells in that condition (GDM). Due to their significance in the development of postpartum diabetes mellitus, inflammation markers in GDM have been widely researched. Inflammation during GDM induces adaptive reactions in the placenta, which can have a substantial effect on the programming of foetal development.

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19

Senn, J. J., P. J. Klover, I. A. Nowak und R. A. Mooney. „Interleukin-6 Induces Cellular Insulin Resistance in Hepatocytes“. Diabetes 51, Nr. 12 (01.12.2002): 3391–99. http://dx.doi.org/10.2337/diabetes.51.12.3391.

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20

Spurlin, B. A., R. M. Thomas, A. K. Nevins, H. J. Kim, Y. J. Kim, H. L. Noh, G. I. Shulman, J. K. Kim und D. C. Thurmond. „Insulin Resistance in Tetracycline-Repressible Munc18c Transgenic Mice“. Diabetes 52, Nr. 8 (25.07.2003): 1910–17. http://dx.doi.org/10.2337/diabetes.52.8.1910.

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21

Pocai, A., K. Morgan, C. Buettner, R. Gutierrez-Juarez, S. Obici und L. Rossetti. „Central Leptin Acutely Reverses Diet-Induced Hepatic Insulin Resistance“. Diabetes 54, Nr. 11 (25.10.2005): 3182–89. http://dx.doi.org/10.2337/diabetes.54.11.3182.

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22

Wang, C. C. L., M. L. Goalstone und B. Draznin. „Molecular Mechanisms of Insulin Resistance That Impact Cardiovascular Biology“. Diabetes 53, Nr. 11 (25.10.2004): 2735–40. http://dx.doi.org/10.2337/diabetes.53.11.2735.

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23

Banks, W. A., A. B. Coon, S. M. Robinson, A. Moinuddin, J. M. Shultz, R. Nakaoke und J. E. Morley. „Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier“. Diabetes 53, Nr. 5 (26.04.2004): 1253–60. http://dx.doi.org/10.2337/diabetes.53.5.1253.

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24

Raymond, R. M., M. P. McLane, W. R. Law, N. F. King und D. W. Leutz. „Myocardial insulin resistance during acute endotoxin shock in dogs“. Diabetes 37, Nr. 12 (01.12.1988): 1684–88. http://dx.doi.org/10.2337/diabetes.37.12.1684.

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25

Veroni, M. C., J. Proietto und R. G. Larkins. „Evolution of insulin resistance in New Zealand obese mice“. Diabetes 40, Nr. 11 (01.11.1991): 1480–87. http://dx.doi.org/10.2337/diabetes.40.11.1480.

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26

Haffner, S. M., R. A. Valdez, H. P. Hazuda, B. D. Mitchell, P. A. Morales und M. P. Stern. „Prospective analysis of the insulin-resistance syndrome (syndrome X)“. Diabetes 41, Nr. 6 (01.06.1992): 715–22. http://dx.doi.org/10.2337/diabetes.41.6.715.

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27

Kohrt, W. M., J. P. Kirwan, M. A. Staten, R. E. Bourey, D. S. King und J. O. Holloszy. „Insulin resistance in aging is related to abdominal obesity“. Diabetes 42, Nr. 2 (01.02.1993): 273–81. http://dx.doi.org/10.2337/diabetes.42.2.273.

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28

Chaiken, R. L., M. A. Banerji, H. Huey und H. E. Lebovitz. „Do blacks with NIDDM have an insulin-resistance syndrome?“ Diabetes 42, Nr. 3 (01.03.1993): 444–49. http://dx.doi.org/10.2337/diabetes.42.3.444.

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29

Hunnicutt, J. W., R. W. Hardy, J. Williford und J. M. McDonald. „Saturated fatty acid-induced insulin resistance in rat adipocytes“. Diabetes 43, Nr. 4 (01.04.1994): 540–45. http://dx.doi.org/10.2337/diabetes.43.4.540.

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30

Barzilai, N., L. She, B. Q. Liu, P. Vuguin, P. Cohen, J. Wang und L. Rossetti. „Surgical removal of visceral fat reverses hepatic insulin resistance“. Diabetes 48, Nr. 1 (01.01.1999): 94–98. http://dx.doi.org/10.2337/diabetes.48.1.94.

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31

Kido, Y., N. Philippe, A. A. Schaffer und D. Accili. „Genetic modifiers of the insulin resistance phenotype in mice“. Diabetes 49, Nr. 4 (01.04.2000): 589–96. http://dx.doi.org/10.2337/diabetes.49.4.589.

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32

Gabriely, I., X. H. Ma, X. M. Yang, L. Rossetti und N. Barzilai. „Leptin Resistance During Aging Is Independent of Fat Mass“. Diabetes 51, Nr. 4 (01.04.2002): 1016–21. http://dx.doi.org/10.2337/diabetes.51.4.1016.

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33

Haffner, S. M., R. D'Agostino, M. F. Saad, M. Rewers, L. Mykkanen, J. Selby, G. Howard et al. „Increased insulin resistance and insulin secretion in nondiabetic African-Americans and Hispanics compared with non-Hispanic whites. The Insulin Resistance Atherosclerosis Study“. Diabetes 45, Nr. 6 (01.06.1996): 742–48. http://dx.doi.org/10.2337/diabetes.45.6.742.

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34

Premkumar, Daivasikamani. „The Role of Obesity in Producing Type 2 Diabetes by Insulin Resistance“. Diabetes & Obesity International Journal 5, Nr. 2 (2020): 1–9. http://dx.doi.org/10.23880/doij-16000227.

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Obesity is a common condition due wrong eating habits and less physical activity. But it can produce serious illness like type 2 diabetes. In Malaysia 18 years and above 33.3% (5.4 million) are pre-obese and 27.2% (4.4 million) are obese. 7.2% are known to have diabetes and 8.0% are previously undiagnosed with diabetes. There is a strong relationship between obesity and diabetes mellitus. We must understand the mechanism by which obesity causes diabetes through and insulin resistance. When the fat distribution is more peripheral have more insulin sensitivity than whose fat distribution is more in the waist. The insulin resistance is caused by variety of substances like non-esterified fatty acids, glycerol, hormones, cytokines, proinflammatory markers which leads to the development of insulin resistance. The development of diabetes is a combination of the failure of β-islet cells of the pancreas and insulin resistance. There is a rising incidence of type 1 and type 2 diabetes due to obesity and weight gain. The obesity is more common in females. Obesity increases with age. Similarly, the incidence of diabetes also increases with and in male sex. Out of 219 persons 77 had normal BMI (less than 25), 83 were overweight (BMI 25 to 30) and 59 were obese (more than 30). The incidence of overweight (37.8%) and obese (26%). People who are overweight (BMI 25- 30) below 40 years are 8, between 40-60 years are 36 and above 60 years are 39. The people who are obese in the 40 years age group 6, 40-60 years 23 and above 60 years 30. Incidence of overweight and obese is more in the females 72.7% and males 58.4%. Incidence of overweight among female is 42% and obese are 30%. Comparatively among male 34.4% are overweight and 24% are obese.

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35

Bloomgarden, Zachary T. „Developments in Diabetes and Insulin Resistance“. Diabetes Care 29, Nr. 1 (22.12.2005): 161–67. http://dx.doi.org/10.2337/diacare.29.01.06.dc06-zb01.

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36

Taylor, R. „Insulin Resistance and Type 2 Diabetes“. Diabetes 61, Nr. 4 (22.03.2012): 778–79. http://dx.doi.org/10.2337/db12-0073.

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37

Gedela, Vasavi, und Sree Lakshmi Gosala. „Diabetes a risk for antimicrobial resistance?“ International Journal of Basic & Clinical Pharmacology 6, Nr. 12 (23.11.2017): 2811. http://dx.doi.org/10.18203/2319-2003.ijbcp20175103.

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Background: Diabetic foot infections can cause substantial morbidity. The role of Diabetes mellitus in the antimicrobial resistance of pathogens in patients with foot infections is not well clarified. So, we compared the profile of antibiotic resistance in diabetic and non-diabetic foot ulcer infections. Objectives were to compare the antimicrobial resistance pattern in diabetic and non-diabetic lower limb infections.Methods: T Pus was isolated in 50 Diabetic and 50 non-diabetic foot ulcer infections. The organisms were isolated on specific media and antibiotic susceptibility was done by using Kirby-Bauer disc diffusion method.Results: The most frequent causative organism in diabetic and non-diabetics is Pseudomonas 27.5% vs 27.1%, Staphylococcus 24.1% vs 27.1%, Klebsiella 24.1% vs 22.03%, E. coli 10.3% vs 10.16%, Proteus 5.17% vs 5.08%. No significant differences in resistance rates to Amikacin, Penicillin, Ofloxacin, Vancomycin, Piperacillin + Tazobactum were observed between diabetic and non-diabetic patients. There is significant difference in resistance to Ampicillin (p=0.017).Conclusions: Diabetes per se does not seem to influence the susceptibility pattern to antimicrobials in our group of patients with foot ulcer infections.

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38

Flack, Kyle D., Kevin P. Davy, Matthew W. Hulver, Richard A. Winett, Madlyn I. Frisard und Brenda M. Davy. „Aging, Resistance Training, and Diabetes Prevention“. Journal of Aging Research 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/127315.

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With the aging of the baby-boom generation and increases in life expectancy, the American population is growing older. Aging is associated with adverse changes in glucose tolerance and increased risk of diabetes; the increasing prevalence of diabetes among older adults suggests a clear need for effective diabetes prevention approaches for this population. The purpose of paper is to review what is known about changes in glucose tolerance with advancing age and the potential utility of resistance training (RT) as an intervention to prevent diabetes among middle-aged and older adults. Age-related factors contributing to glucose intolerance, which may be improved with RT, include improvements in insulin signaling defects, reductions in tumor necrosis factor-α, increases in adiponectin and insulin-like growth factor-1 concentrations, and reductions in total and abdominal visceral fat. Current RT recommendations and future areas for investigation are presented.

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39

Hannah, Judy S., und Barbara V. Howard. „Dietary fats, insulin resistance, and diabetes“. Journal of Cardiovascular Risk 1, Nr. 1 (Juni 1994): 31–37. http://dx.doi.org/10.1097/00043798-199406000-00006.

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40

Reusch, Jane E. B., und Boris B. Draznin. „Atherosclerosis in diabetes and insulin resistance“. Diabetes, Obesity and Metabolism 9, Nr. 4 (Juli 2007): 455–63. http://dx.doi.org/10.1111/j.1463-1326.2006.00620.x.

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41

Mestman, MD, Jorge H. „INSULIN RESISTANCE SYNDROME AND GESTATIONAL DIABETES“. Endocrine Practice 9, Supplement 2 (Oktober 2003): 90–92. http://dx.doi.org/10.4158/ep.9.s2.90.

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42

ANG, Christine, und Mary Ann LUMSDEN. „Diabetes and the maternal resistance vasculature“. Clinical Science 101, Nr. 6 (01.12.2001): 719. http://dx.doi.org/10.1042/cs20010153.

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43

Cowley, Cheryl. „Insulin resistance in type 2 diabetes“. Practice Nursing 11, Nr. 15 (Oktober 2000): 27–29. http://dx.doi.org/10.12968/pnur.2000.11.15.13037.

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44

Hannah, J. S., und B. V. Howard. „Dietary Fats, Insulin Resistance, and Diabetes“. European Journal of Cardiovascular Prevention & Rehabilitation 1, Nr. 1 (01.06.1994): 31–37. http://dx.doi.org/10.1177/174182679400100106.

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45

ANG, Christine, und Mary Ann LUMSDEN. „Diabetes and the maternal resistance vasculature“. Clinical Science 101, Nr. 6 (21.11.2001): 719–29. http://dx.doi.org/10.1042/cs1010719.

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Diabetes is the most common endocrine disorder worldwide, with complications that include the development of both macro- and micro-vascular disease that contribute significantly to patient morbidity and mortality. The severity of diabetic complications is amplified during pregnancy, resulting in a higher incidence of adverse pregnancy outcomes such as pre-eclampsia, placental insufficiency and stillbirth than in non-diabetics. Vascular dysfunction is thought to underlie many of these complications, with the greatest impact occurring at the level of the resistance vasculature, where alterations in vascular reactivity can significantly affect blood flow and tissue perfusion. It is likely that problems associated with diabetic pregnancies are related, in part, to abnormal vascular function, particularly dysfunction of the vascular endothelium.

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46

Lima, Luís Maurício T. R. „Insulin resistance underlying type 2 diabetes“. Lancet Diabetes & Endocrinology 7, Nr. 6 (Juni 2019): 424. http://dx.doi.org/10.1016/s2213-8587(19)30147-0.

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47

Feroe, Aliya G., Roberta Attanasio und Franco Scinicariello. „Acrolein metabolites, diabetes and insulin resistance“. Environmental Research 148 (Juli 2016): 1–6. http://dx.doi.org/10.1016/j.envres.2016.03.015.

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48

Bray, George A. „Models of insulin resistance and diabetes“. Pathophysiology 1 (November 1994): 37. http://dx.doi.org/10.1016/0928-4680(94)90098-1.

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49

Nicolau, Julia, Thierry Lequerré, Hélène Bacquet und Olivier Vittecoq. „Rheumatoid arthritis, insulin resistance, and diabetes“. Joint Bone Spine 84, Nr. 4 (Juli 2017): 411–16. http://dx.doi.org/10.1016/j.jbspin.2016.09.001.

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50

Stolar, Mark W. „Insulin resistance, diabetes, and the adipocyte“. American Journal of Health-System Pharmacy 59, suppl_9 (01.12.2002): S3—S8. http://dx.doi.org/10.1093/ajhp/59.suppl_9.s3.

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