Journal articles: 'Diabetes – Etiology'

1

Cinek, Ondřej, and Zdeněk Šumník. "Type 1 diabetes: etiology and epidemiology." Vnitřní lékařství 65, no. 4 (April 1, 2019): 235–47. http://dx.doi.org/10.36290/vnl.2019.041.

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Bratchikova, N. A., A. I. Zhelnina, D. V. Lopatin, and L. V. Sivakova. "DIABETES MELLITUS: ETIOLOGY, PATHOGENESIS, TREATMENT." Международный студенческий научный вестник (International Student Scientific Herald), no. 1 2020 (2020): 13. http://dx.doi.org/10.17513/msnv.19902.

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3

Todd, John A. "Etiology of Type 1 Diabetes." Immunity 32, no. 4 (April 2010): 457–67. http://dx.doi.org/10.1016/j.immuni.2010.04.001.

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4

Rossini, A. A., J. P. Mordes, and E. S. Handler. "Speculations on etiology of diabetes mellitus. Tumbler hypothesis." Diabetes 37, no. 3 (March 1, 1988): 257–61. http://dx.doi.org/10.2337/diabetes.37.3.257.

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5

Schade, D. S., D. A. Drumm, W. C. Duckworth, and R. Philip Eaton. "The Etiology of Incapacitating, Brittle Diabetes." Diabetes Care 8, no. 1 (January 1, 1985): 12–20. http://dx.doi.org/10.2337/diacare.8.1.12.

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6

Taylor, R. "Type 2 Diabetes: Etiology and reversibility." Diabetes Care 36, no. 4 (March 21, 2013): 1047–55. http://dx.doi.org/10.2337/dc12-1805.

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7

Ambler, GR. "Type 1 Diabetes: Etiology And Treatment." Journal of Paediatrics and Child Health 40, no. 4 (April 2004): 243–44. http://dx.doi.org/10.1111/j.1440-1754.2004.00351.x.

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8

Rodger, N. Wilson. "Type 1 Diabetes: Etiology and Treatment." Annals of Internal Medicine 139, no. 10 (November 18, 2003): 874. http://dx.doi.org/10.7326/0003-4819-139-10-200311180-00036.

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9

Tolstoi, Linda G., and John B. Josimovich. "Gestational Diabetes Mellitus: Etiology and Management." Nutrition Today 34, no. 5 (September 1999): 178–88. http://dx.doi.org/10.1097/00017285-199909000-00003.

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Tolstoi, Linda G., and John B. Josimovich. "Gestational Diabetes Mellitus: Etiology and Management." Nutrition Today 34, no. 5 (September 1999): 178–88. http://dx.doi.org/10.1097/00017285-199934050-00003.

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11

Javeed, Naureen, and Aleksey V. Matveyenko. "Circadian Etiology of Type 2 Diabetes Mellitus." Physiology 33, no. 2 (March 1, 2018): 138–50. http://dx.doi.org/10.1152/physiol.00003.2018.

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The epidemic of Type 2 diabetes mellitus necessitates development of novel therapeutic and preventative strategies to attenuate expansion of this debilitating disease. Evidence links the circadian system to various aspects of diabetes pathophysiology and treatment. The aim of this review will be to outline the rationale for therapeutic targeting of the circadian system in the treatment and prevention of Type 2 diabetes mellitus and consequent metabolic comorbidities.

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12

Hoffman, M. "New theory of diabetes etiology riles immunologists." Science 255, no. 5044 (January 31, 1992): 532–33. http://dx.doi.org/10.1126/science.1736357.

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13

Korsgren, Stella, Ylva Molin, Kaija Salmela, Torbjörn Lundgren, Åsa Melhus, and Olle Korsgren. "On the Etiology of Type 1 Diabetes." American Journal of Pathology 181, no. 5 (November 2012): 1735–48. http://dx.doi.org/10.1016/j.ajpath.2012.07.022.

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14

Acharjee, Satarupa, Bijaya Ghosh, Bandar E. Al-Dhubiab, and Anroop B. Nair. "Understanding Type 1 Diabetes: Etiology and Models." Canadian Journal of Diabetes 37, no. 4 (August 2013): 269–76. http://dx.doi.org/10.1016/j.jcjd.2013.05.001.

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15

Kavvoura, Fotini K., Anne Raimondo, Gayathiry Thanabalasingham, Amy Barrett, Amanda L. Webster, Debbie Shears, Nicholas P. Mann, Sian Ellard, Anna L. Gloyn, and Katharine R. Owen. "Reclassification of Diabetes Etiology in a Family With Multiple Diabetes Phenotypes." Journal of Clinical Endocrinology & Metabolism 99, no. 6 (June 1, 2014): E1067—E1071. http://dx.doi.org/10.1210/jc.2013-3641.

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16

Kuhl, C., P. J. Hornnes, and O. Andersen. "Review: Etiology and Pathophysiology of Gestational Diabetes Mellitus." Diabetes 34, Supplement_2 (June 1, 1985): 66–70. http://dx.doi.org/10.2337/diab.34.2.s66.

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17

Rossini, A. A., J. P. Mordes, and E. S. Handler. "Speculations on Etiology of Diabetes Mellitus: Tumbler Hypothesis." Diabetes 37, no. 3 (March 1, 1988): 257–61. http://dx.doi.org/10.2337/diab.37.3.257.

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18

Viberti, G. "Etiology and Prognostic Significance of Albuminuria in Diabetes." Diabetes Care 11, no. 10 (November 1, 1988): 840–45. http://dx.doi.org/10.2337/diacare.11.10.840.

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19

Skyler, Jay S., and Alexander Rabinovitch. "Etiology and Pathogenesis of Insulin Dependent Diabetes Mellitus." Pediatric Annals 16, no. 9 (September 1, 1987): 682–92. http://dx.doi.org/10.3928/0090-4481-19870901-06.

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20

Ananthakrishnan, Sonia. "Diabetes Insipidus in Pregnancy: Etiology, Evaluation, and Management." Endocrine Practice 15, no. 4 (May 2009): 377–82. http://dx.doi.org/10.4158/ep09090.ra.

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21

Léyy-Marchal, C. "INCIDENCE VARIATION AND ETIOLOGY OF TYPE 1 DIABETES." Pediatric Research 33 (May 1993): S8. http://dx.doi.org/10.1203/00006450-199305001-00034.

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22

Haller, Michael J., Mark A. Atkinson, and Desmond Schatz. "Type 1 Diabetes Mellitus: Etiology, Presentation, and Management." Pediatric Clinics of North America 52, no. 6 (December 2005): 1553–78. http://dx.doi.org/10.1016/j.pcl.2005.07.006.

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23

Zhang, Jiayue, Shujuan Ma, Chuhao Guo, Sisi Long, Shilan Wu, and Hongzhuan Tan. "Research progress on etiology of gestational diabetes mellitus." Global Health Journal 2, no. 4 (December 2018): 19–27. http://dx.doi.org/10.1016/s2414-6447(19)30179-4.

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24

Van Belle, Tom L., Ken T. Coppieters, and Matthias G. Von Herrath. "Type 1 Diabetes: Etiology, Immunology, and Therapeutic Strategies." Physiological Reviews 91, no. 1 (January 2011): 79–118. http://dx.doi.org/10.1152/physrev.00003.2010.

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Type 1 diabetes (T1D) is a chronic autoimmune disease in which destruction or damaging of the beta-cells in the islets of Langerhans results in insulin deficiency and hyperglycemia. We only know for sure that autoimmunity is the predominant effector mechanism of T1D, but may not be its primary cause. T1D precipitates in genetically susceptible individuals, very likely as a result of an environmental trigger. Current genetic data point towards the following genes as susceptibility genes: HLA, insulin, PTPN22, IL2Ra, and CTLA4. Epidemiological and other studies suggest a triggering role for enteroviruses, while other microorganisms might provide protection. Efficacious prevention of T1D will require detection of the earliest events in the process. So far, autoantibodies are most widely used as serum biomarker, but T-cell readouts and metabolome studies might strengthen and bring forward diagnosis. Current preventive clinical trials mostly focus on environmental triggers. Therapeutic trials test the efficacy of antigen-specific and antigen-nonspecific immune interventions, but also include restoration of the affected beta-cell mass by islet transplantation, neogenesis and regeneration, and combinations thereof. In this comprehensive review, we explain the genetic, environmental, and immunological data underlying the prevention and intervention strategies to constrain T1D.

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25

Sjöholm, Åke, and Thomas Nyström. "Inflammation and the etiology of type 2 diabetes." Diabetes/Metabolism Research and Reviews 22, no. 1 (2005): 4–10. http://dx.doi.org/10.1002/dmrr.568.

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26

Porte, D., and S. E. Kahn. "Hyperproinsulinemia and amyloid in NIDDM. Clues to etiology of islet beta-cell dysfunction?" Diabetes 38, no. 11 (November 1, 1989): 1333–36. http://dx.doi.org/10.2337/diabetes.38.11.1333.

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27

Xu, Hang, Xiaopeng Li, Hannah Adams, Karen Kubena, and Shaodong Guo. "Etiology of Metabolic Syndrome and Dietary Intervention." International Journal of Molecular Sciences 20, no. 1 (December 31, 2018): 128. http://dx.doi.org/10.3390/ijms20010128.

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The growing prevalence of metabolic syndrome (MetS) in the U.S. and even worldwide is becoming a serious health problem and economic burden. MetS has become a crucial risk factor for the development of type 2 diabetes mellitus (T2D) and cardiovascular diseases (CVD). The rising rates of CVD and diabetes, which are the two leading causes of death, simultaneously exist. To prevent the progression of MetS to diabetes and CVD, we have to understand how MetS occurs and how it progresses. Too many causative factors interact with each other, making the investigation and treatment of metabolic syndrome a very complex issue. Recently, a number of studies were conducted to investigate mechanisms and interventions of MetS, from different aspects. In this review, the proposed and demonstrated mechanisms of MetS pathogenesis are discussed and summarized. More importantly, different interventions are discussed, so that health practitioners can have a better understanding of the most recent research progress and have available references for their daily practice.

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28

Morovatdar, Negar, Gholamreza Tayebi Nasrabad, Konstantinos Tsarouhas, and Ramin Rezaee. "Etiology of Renal Replacement Therapy in Iran." International Journal of Nephrology 2019 (November 26, 2019): 1–5. http://dx.doi.org/10.1155/2019/5010293.

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Introduction. End-stage renal disease (ESRD) is one of the most common life-threatening diseases. In the past two decades, several factors were held responsible as the cause of this condition. The present study aimed to determine the causes of ESRD in the province of Khorasan Razavi, Iran. Materials and Methods. This cross-sectional study was conducted on 2404 ESRD patients who referred to 39 hemodialysis centers in Khorasan Razavi province, Iran, and were registered in the Mashhad University of Medical Sciences (MUMS), between 2000 and December 2018. Sociodemographic data and causes of ESRD were extracted from data registry. Results. The mean age at onset of hemodialysis for 2404 patients was 52.8 ± 16.4 years, and 57.1% of the patients were male. Clinical profile of hypertension (28.3%) and diabetes mellitus (24.8%) were the most common known causes of ESRD in our patients. Hypertension was more prevalent in male patients compared with females (30 vs 25%, respectively) while diabetes was more prevalent in females compared with males (25.4 vs 24.4%, respectively), p=0.009. Educational level was significantly associated with the cause of ESRD (p<0.001). Age of onset of ESRD in hypertensive patients was significantly lower compared with diabetic patients (51.5 ± 16.3 vs 58.28 ± 12.9 years, respectively; p<0.001). Conclusions. In the current study, the most common causes of ESRD were hypertension and diabetes mellitus. Primary prevention of hypertension and diabetes and proper treatment must be considered to reduce the burden of ESRD in Iran.

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29

Sullivan, Beverly A., Scott T. Henderson, Julie M. Davis, and Martin B. Steffenson. "Etiology, Detection, Diagnosis, and Clinical Management of Gestational Diabetes Mellitus." Journal of Pharmacy Practice 12, no. 1 (February 1999): 65–71. http://dx.doi.org/10.1177/089719009901200108.

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Healthy outcomes for both mother and child are expected and fortunately seen in most pregnancies. In some cases, serious or potentially serious problems arise during the pregnancy that mandate a need for both close monitoring and treatment interventions by health care providers. Gestational diabetes mellitus (GDM) is such a condition that may evolve during pregnancy. Women who experienced gestational diabetes during pregnancy are at increased risk of developing Type 2 diabetes as are their offspring. As defined, GDM is a type of diabetes restricted to pregnant women in whom the recognition of glucose intolerance first occurs during pregnancy.1 Physicians and pharmacists who are trained in the management of diabetes can help guide the patient with GDM through the pregnancy and after delivery, monitor her and the infant. This article reviews the current concepts pertaining to the basic pathophysiology, detection, diagnosis, and management of gestational diabetes mellitus.

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30

O’Connor, M. Rebecca, Ardith Doorenbos, and Joachim Voss. "Clinical Update on Genetic and Autoimmune Biomarkers in Pediatric Diabetes." Biological Research For Nursing 16, no. 2 (February 2, 2013): 218–27. http://dx.doi.org/10.1177/1099800412473820.

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Purpose: The purpose of this clinical update is to review the etiology of diabetes types affecting youth under 20 and describe diabetes-related genetic and autoimmune biomarkers based on the most recent literature. This information will support diabetes care providers’ efforts to better explain the complex topic to patients and families. Method: A PubMed search identified 396 reviews published from 2008 to 2011 that included the topics of etiology, epidemiology, genetics/epigenetics, pathogenesis, or immunology related to diabetes in youth. The current clinical update includes 19 of these. Results: The majority of youth under 20 years with diabetes have Type 1 diabetes. Other forms of the disease affecting this population include Type 2, monogenic, and secondary diabetes. Genetic and autoimmune biomarkers can help determine the risk and diagnosis of both Type 1 and monogenic diabetes. An accurate diagnosis of diabetes type allows for determination of optimal treatment options. Conclusion: The complexity of determining etiology, risk, diagnosis, and treatment for diabetes in youth is increasing with the rate of related genetic and immunologic advances. Diabetes care providers must be able to explain the complex genetic and autoimmune biomarkers used in determining the risk of diabetes, diagnosis of the disease, and identification of treatment options to patients and families.

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31

Hegedüs, Laszlo, Thomas H. Brix, and Ralf Paschke. "Etiology of Simple Goiter." Thyroid 19, no. 3 (March 2009): 209–11. http://dx.doi.org/10.1089/thy.2009.0047.

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32

Melmed, Shlomo. "Etiology of Pituitary Acromegaly." Endocrinology and Metabolism Clinics of North America 21, no. 3 (September 1992): 539–51. http://dx.doi.org/10.1016/s0889-8529(18)30201-9.

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33

Korpaisarn, Sira, and Joshua D. Safer. "Etiology of Gender Identity." Endocrinology and Metabolism Clinics of North America 48, no. 2 (June 2019): 323–29. http://dx.doi.org/10.1016/j.ecl.2019.01.002.

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34

LaMonte, Michael J., Steven N. Blair, and Timothy S. Church. "Physical activity and diabetes prevention." Journal of Applied Physiology 99, no. 3 (September 2005): 1205–13. http://dx.doi.org/10.1152/japplphysiol.00193.2005.

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Diabetes has reached epidemic proportions worldwide and is associated with a large economic burden, increased risk of cardiovascular disease, and premature mortality. Hyperglycemia is the hallmark clinical manifestation of diabetes and evolves through a multifactorial etiology of genetic, environmental, and behavioral enablers. Approximately 90% of diabetes cases are the non-insulin-dependent phenotype, which is characterized by a progressive deterioration in insulin-mediated glucose disposal, particularly by peripheral tissues. Our hypothesis is that the most proximal behavioral cause of insulin resistance is physical inactivity. Indeed, several streams of scientific research have demonstrated a role for physical activity in the etiology and prevention of diabetes and its related morbidity. In this review we will discuss some of the key observational and experimental studies that have examined associations among physical activity, cardiorespiratory fitness, and non-insulin-dependent diabetes.

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35

McGarry, J. D. "Banting Lecture 2001: Dysregulation of Fatty Acid Metabolism in the Etiology of Type 2 Diabetes." Diabetes 51, no. 1 (January 1, 2002): 7–18. http://dx.doi.org/10.2337/diabetes.51.1.7.

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36

Jannetta, PeterJ, LynnH Fletcher, PeterM Grondziowski, KennethF Casey, and RaymondF Sekula. "Type 2 diabetes mellitus: A central nervous system etiology." Surgical Neurology International 1, no. 1 (2010): 31. http://dx.doi.org/10.4103/2152-7806.66460.

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37

Fischman, Daniel, and Vinod Nookala. "Cystic Fibrosis-Related Diabetes Mellitus: Etiology, Evaluation, and Management." Endocrine Practice 14, no. 9 (December 2008): 1169–79. http://dx.doi.org/10.4158/ep.14.9.1169.

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38

Clark, Charles M., and R. Clark Perry. "Type 2 diabetes and macrovascular disease: Epidemiology and etiology." American Heart Journal 138, no. 5 (November 1999): S330—S333. http://dx.doi.org/10.1016/s0002-8703(99)70031-1.

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39

CLARK, C., and R. CLARKPERRY. "Type 2 diabetes and macrovascular disease: Epidemiology and etiology." American Heart Journal 138, no. 4 (October 1999): s330—s333. http://dx.doi.org/10.1016/s0167-0115(99)90001-7.

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40

Shimada, Akira. "Autoimmunity as an etiology of fulminant type 1 diabetes." Diabetology International 7, no. 2 (March 9, 2016): 104–5. http://dx.doi.org/10.1007/s13340-016-0262-2.

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41

Richardson, Donald, and Aaron Vinik. "Etiology and treatment of erectile failure in diabetes mellitus." Current Diabetes Reports 2, no. 6 (November 2002): 501–9. http://dx.doi.org/10.1007/s11892-002-0120-4.

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42

Cerna, Marie. "Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus." International Journal of Molecular Sciences 21, no. 1 (December 19, 2019): 36. http://dx.doi.org/10.3390/ijms21010036.

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Type 1 diabetes mellitus (T1DM) is caused by an autoimmune destruction of the pancreatic β-cells, a process in which autoreactive T cells play a pivotal role, and it is characterized by islet autoantibodies. Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused by the interaction of multiple environmental and genetic factors. The integrations of environments and genes occur via epigenetic regulations of the genome, which allow adaptation of organism to changing life conditions by alternation of gene expression. T1DM has increased several-fold over the past half century. Such a short time indicates involvement of environment factors and excludes genetic changes. This review summarizes the most current knowledge of epigenetic changes in that process leading to autoimmune diabetes mellitus.

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43

Groop, Leif C., and Johan G. Eriksson. "The Etiology and Pathogenesis of Non-insulin-dependent Diabetes." Annals of Medicine 24, no. 6 (January 1992): 483–89. http://dx.doi.org/10.3109/07853899209167000.

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44

Santamaria, Pere, Masao Nagata, and Ji-Won Yoon. "Autoimmune Mechanisms in The Etiology of Type I Diabetes." Clinical Pediatric Endocrinology 3, no. 1 (1994): 1–23. http://dx.doi.org/10.1297/cpe.3.1.

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45

Vora, Amit C. "Type 1 Diabetes. Etiology and Treatment (Contemporary Endocrinology Series)." Diabetes Technology & Therapeutics 6, no. 4 (August 2004): 556–57. http://dx.doi.org/10.1089/1520915041705857.

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46

Åkerblom, Hans K., Outi Vaarala, Heikki Hyöty, Jorma Ilonen, and Mikael Knip. "Environmental factors in the etiology of type 1 diabetes." American Journal of Medical Genetics 115, no. 1 (March 26, 2002): 18–29. http://dx.doi.org/10.1002/ajmg.10340.

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47

Kommoju, Uma Jyothi, and Battini Mohan Reddy. "Genetic etiology of type 2 diabetes mellitus: a review." International Journal of Diabetes in Developing Countries 31, no. 2 (April 2011): 51–64. http://dx.doi.org/10.1007/s13410-011-0020-8.

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48

Grafton, G., C. M. Bunce, M. C. Sheppard, G. Brown, and M. A. Baxter. "Effect of Mg2+ on Na(+)-dependent inositol transport. Role for Mg2+ in etiology of diabetic complications." Diabetes 41, no. 1 (January 1, 1992): 35–39. http://dx.doi.org/10.2337/diabetes.41.1.35.

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49

Bodmer, C. W., A. W. Patrick, T. V. How, and G. Williams. "Exaggerated sensitivity to NE-induced vasoconstriction in IDDM patients with microalbuminuria. Possible etiology and diagnostic implications." Diabetes 41, no. 2 (February 1, 1992): 209–14. http://dx.doi.org/10.2337/diabetes.41.2.209.

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50

Buchanan, T. A., K. M. Denno, G. F. Sipos, and T. W. Sadler. "Diabetic teratogenesis. In vitro evidence for a multifactorial etiology with little contribution from glucose per se." Diabetes 43, no. 5 (May 1, 1994): 656–60. http://dx.doi.org/10.2337/diabetes.43.5.656.

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Journal articles on the topic 'Diabetes – Etiology'

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