Articoli di riviste: "Insulin resistance"

1

Kumar, Sinha Ritesh, and Chandra Satish. "Insulin resistance." Asian Pacific Journal of Health Sciences, Supplimentary 2014 (2014): 71–78. http://dx.doi.org/10.21276/apjhs.2014.1.1s.15.

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2

Demir, Şevin, and Çelik Banu Arslan. "Ability of Metabolic Score for Insulin Resistance to Detect Insulin Resistance." Chronicles of Precision Medical Researchers 3, no. 3 (October 13, 2022): 187–92. https://doi.org/10.5281/zenodo.7195874.

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Aim: To evaluate the usability of metabolic score for insulin resistance (METS-IR), a novel insulin resistance index, in our country and to determine the optimal cut-off value of this index for detecting insulin resistance. Material and Method: One thousand five hundred sixty seven individuals who participated in our check-up program between 2020 and 2021 were retrospectively evaluated with the patient files for inclusion in the study. Insulin resistance was accepted when HOMA-IR≥2.7. Subjects were divided into 4 quartiles according to their METS-IR levels. Receiver-operating characteristic curve was used to determine the indices’ predictive performance and the optimal cut-off value of METS-IR to identify insulin resistance. Binary logistic regression model was used to associate insulin resistance with the varying indexes. Results: Among the 494 participants, 294 (59.5%) were women and the mean age of the subjects was 48.61±12.90 years. As the quartile of METS-IR increased, prevalence of male gender, metabolic syndrome, fatty liver, and levels of age, blood pressure, cigarette smoking, obesity, and insulin resistance indexes, HbA1c increased (all, p<0.001). METS-IR had the highest predictive value for the presence of insulin resistance (AUC=0.813, p<0.001). The highest sensitivity and specificity were achieved at METSIR between 39–42. The increase in METS-IR is more significant when compared to other indexes for the prediction of insulin resistance (OR=1.332, p<0.001). Conclusions: METS-IR can be used as a screening test for insulin resistance in settings such as primary care centers where insulin levels cannot be measured.  

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Sowers, James R., and Edward D. Frohlich. "Insulin and insulin resistance:." Medical Clinics of North America 88, no. 1 (January 2004): 63–82. http://dx.doi.org/10.1016/s0025-7125(03)00128-7.

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Jeffery, Alison. "Insulin resistance." Nursing Standard 17, no. 32 (April 23, 2003): 47–53. http://dx.doi.org/10.7748/ns2003.04.17.32.47.c3381.

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Tomono, Syouichi. "Insulin Resistance :." Kitakanto Medical Journal 62, no. 1 (2012): 73–74. http://dx.doi.org/10.2974/kmj.62.73.

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Jeffery, Alison. "Insulin resistance." Nursing Standard 17, no. 32 (April 23, 2003): 47–55. http://dx.doi.org/10.7748/ns.17.32.47.s62.

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7

Park, Kyong Soo. "Insulin Resistance." Journal of the Korean Medical Association 44, no. 3 (2001): 302. http://dx.doi.org/10.5124/jkma.2001.44.3.302.

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8

Bell, David S. H. "Insulin resistance." Postgraduate Medicine 93, no. 7 (May 15, 1993): 99–107. http://dx.doi.org/10.1080/00325481.1993.11701704.

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9

Carroll, P. B., and R. C. Eastman. "Insulin Resistance." Endocrinologist 1, no. 2 (April 1991): 89–97. http://dx.doi.org/10.1097/00019616-199104000-00005.

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10

DeFronzo, Ralph A. "Insulin resistance." Current Opinion in Cardiology 5, no. 5 (October 1990): 592–98. http://dx.doi.org/10.1097/00001573-199010000-00003.

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11

Whitelaw, D. C., and S. G. Gilbey. "Insulin Resistance." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 35, no. 5 (September 1998): 567–83. http://dx.doi.org/10.1177/000456329803500501.

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12

Sinaiko, Alan R., and Sonia Caprio. "Insulin Resistance." Journal of Pediatrics 161, no. 1 (July 2012): 11–15. http://dx.doi.org/10.1016/j.jpeds.2012.01.012.

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13

VOLL, ARTUR, and JOHAN KLOSTER. "Insulin Resistance." Acta Medica Scandinavica 157, no. 3 (April 24, 2009): 223–32. http://dx.doi.org/10.1111/j.0954-6820.1957.tb14430.x.

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14

El Ray, Ahmed, Tarik Asselah, Rami Moucari, Maged El Ghannam, Alaa A. Taha, Mohamed A. Saber, Maha Akl, et al. "Insulin resistance." European Journal of Gastroenterology & Hepatology 25, no. 4 (April 2013): 421–27. http://dx.doi.org/10.1097/meg.0b013e32835c9f69.

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15

O'Doherty, R., D. Stein, and J. Foley. "Insulin resistance." Diabetologia 40 (September 19, 1997): S10—S15. http://dx.doi.org/10.1007/s001250051389.

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16

El-Zayadi, Abdel-Rahman. "Insulin resistance." Arab Journal of Gastroenterology 11, no. 2 (June 2010): 66–69. http://dx.doi.org/10.1016/j.ajg.2010.04.010.

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17

Altunoglu, Esma Guldal. "Insulin resistance." Istanbul Medical Journal 13, no. 3 (2012): 0. http://dx.doi.org/10.5505/1304.8503.2012.78941.

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18

Krenkel, Jessica A. "Insulin Resistance." Topics in Clinical Nutrition 17, no. 5 (December 2002): 85. http://dx.doi.org/10.1097/00008486-200212000-00011.

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19

Nesbitt, Alexander. "Insulin Resistance." Journal of Advanced Nursing 44, no. 3 (October 20, 2003): 327–28. http://dx.doi.org/10.1046/j.1365-2648.2003.02826_3.x.

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20

Wolfrum, C., E. Asilmaz, E. Luca, J. M. Friedman, and M. Stoffel. "Insulin Resistance." Journal of the American Society of Nephrology 16, no. 3 (March 2005): 569–71. http://dx.doi.org/10.1681/01.asn.0000926692.88991.55.

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21

Chaoji, Sunanda Ashutosh. "Insulin Resistance." Vidarbha Journal of Internal Medicine 33 (April 6, 2023): 27–31. http://dx.doi.org/10.25259/vjim_41_2022.

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Abstract (sommario):

The twin epidemic of ‘Diabesity’-diabetes and obesity, all over the world, both in developed and developing countries, has brought the issue of insulin resistance (IR) into new focus of research. Apart from Type 2 diabetes mellitus (DM), IR is implicated in many other clinical syndromes because of its varied metabolic and mitogenic actions. IR has been found to play important pivotal role in pathophysiology of diabesity. IR is defined as when a normal or higher insulin level fails to produce expected biological response; one predominantly affecting insulin mediated glucose disposal 20–30% reduction in the number of insulin receptors on the target cells is observed in majority of Type 2 DM patients but 1/3 of the patients may not manifest loss of number of receptors; therefore, defective post-receptor signalling is considered as the main cause of IR. Main sites of IR are liver, adipose tissue and skeletal muscles. Apart from Type 2 DM, many other clinical and genetic syndromes are associated with IR.

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22

O’Doherty, R., D. Stein, and J. Foley. "Insulin resistance." Diabetologia 40, S3 (March 1997): B10—B15. http://dx.doi.org/10.1007/bf03168180.

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23

Perkins, Amanda. "Insulin resistance." Nursing Made Incredibly Easy! 22, no. 3 (April 10, 2024): 5–13. http://dx.doi.org/10.1097/nme.0000000000000046.

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Insulin resistance is believed to be a precursor to type 2 diabetes mellitus, metabolic syndrome, and nonalcoholic fatty liver disease. Through education, nurses can understand their role in helping patients manage this condition.

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24

Beale, Elmus G. "Insulin Signaling and Insulin Resistance." Journal of Investigative Medicine 61, no. 1 (January 1, 2013): 11–14. http://dx.doi.org/10.2310/jim.0b013e3182746f95.

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25

OʼHare, James A. "Insulin, insulin resistance, and hypertension." Current Opinion in Endocrinology and Diabetes 1, no. 1 (January 1994): 147–52. http://dx.doi.org/10.1097/00060793-199400010-00027.

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26

Stumvoll, Michael, and Hans Häring. "Insulin Resistance and Insulin Sensitizers." Hormone Research in Paediatrics 55, no. 2 (2001): 3–13. http://dx.doi.org/10.1159/000063466.

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27

HOWARD, BARBARA V. "Insulin, Insulin Resistance, and Dyslipidemia." Annals of the New York Academy of Sciences 683, no. 1 Dietary Lipid (June 1993): 1–8. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35687.x.

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28

Dr., R. Anil Kumar. "Comparison of insulin resistance scoring system with indirect methods of estimating insulin resistance in Indian type 2 diabetes subjects." International Journal of Medical Research and Review 7, no. 5 (October 31, 2019): 361–69. https://doi.org/10.17511/ijmrr.2019.i05.04.

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Background: Identification of insulin resistance is very important in management of type 2 diabetes. The euglycemic insulin clamp method, intravenous glucose tolerance tests (IVGTT) and minimal model approximation of glucose (MMAMG) are standard methods of measurement of insulin resistance in research. However, they are impractical in clinical practice and are difficult to perform in population-based research studies. So, a simple scoring system was designed to estimate the insulin resistance. Methods: 200 type 2 diabetes individuals who attended Karnataka Institute of endocrinology and research outpatient department. Fasting plasma glucose, post prandial plasma glucose, fasting insulin, lipid profile, BMI, waist circumference and BP of these subjects were checked. Results: Out of 200 type 2 diabetes subjects 69.5% were males and age group ranging from 26 to 85 years. Duration of diabetes range from 0 to 20 years and 53% of patients had hypertension and 46.5% have hypertriglyceridemia. Insulin resistance calculated by KIER scoring system, HOMA-1, QUICKI, HOMA2 and Fasting Insulin was present in 82%, 63%, 63.5%, 33.5% and 37.5% 0f individuals respectively. KIER scoring system had a statistically significant correlation with HOMA and QUICKY indices. (P value < 0.001) Conclusions: (1) KIER scoring system detects insulin resistance in 82% of type 2 diabetes individuals. (2) HOMA 1 and QUICKI are identical and similarly HOMA 2 and fasting insulin levels are almost identical in estimation of insulin resistance. (3) The KIER scoring system designed is very simple and economical. It takes into consideration the different factors which contribute to insulin resistance.

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29

Petersen, Max C., and Gerald I. Shulman. "Mechanisms of Insulin Action and Insulin Resistance." Physiological Reviews 98, no. 4 (October 1, 2018): 2133–223. http://dx.doi.org/10.1152/physrev.00063.2017.

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The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pathophysiological processes involved in T2D: insulin resistance. Understanding insulin resistance, in turn, requires knowledge of normal insulin action. In this review, both the physiology of insulin action and the pathophysiology of insulin resistance are described, focusing on three key insulin target tissues: skeletal muscle, liver, and white adipose tissue. We aim to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response. First, in section II, the effectors and effects of direct, cell-autonomous insulin action in muscle, liver, and white adipose tissue are reviewed, beginning at the insulin receptor and working downstream. Section III considers the critical and underappreciated role of tissue crosstalk in whole body insulin action, especially the essential interaction between adipose lipolysis and hepatic gluconeogenesis. The pathophysiology of insulin resistance is then described in section IV. Special attention is given to which signaling pathways and functions become insulin resistant in the setting of chronic overnutrition, and an alternative explanation for the phenomenon of ‟selective hepatic insulin resistanceˮ is presented. Sections V, VI, and VII critically examine the evidence for and against several putative mediators of insulin resistance. Section V reviews work linking the bioactive lipids diacylglycerol, ceramide, and acylcarnitine to insulin resistance; section VI considers the impact of nutrient stresses in the endoplasmic reticulum and mitochondria on insulin resistance; and section VII discusses non-cell autonomous factors proposed to induce insulin resistance, including inflammatory mediators, branched-chain amino acids, adipokines, and hepatokines. Finally, in section VIII, we propose an integrated model of insulin resistance that links these mediators to final common pathways of metabolite-driven gluconeogenesis and ectopic lipid accumulation.

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30

Chandra, Nimai Chand. "Hyperlipidimia, Hyperleptinemia and Insulin Resistance Intercorrelation with Obesity." Diabetes & Obesity International Journal 5, no. 1 (2020): 1–6. http://dx.doi.org/10.23880/doij-16000223.

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The present study has shown a parallel increase of triacylglycerol, cholesterol, and low density lipoprotein (LDL) along with an increase in body mass and BMI of human obese subjects. Conversely a fall in HDL concentration was observed. Plasma leptin level increased proportionately with increase of body weight as obesity advanced from obese to morbid type. A positive correlation was observed between leptin and insulin concentrations in obese subjects. A parallel increase of plasma glucose concentration was followed with decreased expression of insulin receptor, measured in adipose tissue, with the progress of obesity. The decreased insulin receptor concentration might be the reason for seen insulin resistance and increased insulin level which marked the positive correlation with associated liptin level in obese subjects.

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31

Zhang, Li, Tao Liu, Pei-Yong Zheng, and Guang Ji. "Leptin resistance and insulin resistance." World Chinese Journal of Digestology 17, no. 15 (2009): 1534. http://dx.doi.org/10.11569/wcjd.v17.i15.1534.

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32

Fahimeh, Kazemi Maryam Nourshahi. "Acute and delayed response of myostatin and insulin resistance to circuit resistance exercise." Sport Biosciences (HARAKAT) 4, no. 14 (January 21, 2013): 129–43. https://doi.org/10.5281/zenodo.3344749.

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<strong>ABSTRACT</strong> Recently, the role of myostatin (MSTN) in control of insulin resistance (IR( has been known. The purpose of this study was to determine of acute and delayed response of MSTN and IR to circuit resistance exercise. For this reason, 12 healthy men volunteered and participated in 2 sessions of the resistance exercise and control with one week apart from each others. After a session to be instructed on how to perform the resistance exercise and to be measured 1-RM, circuit resistance exercise program was performed including 7 movements, and at each movement, 3 sets of 15 repetitions with a load 55% of 1 repetition maximum (1RM). In each session, blood samples were collected before, immediately after, 1 hour after and 24 hour after the exercise for measuring plasma myostatin, glucose and insulin concentration and IR was calculated. Using 2×4 repeated measures analysis of variance (ANOVA), exercise time had no significant effect on plasma myostatin concentration, so that plasma myostatin concentration increased immediately after the exercise and 1 and 24 hour after the exercise decreased gradually. Exercise time had a significant effect on plasma glucose and insulin concentration and IR, nevertheless, plasma glucose and insulin concentration and IR increased immediately after the exercise and 1 and 24 hour after the exercise decreased gradually. Interaction of session and time had no significant effect on plasma myostatin and glucose concentration, but a significant effect on plasma insulin concentration and IR. In conclusion, circuit resistance exercise can’t have remarkable effects on acute and delayed response of MSTN and IR.

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33

MARKO, R. CINCOVIĆ, BELIĆ BRANISLAVA, ĐOKOVIĆ RADOJICA, TOHOLJ BOJAN, HRISTOVSKA TALIJA, DELIĆ BILJANA, and DOŠENOVIĆ MAJA. "INSULIN RESISTANCE IN COWS DURING DRY PERIOD AND EARLY LACTATION." Contemporary Agriculture (2014) 63, no. 1-2 (June 15, 2014): 98–105. https://doi.org/10.5281/zenodo.5913040.

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Insulin resistance is pathophisiological term defined as change in insulin responsiveness (insulin response to glucose) or insulin sensitivity (tissue response to insulin) or both. The aim of this study was to investigate insulin resistance in dairy cows during dry period and early lactation, and determine influence of insulin, glucose and NEFA to RQUICKI index of insulin resistance. Cows in early lactation showed lower concentration of glucose and insulin and higher concentration of NEFA compared to cows in dry period. Insulin:glucose index are 2.5 in dry period and 2.05 in early lactation. RQUICKI index was lower during early lactation. Determination of RQUICKI value using a concentration of glucose, insulin and NEFA was correct in 78.9% in dry period and 84.5% in early lactation. During dry period insulin and glucose showed significant influence to RQUICKI value (negative correlation), but there was found absence of NEFA influences. However, NEFA only showed significant influences to RQUICKI in early lactation (negative correlation). Insulin and glucose determined RQUICKI in 56% from 78.9% of whole model, but in early lactation NEFA determined 32% from 84.5%. Higher glucose concentration means higher insulin response in dry period with consequently poor insulin binding and glucose transport. In this condition it is need higher concentration of insulin to neutralize same concentration of glucose. Therefore, found higher insulin:glucose ration was found in dry period in relation to early lactation. Insulin resistance is more intense in early lactation compared to dry period. Based on metabolic change insulin resistance in dry period is consequence of decreased insulin sensitivity of peripheral tissue with compensatory increased insulin:glucose ration. During early lactation there is decrease insulin and glucose concentration with lower insulin response to glucose. Absence of insulin increases lipid mobilization which determined insulin resistance level.

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Limoncini, A., C. Smirne, F. Corliano, C. Marconi, E. Scaglia, G. Carnevale, P. Toniutto, C. Fabris, and M. Pirisi. "[725] INSULIN RESISTANCE, INSULIN SECRETION AND." Journal of Hepatology 46 (April 2007): S273. http://dx.doi.org/10.1016/s0168-8278(07)62323-x.

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35

MAGSINO, CESAR H., and JUDY SPENCER. "Insulin Receptor Antibodies and Insulin Resistance." Southern Medical Journal 92, no. 7 (July 1999): 717–19. http://dx.doi.org/10.1097/00007611-199907000-00013.

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36

Gallagher, Emily Jane, and Derek LeRoith. "Insulin, Insulin Resistance, Obesity, and Cancer." Current Diabetes Reports 10, no. 2 (March 6, 2010): 93–100. http://dx.doi.org/10.1007/s11892-010-0101-y.

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37

Sivitz, William I. "Understanding insulin resistance." Postgraduate Medicine 116, no. 1 (July 2004): 41–48. http://dx.doi.org/10.3810/pgm.2004.07.1550.

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38

SARUTA, TAKAO. "Insulin resistance syndrome." Nihon Naika Gakkai Zasshi 85, no. 2 (1996): 285–91. http://dx.doi.org/10.2169/naika.85.285.

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39

Bloomgarden, Z. T. "Insulin Resistance Concepts." Diabetes Care 30, no. 5 (April 27, 2007): 1320–26. http://dx.doi.org/10.2337/dc07-zb05.

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40

Fletcher, Barbara, and Cindy Lamendola. "Insulin Resistance Syndrome." Journal of Cardiovascular Nursing 19, no. 5 (September 2004): 339–45. http://dx.doi.org/10.1097/00005082-200409000-00009.

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41

Leslie, M. "Outfoxing Insulin Resistance." Science of Aging Knowledge Environment 2002, no. 36 (September 11, 2002): 125nw—125. http://dx.doi.org/10.1126/sageke.2002.36.nw125.

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42

Polonsky, William. "Psychological Insulin Resistance." Diabetes Educator 33, no. 7s (July 2007): 241S—244S. http://dx.doi.org/10.1177/0145721707305701.

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43

Montminy, Marc, and Seung-Hoi Koo. "Outfoxing insulin resistance?" Nature 432, no. 7020 (December 2004): 958–59. http://dx.doi.org/10.1038/432958a.

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44

Funnell, Martha Mitchell. "Understanding insulin resistance." Nursing 42, no. 3 (March 2012): 62. http://dx.doi.org/10.1097/01.nurse.0000411421.44527.bf.

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45

Cheng, Tsung O. "Insulin Resistance Syndrome." Southern Medical Journal 91, no. 7 (July 1998): 697. http://dx.doi.org/10.1097/00007611-199807000-00041.

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46

GRANBERRY, MARK C., and VIVIAN A. FONSECA. "Insulin Resistance Syndrome." Southern Medical Journal 92, no. 1 (January 1999): 2–14. http://dx.doi.org/10.1097/00007611-199901000-00002.

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47

Cummings, Doyle M., Sarah Henes, Kathryn M. Kolasa, John Olsson, and David Collier. "Insulin Resistance Status." Archives of Pediatrics & Adolescent Medicine 162, no. 8 (August 1, 2008): 764. http://dx.doi.org/10.1001/archpedi.162.8.764.

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48

DeFronzo, Ralph A. "Introduction: Insulin Resistance." Diabetes / Metabolism Reviews 5, no. 5 (August 1989): iii. http://dx.doi.org/10.1002/dmr.5610050505.

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Willette, Auriel A., Christine M. Burns та Barbara B. Bendlin. "Insulin Resistance andAPOEε4". JAMA Neurology 72, № 12 (1 грудня 2015): 1536. http://dx.doi.org/10.1001/jamaneurol.2015.3285.

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Jeffery, Alison. "Prepubertal insulin resistance." Practical Diabetes 29, no. 4 (May 2012): 130–31. http://dx.doi.org/10.1002/pdi.1676.

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