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1

Costa, ??ngels, Ignacio Conget, and Ramon Gomis. "Impaired Glucose Tolerance." Treatments in Endocrinology 1, no. 4 (2002): 205–10. http://dx.doi.org/10.2165/00024677-200201040-00001.

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2

Newman, Byron Y. "Impaired glucose tolerance." Optometry - Journal of the American Optometric Association 78, no. 12 (December 2007): 622–23. http://dx.doi.org/10.1016/j.optm.2007.11.001.

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3

Davies, M. J., and I. P. Gray. "Impaired glucose tolerance." BMJ 312, no. 7026 (February 3, 1996): 264–65. http://dx.doi.org/10.1136/bmj.312.7026.264.

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4

Yudkin, J. S., K. G. Alberti, D. G. McLarty, and A. B. Swai. "Impaired glucose tolerance." BMJ 301, no. 6749 (September 1, 1990): 397–402. http://dx.doi.org/10.1136/bmj.301.6749.397.

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5

Shen, Xiaoxia, Ping Zhang, Jinping Wang, Yali An, Edward W. Gregg, Bo Zhang, Hui Li, et al. "Influence of improvement or worsening of glucose tolerance on risk of stroke in persons with impaired glucose tolerance." International Journal of Stroke 13, no. 9 (June 29, 2018): 941–48. http://dx.doi.org/10.1177/1747493018784432.

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Background and aim We sought to determine the effect of regression to normal glucose tolerance (NGT) or progression to diabetes in early years of impaired glucose tolerance (IGT) on subsequent risk of stroke. Methods In 1986, 576 adults aged 25 years and older with impaired glucose tolerance in Da Qing, China, were randomly assigned by clinic to control, diet, exercise, or diet plus exercise intervention groups for a six-year period. Subsequently participants received medical care in their local clinics. We tracked participants for additional 17 years to ascertain stroke events and other outcomes. Results At the end of 6-year intervention trial follow-up, 272 (50.2%) had progressed to diabetes, 169 (31.2%) regressed to normal glucose tolerance, and 101 (18.6%) remained impaired glucose tolerance. During the subsequent 17-year follow-up, 173 (31.9%) developed a stroke, 26.7% of normal glucose tolerances, 30.7% of impaired glucose tolerances, and 36.1% of those with diabetes. After controlling for age, sex, baseline blood pressure, smoking, total cholesterol, previous cardiovascular disease and intervention group, those who developed diabetes in the first six years had a higher incidence of stroke than those who reverted to normal glucose tolerance (HR = 1.49, 95% CI 1.01–2.19, p = 0.04), whereas for those who remained impaired glucose tolerance compared to those who regressed to normal glucose tolerance the HR was 1.25 (95% CI 0.80–1.93; p = 0.30). A 1-mmol/L increase in both fasting and 2-h post-load plasma glucose from entry to end of the six-year trial was significantly associated with a higher risk of development of stroke in the subsequent 17 years, respectively (HR = 1.07, 95% CI 1.03–1.11, p < 0.0001 for fasting glucose, HR = 1.05, 95% CI 1.02–1.09, p = 0.007 for 2-h post-load plasma glucose). Conclusions Among Chinese adults with impaired glucose tolerance, early progression to diabetes predicted a higher risk of stroke, compared those who regressed to normal glucose tolerance.
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6

Berkus, M. D., E. M. J. Xenakis, and O. Langer. "Glucose tolerance test periodicity as a descriptor of glucose tolerance abnormality." International Journal of Gynecology & Obstetrics 40, no. 2 (February 1993): 187. http://dx.doi.org/10.1016/0020-7292(93)90423-t.

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7

Santos, Maria Luiza dos, Flávio F. Aragon, Carlos R. Padovani, and Walkyria P. Pimenta. "Daytime variations in glucose tolerance in people with impaired glucose tolerance." Diabetes Research and Clinical Practice 74, no. 3 (December 2006): 257–62. http://dx.doi.org/10.1016/j.diabres.2006.04.007.

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8

Diamond, Michael P., Subodhsingh Chauhan, Michael Kruger, and Marappa Subramanian. "Values of fasting glucose levels, glucose tolerance tests, and glucose-insulin ratios as predictors of glucose tolerance." Fertility and Sterility 80, no. 4 (October 2003): 1022–25. http://dx.doi.org/10.1016/s0015-0282(03)01016-1.

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9

Foley, J. E., P. Thuillez, S. Lillioja, J. Zawadzki, and C. Bogardus. "Insulin sensitivity in adipocytes from subjects with varying degrees of glucose tolerance." American Journal of Physiology-Endocrinology and Metabolism 251, no. 3 (September 1, 1986): E306—E310. http://dx.doi.org/10.1152/ajpendo.1986.251.3.e306.

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Previous studies showed that the sensitivity of glucose transport to insulin is lower in adipocytes isolated from subjects with noninsulin-dependent diabetes mellitus and impaired glucose tolerance compared with subjects with normal glucose tolerance. This study analyzed the relationship between insulin sensitivity of glucose transport and glycemia in a large group of nondiabetic-nonglucose-intolerant subjects with a wide range of glycemic response to oral glucose. Seventy-four Pima Indians with 2-h postglucose load glucoses between 77 and 197 mg/100 ml, fasting plasma glucoses between 76 and 108 mg/100 ml, and no postload glucoses less than 199 mg/100 ml were studied. Isolated adipocytes were prepared in vitro after an abdominal fat biopsy, ED50 of insulin for glucose transport was correlated with 2-h postload glucoses, but not between insulin binding per cell or per cell surface area or in ED50 of insulin for antilipolysis and 2-h postglucose load glucoses. Although only 17% of the variation in glucose tolerance could be explained by a change in the sensitivity of glucose transport to insulin, the data suggests that a postinsulin-binding defect in the coupling of insulin binding to glucose transport may be an early step in the development of insulin resistance in human adipocytes.
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10

Stout, Robert W. "Glucose Tolerance and Ageing." Journal of the Royal Society of Medicine 87, no. 10 (October 1994): 608–9. http://dx.doi.org/10.1177/014107689408701015.

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Hyperglycaemia, impaired glucose tolerance and non-insulin dependent diabetes become progressively more common with advancing age. The mechanism is insensitivity to the actions of insulin at the postreceptor level. Inadequate secretion of insulin and decreased hepatic sensitivity to insulin's action in suppressing glucose output also occur. The age-related changes may be made worse by obesity, renal failure or the ingestion of certain drugs, or may be lessened by increased physical activity.
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11

Zetterman, Teemu, Ritva Markkula, and Eija Kalso. "Glucose tolerance in fibromyalgia." Medicine 100, no. 46 (November 19, 2021): e27803. http://dx.doi.org/10.1097/md.0000000000027803.

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12

Eiks, M. L. "Oral Glucose Tolerance Tests." Diabetes Care 19, no. 3 (March 1, 1996): 271. http://dx.doi.org/10.2337/diacare.19.3.271a.

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13

Fraser, RobertB, FionaA Ford, Christine Bruce, J. David Fachnie, and FredW Whitehouse. "GLUCOSE TOLERANCE IN PREGNANCY." Lancet 333, no. 8629 (January 1989): 109–10. http://dx.doi.org/10.1016/s0140-6736(89)91474-8.

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14

Sutherland, H. W., D. W. M. Pearson, D. M. Campbell, and R. J. Jarrett. "GLUCOSE TOLERANCE IN PREGNANCY." Lancet 332, no. 8626-8627 (December 1988): 1482. http://dx.doi.org/10.1016/s0140-6736(88)90948-8.

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15

Greenspoon, Jeffrey S. "Oral Glucose Tolerance Test." Mayo Clinic Proceedings 63, no. 8 (August 1988): 838. http://dx.doi.org/10.1016/s0025-6196(12)62371-4.

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16

Taylor, Roy. "DRUGS AND GLUCOSE TOLERANCE." Adverse Drug Reaction Bulletin 121, no. 1 (December 1986): 452–55. http://dx.doi.org/10.1097/00012995-198612000-00001.

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17

Hurel, Steven J., and Roy Taylor. "Drugs and glucose tolerance." Adverse Drug Reaction Bulletin 174, no. 1 (October 1995): 659–62. http://dx.doi.org/10.1097/00012995-199510000-00001.

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18

DYCKNER, THOMAS, and PER-OLOV WESTER. "Peroral Glucose Tolerance Test." Acta Medica Scandinavica 220, no. 4 (April 24, 2009): 315–19. http://dx.doi.org/10.1111/j.0954-6820.1986.tb02771.x.

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19

Voelker, R. "Famine and Glucose Tolerance." JAMA: The Journal of the American Medical Association 279, no. 6 (February 11, 1998): 420—b—420. http://dx.doi.org/10.1001/jama.279.6.420-b.

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20

Voelker, Rebecca. "Famine and Glucose Tolerance." JAMA 279, no. 6 (February 11, 1998): 420. http://dx.doi.org/10.1001/jama.279.6.420-jwm81008-3-1.

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21

Giugliano, D. "Height and glucose tolerance." Diabetologia 35, no. 7 (July 1992): 698–99. http://dx.doi.org/10.1007/bf00400266.

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22

Williams, D. R. R., and R. J. Jarrett. "Height and glucose tolerance." Diabetologia 35, no. 2 (February 1992): 191–92. http://dx.doi.org/10.1007/bf00402557.

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23

Haffner, S. M., A. Agil, L. Mykkanen, M. P. Stern, and I. Jialal. "Plasma Oxidizability in Subjects With Normal Glucose Tolerance, Impaired Glucose Tolerance, and NIDDM." Diabetes Care 18, no. 5 (May 1, 1995): 646–53. http://dx.doi.org/10.2337/diacare.18.5.646.

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24

Hung, Yi-Jen, Chang-Hsun Hsieh, Dee Pei, Shi-Wen Kuo, Jiunn-Tay Lee, Ling-Yi Wu, Chih-Tsueng He, Chien Hsing Lee, Sandra Chyi Fan, and Wayne Huey-Herng Sheu. "Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose tolerance." Clinical Endocrinology 62, no. 1 (January 2005): 85–91. http://dx.doi.org/10.1111/j.1365-2265.2004.02178.x.

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25

Cockram, C. S. "Fasting glucose and progression of impaired glucose tolerance." Diabetes Care 22, no. 2 (February 1, 1999): 369–70. http://dx.doi.org/10.2337/diacare.22.2.369.

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26

Henriksen, J. E., F. Alford, A. Handberg, A. Vaag, and H. Beck-Nielsen. "Glucose processing during the intravenous glucose tolerance test." Metabolism 45, no. 5 (May 1996): 598–605. http://dx.doi.org/10.1016/s0026-0495(96)90030-x.

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27

Wu, Tongzhi, Christopher K. Rayner, Karen L. Jones, Cong Xie, Chinmay Marathe, and Michael Horowitz. "Role of intestinal glucose absorption in glucose tolerance." Current Opinion in Pharmacology 55 (December 2020): 116–24. http://dx.doi.org/10.1016/j.coph.2020.10.017.

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28

Buch, Inge, Peter J. Hornnes, and Claus Kühl. "Glucose tolerance in early pregnancy." Acta Endocrinologica 112, no. 2 (June 1986): 263–66. http://dx.doi.org/10.1530/acta.0.1120263.

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Abstract. The effect of pregnancy on oral glucose tolerance (50 g of glucose) and plasma insulin and glucagon responses to oral glucose was studied in weeks 10 and 32 of pregnancy and again 1 year post partum in 12 normal women. Already in week 10, fasting plasma glucose was decreased and the glucose-induced insulin secretion increased as compared with post partum. However, glucose tolerance was not affected at this time. In week 32, glucose tolerance had deteriorated, although the levels of both fasting and glucose-induced insulin were higher than those found in early pregnancy and post partum. At all investigations fasting plasma glucagon and the suppression of plasma glucagon after oral glucose were similar, indicating that glucagon is not implicated in the changes in glucose homeostasis seen in pregnancy. It is concluded that glucose tolerance is unaltered by pregnancy in week 10. Pregnancy has, however, at this very early stage already affected glucose homeostasis as seen by the decrease in fasting plasma glucose and the increase in the insulin response to glucose.
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29

Lages, Marlene, Renata Barros, Pedro Moreira, and Maria P. Guarino. "Metabolic Effects of an Oral Glucose Tolerance Test Compared to the Mixed Meal Tolerance Tests: A Narrative Review." Nutrients 14, no. 10 (May 12, 2022): 2032. http://dx.doi.org/10.3390/nu14102032.

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The oral glucose tolerance test (OGTT) is recommended for assessing abnormalities in glucose homeostasis. Recognised as the gold standard test for diagnosing diabetes, the OGTT provides useful information about glucose tolerance. However, it does not replicate the process of absorption and digestion of complex foods, such as that which occurs with a mixed meal tolerance test (MMTT), an alternative that is still not well explored in the diagnosis of metabolic alterations. The MMTT could be an asset in detecting glucose homeostasis disorders, including diabetes since it has more similarities to the common dietary pattern, allowing early detection of subtle changes in metabolic homeostasis in response to combined nutrients. This alternative has the advantage of being more tolerable and pleasant to patients since it induces a more gradual increase in blood glucose, thus reducing the risk of rebound hypoglycemia and other related complications. The present article reviewed the clinical data available regarding the possibility of screening or diagnosing altered glucose homeostasis, including type 2 diabetes mellitus, with the MMTT.
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30

&NA;. "Protease inhibitors impair glucose tolerance." Reactions Weekly &NA;, no. 738 (February 1999): 5. http://dx.doi.org/10.2165/00128415-199907380-00007.

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31

&NA;. "Protease inhibitors impair glucose tolerance." Inpharma Weekly &NA;, no. 1174 (February 1999): 21. http://dx.doi.org/10.2165/00128413-199911740-00042.

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32

Kidd, G. S., G. E. Graff, B. F. Davies, M. T. McDermott, J. L. Aeling, and F. D. Hofeldt. "Glucose Tolerance in Granuloma Annulare." Diabetes Care 8, no. 4 (July 1, 1985): 380–84. http://dx.doi.org/10.2337/diacare.8.4.380.

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33

Mobin, Ahsan, Imtiaz Manzoor, Jawahar Lal, and Jawahar Kumar. "HYPERTENSIVE PATIENTS; IMPAIRED GLUCOSE TOLERANCE." Professional Medical Journal 24, no. 10 (October 1, 2017): 1480–83. http://dx.doi.org/10.17957/tpmj/17.4077.

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34

Machtey, I. "Tendinitis and Abnormal Glucose Tolerance." Scandinavian Journal of Rheumatology 15, no. 2 (January 1986): 224. http://dx.doi.org/10.3109/03009748609102093.

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35

Reaven, P. D., E. L. Barrett-Connor, and D. K. Browner. "Abnormal Glucose Tolerance and Hypertension." Diabetes Care 13, no. 2 (February 1, 1990): 119–25. http://dx.doi.org/10.2337/diacare.13.2.119.

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36

Laposata, Michael, Donna H. MacMillan, and Jirina Vasek. "Reflex Testing; Glucose Tolerance Testing." Laboratory Medicine 29, no. 10 (October 1, 1998): 595–97. http://dx.doi.org/10.1093/labmed/29.10.595.

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37

Marre, M., C. Gauville, and Ph Passa. "Calcium Antagonists and Glucose Tolerance." Journal of Hypertension 3, no. 5 (October 1985): 540. http://dx.doi.org/10.1097/00004872-198510000-00035.

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38

&NA;. "CS-045 improves glucose tolerance." Inpharma Weekly &NA;, no. 815 (November 1991): 8. http://dx.doi.org/10.2165/00128413-199108150-00022.

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39

Prasad, M. C., and P. L. Kaul. "Glucose Tolerance Test in Goats." Zentralblatt für Veterinärmedizin Reihe A 28, no. 9-10 (May 13, 2010): 732–36. http://dx.doi.org/10.1111/j.1439-0442.1981.tb01244.x.

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40

Suntsov, Yu I., and S. V. Kudryakova. "Epidemiology of impaired glucose tolerance." Problems of Endocrinology 45, no. 2 (April 4, 1999): 48–52. http://dx.doi.org/10.14341/probl11750.

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In 1980, the WHO Expert Committee on Diabetes Mellitus (DM) proposed a new classification of diabetes. In it, impaired glucose tolerance (NTG) was identified as an independent clinical class. This was due to the following: diabetes, primarily non-insulin-dependent (NIDDM), as a rule, develops gradually, and several stages can be distinguished in its development [35, 55]. The first of them, according to many experts, is NTG.
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41

Ake-Uzoigwe, Rukeme, Anubha Arora, Dongping Zhang, Carolyn Salafia, Kolawole Akinnawonu, and Aleksandr Fuks. "Postpartum Oral Glucose Tolerance Test." Obstetrics & Gynecology 129 (May 2017): 40S—41S. http://dx.doi.org/10.1097/01.aog.0000514347.83223.e8.

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42

Barnett, Anthony H. "Glucose tolerance testing for all?" International Journal of Clinical Practice 61, no. 4 (March 22, 2007): 541–43. http://dx.doi.org/10.1111/j.1742-1241.2007.01307.x.

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43

Hubbard, Kathryn, Jean-Marc Pavard, and Roy Forster. "Glucose tolerance testing in primates." Toxicology Letters 88 (October 1996): 93. http://dx.doi.org/10.1016/s0378-4274(96)80336-5.

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44

Pozzilli, P. "Osteocalcin, glucose tolerance and diabetes." Annales d'Endocrinologie 76, no. 4 (September 2015): 302. http://dx.doi.org/10.1016/j.ando.2015.07.042.

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45

FERRI, C. "Glucose tolerance and non-modulation." American Journal of Hypertension 8, no. 4 (April 1995): 57A. http://dx.doi.org/10.1016/0895-7061(95)97574-b.

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46

Leong, Ivone. "Follistatin inactivation improves glucose tolerance." Nature Reviews Endocrinology 14, no. 8 (June 26, 2018): 439. http://dx.doi.org/10.1038/s41574-018-0052-y.

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47

MARSHALL, JULIE A., and RICHARD F. HAMMAN. "Dietary Lipids and Glucose Tolerance." Annals of the New York Academy of Sciences 683, no. 1 Dietary Lipid (June 1993): 46–56. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35691.x.

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48

Smith, A. Gordon, and J. Robinson Singleton. "Impaired Glucose Tolerance and Neuropathy." Neurologist 14, no. 1 (January 2008): 23–29. http://dx.doi.org/10.1097/nrl.0b013e31815a3956.

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49

Krentz, Andrew J., Penelope M. Clark, Lorna Cox, and Malcolm Nattrass. "Hyperproinsulinaemia in Impaired Glucose Tolerance." Clinical Science 85, no. 1 (July 1, 1993): 97–100. http://dx.doi.org/10.1042/cs0850097.

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1. Basal circulating concentrations of islet B cell products were measured using two-site monoclonal antibody-based immunoradiometric assays after a 10 h overnight fast in a group of non-obese subjects with recently diagnosed impaired glucose tolerance (World Health Organization criteria). A group of healthy subjects with normal oral glucose tolerance matched for age and body mass index served as normal controls. 2. Fasting blood glucose concentration was normal in all subjects with mean (±SEM) levels of 5.1 ± 0.2 and 4.8 ± 0.2 mmol/l (P >0.1) for the group with impaired glucose tolerance and the healthy control group, respectively. 3. There was no significant difference (P >0.1) in fasting plasma insulin or C-peptide concentrations between the groups. 4. By contrast, the fasting concentration of intact proinsulin was nearly four-fold higher in the subjects with impaired glucose tolerance than in the matched healthy control subjects (4.5 ± 1.0 versus 1.2 ± 0.2 pmol/l, P <0.005). 5. Similarly, the fasting plasma concentration of 32–33 split proinsulin in the subjects with impaired glucose tolerance was almost twice that of the control subjects (7.4 ± 1.3 versus 3.9 ± 0.8 pmol/l, P <0.02). 6. In conclusion, fasting concentrations of proinsulin-like molecules are elevated in non-obese subjects with newly diagnosed impaired glucose tolerance. This observation is consistent with defective islet B cell proinsulin processing in this syndrome.
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50

Saliani, Negar, Soheila Montazersaheb, and Shideh Montasser Kouhsari. "Micromanaging Glucose Tolerance and Diabetes." Advanced Pharmaceutical Bulletin 7, no. 4 (December 31, 2017): 547–56. http://dx.doi.org/10.15171/apb.2017.066.

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