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1

Hatfield, Frederick C. Training & the glucose tolerance factor. Woodland Hills, CA: Weider Health & Fitness, 1990.

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2

Pasqualina, Santaguida, United States. Agency for Healthcare Research and Quality., and McMaster University. Evidence-based Practice Center., eds. Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose. [Rockville, Md: Agency for Healthcare Research and Quality, 2005.

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3

Perus̆ic̆ová, Jindra. Glucose tolerance and secretion of insulin in chronic pancreatitis. Praha: Univerzita Karlova, 1990.

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4

National Diabetes Information Clearinghouse (U.S.), ed. Diagnosis of diabetes. [Bethesda, Md.]: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Dept. of Health and Human Services, 2004.

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5

National Institutes of Health (U.S.), ed. From impaired glucose tolerance to diabetes: A two-step process. Bethesda, Md: National Institutes of Health, 1989.

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6

Nathan, David M. Beating diabetes: The first complete program clinically proven to dramatically improve your glucose tolerance. New York: McGraw-Hill, 2005.

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7

Hadden, Wilbur Crane. The prevalence of diagnosed diabetes, undiagnosed diabetes, and impaired glucose tolerance in adults 20-74 years of age, United States, 1976-80. Hyattsville, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Center for Health Statistics, 1987.

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8

Parker, Philip M., and James N. Parker. Glucose test: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

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9

Feuer, Joshua Paul. Assessment of acculturation and its associations with type 2 diabetes, impaired glucose tolerance and obesity in an isolated Canadian Aboriginal community. Ottawa: National Library of Canada, 2001.

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10

Mehling, Christine. Comparison of low glycemic index high carbohydrate, high glycemic index high carbohydrate and monounsaturated fat enriched diets on insulin sensitivity in the treatment of impaired glucose tolerance. Ottawa: National Library of Canada, 2000.

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11

United States. Congress. Senate. A bill to amend title XVIII of the Social Security Act to improve Medicare treatment and education for beneficiaries with diabetes by providing coverage of diabetes outpatient self-management training services and uniform coverage of blood-testing strips for individuals with diabetes. [Washington, D.C.?]: [United States Government Printing Office], 1997.

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12

missing], [name. Diabetes sourcebook: Basic consumer health information about type 1 diabetes (insulin-dependent or juvenile-onset diabetes), type 2 diabetes (noninsulin-dependent or adult-onset diabetes), gestational diabetes, impaired glucose tolerance (IGT) ... 3rd ed. Detroit, MI: Omnigraphics, 2003.

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13

Trumbach, Sabine. Glukose-Toleranz und Insulin-Sekretion unter simulierter Schwerelosigkeit. Koln: DFLVR, 1988.

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14

Engel, Anna Elizabeth. Capillary-muscle fiber morphometry in female diabetic and impaired glucose tolerant rats. Ottawa: National Library of Canada, 1998.

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15

D, Matthews Dawn, ed. Diabetes sourcebook: Basic consumer health information about Type 1 diabetes (insulin-dependent or juvenile-onset diabetes), Type 2 diabetes (noninsulin-dependent or adult-onset diabetes, gestational diabetes, impaired glucose tolerance (IGT), and related complications, such as amputation, eye disease, gum disease, nerve damage, and end-stage renal disease : including facts about insulin, oral diabetes medications, blood sugar testing, and the role of exercise and nutrition in the control of diabetes : along with a glossary and resources for further help and information. 3rd ed. Detroit, Mich: Omnigraphics, 2003.

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16

Chackrewarthy, Sureka, ed. Glucose Tolerance. InTech, 2012. http://dx.doi.org/10.5772/2916.

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17

Passwater, Richard. Glucose Tolerance Factor Chromium (Good Health Guides). Keats Pub Inc, 1986.

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18

The minimal model approach and determinants of glucose tolerance. Baton Rouge: Louisiana State University Press, 1997.

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19

Martinson, Kerry Elizabeth. Changes in plasma pyridoxal 5'-phosphate and red blood cell pyridoxal 5'-phosphate concentration during an oral glucose tolerance test in persons with diabetes mellitus. 1994.

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20

Wagner, Sandra. Impaired Glucose Tolerance and Insulin Resistance: Risk Factors, Management and Health Implications. Nova Science Publishers, Incorporated, 2015.

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21

Handbook Of Bedside Glucose Testing. American Association Clinical Chemistry, 1998.

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22

Publications, ICON Health. Glucose Tolerance Test - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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23

Impaired Glucose Tolerance and Cardiovascular Disease, An Issue of Endocrinology and Metabolism Clinics (The Clinics: Internal Medicine). Saunders, 2006.

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24

Hanley, Anthony James Gordon. Proinsulin and changes in glucose tolerance in a native Canadian community experiencing an epidemic of type 2 diabetes mellitus. 2000.

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25

Vashist, Sandeep Kumar, and John H. T. Luong. Point-Of-care Glucose Detection for Diabetic Monitoring and Management. Taylor & Francis Group, 2017.

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26

Vashist, Sandeep Kumar, and John H. T. Luong. Point-Of-care Glucose Detection for Diabetic Monitoring and Management. Taylor & Francis Group, 2017.

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27

Vashist, Sandeep Kumar, and John H. T. Luong. Point-Of-care Glucose Detection for Diabetic Monitoring and Management. Taylor & Francis Group, 2017.

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28

Point-Of-care Glucose Detection for Diabetic Monitoring and Management. Taylor & Francis Group, 2016.

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29

Vashist, Sandeep Kumar, and John Luong. Point-Of-care Glucose Detection for Diabetic Monitoring and Management. Taylor & Francis Group, 2020.

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30

Butler, Gary, and Jeremy Kirk. Endocrine investigations and laboratory reference ranges. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0101.

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General guidelines 330GH provocation tests 331Tests for GH secretion 332IGF-1 generation test 334Oral glucose tolerance test for investigating excess GH secretion 335TRH test 336LHRH/GnRH (gonadotropin-releasing hormone) stimulation test 337Triple pituitary stimulation test 338Water deprivation test (WDT) 340...
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31

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Macronutrients and fibre requirements during pregnancy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0004.

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In this chapter, the impact of varying intakes of protein, carbohydrate and lipids, which are the key nutrients that contribute to calorie intake, is examined. Fibre is also an important food component that needs to be considered. The maternal macronutrient profile can influence embryonic and fetal development. For instance, both low and excessively high protein intakes during pregnancy are associated with restricted growth, increased adiposity, and impaired glucose tolerance. High-fat maternal diets can significantly increase the susceptibility to diet-induced obesity and percentage total body fat in offspring, although types of fats need to be considered, as intake of polyunsaturated fatty acids is important for fetal development. The type and content of carbohydrate (high- vs low-glycaemic sources) in the maternal diet influences blood glucose concentration, which has a direct effect on fetal glucose levels and metabolism.
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32

Carter, R., and C. W. Imrie. Hepatobiliary surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198510567.003.0008.

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Introduction 306Investigational procedures 308Pancreatic mobilisation 310Management of tumours 312Management of pancreatic necrosis 316Management of pseudocyst 318Management of chronic pancreatitis 320Common pancreatic complications 322As the morbidity and mortality associated with pancreatic surgery are amongst the highest in surgical practice, management of patients should take place within the context of multi-disciplinary team and they should be in optimal condition pre-operatively. They may be suffering from exocrine failure, altered glucose tolerance, or altered coagulation due to post-hepatic biliary obstruction. All these issues should be addressed. Most surgical procedures will require blood to be cross-matched....
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33

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 50-Year-Old Woman with Burning Feet. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0020.

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Small-fiber neuropathy typically presents with burning pain or with widespread brief stabbing pains, by atypical presentations including asymmetric sensory symptoms are common. Nerve conduction studies are usually normal, as this disorder test only interrogates large fiber function; in small-fiber neuropathy the pathology is restricted to smaller unmyelinated fibers. Autonomic neuropathy can accompany the painful peripheral neuropathy but can be difficult to recognize since the symptoms can be protean. In this chapter, clinical characteristics of small-fiber and autonomic neuropathy are discussed. Various diagnostic modalities are described, including the benefits and pitfalls of available options. The most common conditions causing small-fiber and autonomic neuropathy are reviewed. The controversy surrounding impaired glucose tolerance as an etiological factor is dicusssed. We discuss the available medications and outline a rational approach to treatment.
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34

Servais, Aude. Nephropathic Cystinosis in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0060.

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Cystinosis is an autosomal recessive lysosomal storage disorder caused by a defect in the carrier-mediated system that normally transports cystine out of lysosomes. As a consequence, tissues accumulate variable amounts of the disulphide amino acid cystine. Three overlapping clinical phenotypes are recognized, varying in severity and age of onset. The most severe, the infantile nephropathic form (MIM 219800), appears in the first year of life. The late-onset form (MIM 219900) is also nephropathic, while ocular, non-nephropathic cystinosis manifests largely with corneal crystal deposition (MIM 219750). Infantile cystinosis is the most common form. Affected children develop renal proximal tubulopathy at 6 to 12 months of age. In the absence of treatment, renal failure occurs, with progression to end-stage renal disease (ESRD). Cystine crystal deposition in the cornea leads to photophobia and continuous widespread cystine accumulation eventually leads to rickets, retinal, endocrinological (hypothyroidism and impaired glucose tolerance), hepatic, gastrointestinal, muscular, and neurological abnormalities.
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35

Daudon, Michel, and Paul Jungers. Uric acid stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0202_update_001.

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Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°C, UA is in non-dissociated form, whose solubility is at best 100 mg/L, whereas urinary UA excretion normally exceeds 600 mg/day and may exceed 1g/day.Because UA solubility increases up to approximately 500 mg/L at urine pH > 6, urine alkalinization, with a target pH of 6.5–7, is the cornerstone of medical treatment. This most often allows dissolution of existing stones and prevention of recurrent stone formation so that urological intervention is infrequently needed. The preferred agent for alkalinization is potassium citrate (30–60 mEq/day in divided doses), because potassium urate is twice more soluble than sodium urate. However, in patients with poor gastric tolerance to potassium citrate or contraindication to potassium supplements, sodium bicarbonate is an acceptable alternative. Limitation of animal proteins, purine-rich foods (including beer), alcoholic drinks and acidified beverages (sodas) are useful measures, together with large fluid intake (> 2–2.5 L/day). Allopurinol may be indicated in cases of symptomatic hyperuricaemia. Regular observance of alkalinisation, with periodic controls of urine pH by the patient, is needed to prevent the rapid formation of UA stones. Patients affected by UANL, especially if overweight, should be evaluated for type 2 diabetes or glucose intolerance and managed accordingly.
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