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Hyperglycemia

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Not to be confused with the opposite disorder (involving low blood sugar), hypoglycemia.
Hyperglycemia
Other namesHigh blood sugar, hyperglycemia, hyperglycæmia
Artist's depiction of hyperglycemia. White hexagons in the image represent glucose molecules, which are increased in the lower image.
SpecialtyEndocrinology

Hyperglycemia or hyperglycaemia is the situation in which blood glucose level is higher than in a healthy subject. A fasting healthy human shows blood glucose level up to 5.6 mmol/L (100 mg/dL). After a meal (postprandial) containing carbohydrates, healthy subjects show postpandrial euglycemic peaks of less than 7.8 mmol/L (140 mg/dL).[1][2][3][4][5][6][7] Therefore, fasting hyperglycemia are values of blood glucose higher than 5.6 mmol/L (100 mg/dL) whereas postprandial hyperglycemia are values higher than 7.8 mmol/L (140 mg/dL).[2][3] Postprandial hyperglycemic levels as high as 8.6 mmol/L (155 mg/dL) at 1-h are associated with T2DM-related complications, which worsen as the degree of hyperglycemia increases.[8][9][10][11] Patients with diabetes are oriented to avoid exceeding the recommended postprandial threshold of 160 mg/dL (8.89 mmol/L) for optimal glycemic control.[12][11][13] Values of blood glucose higher than 160 mg/dL are classified as ‘very high’ hyperglycemia,[1] a condition in which an excessive amount of glucose (glucotoxicity) circulates in the blood plasma. These values are higher than the renal threshold of 10 mmol/L (180 mg/dL) up to which glucose reabsorption is preserved at physiological rates[8][14][15] and insulin therapy is not necessary.[16][17] Blood glucose values higher than the cutoff level of 11.1 mmol/L (200 mg/dL) are used to diagnose T2DM[18] and strongly associated with metabolic disturbances,[19] although symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent fasting blood glucose range between 5.6–7 mmol/L (~100–126 mg/dL) (American Diabetes Association guidelines) is considered slightly hyperglycemic, and above 7 mmol/L (126 mg/dL) is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

Signs and symptoms

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The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment.[20] Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms.[20] During this asymptomatic period, an abnormality in carbohydrate metabolism can occur, which can be tested by measuring plasma glucose.[20] Chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. Impairment of growth and susceptibility to certain infections can occur as a result of chronic hyperglycemia.[20]

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.[citation needed]

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:[21]

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response.[citation needed]

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis.[citation needed]

Signs and symptoms of diabetic ketoacidosis may include:[citation needed]

  • Ketoacidosis
  • Kussmaul hyperventilation (deep, rapid breathing)
  • Confusion or a decreased level of consciousness
  • Dehydration due to glycosuria and osmotic diuresis
  • Increased thirst
  • 'Fruity' smelling breath odor
  • Sweet sensation that is felt into the mouth without a reason
  • Nausea and vomiting
  • Abdominal pain
  • Impairment of cognitive function, along with increased sadness and anxiety[22][23]
  • Weight loss

Hyperglycemia causes a decrease in cognitive performance, specifically in processing speed, executive function, and performance.[24] Decreased cognitive performance may cause forgetfulness and concentration loss.[24]

Complications

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In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase.[25] The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.[citation needed]

Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth. Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure.[26]

Also, a life-threatening consequence of hyperglycemia can be nonketotic hyperosmolar syndrome.[20]

Perioperative hyperglycemia has been associated with immunosuppression, increased infections, osmotic diuresis, delayed wound healing, delayed gastric emptying, sympatho-adrenergic stimulation, and increased mortality. In addition, it reduces skin graft success, exacerbates brain, spinal cord, and renal damage by ischemia, worsens neurologic outcomes in traumatic head injuries, and is associated with postoperative cognitive dysfunction following CABG.[27]

Furthermore, hyperglycemia has been linked to increased susceptibility to a range of infectious diseases. This susceptibility can be attributed to the impairment of the immune system's response, which is often compromised in hyperglycemic conditions. Hyperglycemia also leads to biochemical changes in the body; both of these factors result in increased severity of respiratory infections and vulnerability to pathogens.[28] Hyperglycemic individuals face the most pronounced risk from such types of ailments, including tuberculosis, the flu, and COVID-19. These risks can be compounded even further by the effects of physiological stress.

Importantly, hyperglycemia affects the function of neutrophils, which are white blood cells responsible for responding to infection. In hyperglycemic individuals, the ability for neutrophils to move towards infection sites, ingest bacteria, and kill them are often impaired, leading to reduced effectiveness in combating infections.[29]

Hyperglycemia also creates microbiological changes within the body: hyperglycemia can lead to rapid changes in blood pH and cell viscosity, weakening the cells and making it more conducive for infectious agents to thrive and dampen inflammatory responses. This is because hyperglycemia impacts a few factors such as microenvironment of immune cells, or even bacteria’s supply of energy, adding on stress to the bacterial proliferation metabolism.[28]

The chronic inflammatory state induced by high glucose levels can also lead to dysfunction in various parts of the immune system. For example, advanced glycation end products (AGEs), which are more prevalent in hyperglycemic conditions, can interfere with the normal function of the immune system and contribute to the pathogenesis of infections.[30] AGEs, whose cross-links are permanent will continue to harm the surrounding tissue until the proteins are destroyed. In addition, they can interact with the RAGE receptor to cause oxidative stress, apoptosis, and inflammation.

Due to neutrophil changes, microbiological changes, and chronic inflammation, patients with hyperglycemia are thus more prone to severe respiratory infections. This increased risk is particularly pronounced with pathogens like Mycobacterium tuberculosis (the bacterium responsible for tuberculosis) and the flu.[31] In recent history, hyperglycemic individuals have also responded more severely to the symptoms of COVID-19. Another example is diabetes. Hyperglycemia and risk of severe infectious outcomes can even further be complicated by physiological stress. For instance, elevated blood glucose levels can actively contribute to pathophysiology of this disease, by exacerbating existing inflammation, impairing cellular immune responses, and increasing oxidative stress, which can also lead to more severe infection. In addition, patients with acute hyperglycemia who don’t have a history of diabetes can experience higher rates of mortality and complications.

Causes

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Hyperglycemia may be caused by: diabetes, various (non-diabetic) endocrine disorders (insulin resistance and thyroid, adrenal, pancreatic, and pituitary disorders), sepsis and certain infections, intracranial diseases (e.g. encephalitis, brain tumors (especially if near the pituitary gland), brain haemorrhages, and meningitis) (frequently overlooked), convulsions, end-stage terminal disease, prolonged/major surgeries,[32] stress,[33] and excessive eating of carbohydrates.[34]

Endocrine

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Chronic, persistent hyperglycaemia is most often a result of diabetes.[citation needed] Several hormones act to increase blood glucose levels and may thus cause hyperglycaemia when present in excess, including: cortisol, catecholamines, growth hormone, glucagon,[35] and thyroid hormones.[36] Hyperglycaemia may thus be seen in: Cushing's syndrome,[37] pheochromocytoma,[38] acromegaly,[39] hyperglucagonemia,[40] and hyperthyroidism.[36]

Diabetes mellitus

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Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus. In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.[citation needed]

In diabetes mellitus, hyperglycemia is usually caused by low insulin levels (diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (diabetes mellitus type 2), depending on the type and state of the disease.[41] Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20–30 minutes, and so glucose levels must be precisely maintained by the body's internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.[citation needed]

Ketoacidosis may be the first symptom of immune-mediated diabetes, particularly in children and adolescents. Also, patients with immune-mediated diabetes can change from modest fasting hyperglycemia to severe hyperglycemia and even ketoacidosis as a result of stress or an infection.[20]

Insulin resistance

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Obesity has been contributing to increased insulin resistance in the global population. Insulin resistance increases hyperglycemia because the body becomes over saturated by glucose. Insulin resistance desensitizes insulin receptors, preventing insulin from lowering blood sugar levels.[42]

The leading cause of hyperglycemia in type 2 diabetes is the failure of insulin to suppress glucose production by glycolysis and gluconeogenesis due to insulin resistance.[43] Insulin normally inhibits glycogenolysis, but fails to do so in a condition of insulin resistance, resulting in increased glucose production.[44] In the liver, Fox06 normally promotes gluconeogenesis in the fasted state, but insulin blocks Fox06 upon feeding.[45] In a condition of insulin resistance insulin fails to block Fox06, resulting in continued gluconeogenesis even upon feeding.[45]

Medications

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Certain medications increase the risk of hyperglycemia, including: corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, statins, niacin, pentamidine, protease inhibitors, L-asparaginase,[46] and antipsychotics.[47] The acute administration of stimulants such as amphetamines typically produces hyperglycemia; chronic use, however, produces hypoglycemia.[citation needed]

Thiazides are used to treat type 2 diabetes but it also causes severe hyperglycemia.[20]

Stress

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A high proportion of patients with an acute stress such as stroke or myocardial infarction may develop hyperglycemia, even in the absence of a diagnosis of diabetes. (Or perhaps stroke or myocardial infarction was caused by hyperglycemia and undiagnosed diabetes.)[citation needed] Human and animal studies suggest that this is not benign, and that stress-induced hyperglycemia is associated with a high risk of mortality after both stroke and myocardial infarction.[48] Somatostatinomas and aldosteronoma-induced hypokalemia can cause hyperglycemia but usually disappears after the removal of the tumour.[20]

Stress causes hyperglycaemia via several mechanisms, including through metabolic and hormonal changes, and via increased proinflammatory cytokines that interrupt carbohydrate metabolism, leading to excessive glucose production and reduced uptake in tissues, can cause hyperglycemia.[49]

Hormones such as the growth hormone, glucagon, cortisol and catecholamines, can cause hyperglycemia when they are present in the body in excess amounts.[20]

Diagnosis

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Monitoring

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It is critical for patients who monitor glucose levels at home to be aware of which units of measurement their glucose meter uses. Glucose levels are measured in either:[citation needed]

  1. Millimoles per liter (mmol/L) is the SI standard unit used in most countries around the world.
  2. Milligrams per deciliter (mg/dL) is used in some countries such as the United States, Japan, France, Egypt and Colombia.

Scientific journals are moving towards using mmol/L; some journals now use mmol/L as the primary unit but quote mg/dL in parentheses.[50]

Glucose levels vary before and after meals, and at various times of day; the definition of "normal" varies among medical professionals. In general, the normal range for most people (fasting adults) is about 4 to 6 mmol/L or 80 to 110 mg/dL. (where 4 mmol/L or 80 mg/dL is "optimal".) A subject with a consistent range above 7 mmol/L or 126 mg/dL is generally held to have hyperglycemia, whereas a consistent range below 4 mmol/L or 70 mg/dL is considered hypoglycemic. In fasting adults, blood plasma glucose should not exceed 7 mmol/L or 126 mg/dL. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply, leading to the complications of diabetes.[51]

Chronic hyperglycemia can be measured via the HbA1c test. The definition of acute hyperglycemia varies by study, with mmol/L levels from 8 to 15 (mg/dL levels from 144 to 270).[52]

Defects in insulin secretion, insulin action, or both, results in hyperglycemia.[20]

Chronic hyperglycemia can be measured by clinical urine tests which can detect sugar in the urine or microalbuminuria which could be a symptom of diabetes.[53]

Group aerobic exercises

Treatment

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Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases and may be lessened by the intake of some natural compounds. For example, a single dose of raw cinnamon before a meal containing complex carbohydrates decreases the postprandial hyperglycemia (higher than 140 mg/dL; >7.8 mmol/L) in patients with type II diabetes.[2] Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.[54]

Replacing white bread by whole wheat bread may help reduce hyperglycemia. Progressively removing bread and reducing carbohydrates may help even more.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc.[citation needed]

Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control.[55] Dipeptidyl peptidase-4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in hospital.[49]

Hyperglycemia can also be improved through minor lifestyle changes. Increasing aerobic exercise to at least 30 minutes a day causes the body to make better use of accumulated glucose since the glucose is being converted to energy by the muscles.[56] Calorie monitoring, with restriction as necessary, can reduce over-eating, which contributes to hyperglycemia.[57]

Diets higher in healthy unsaturated fats and whole wheat carbohydrates such as the Mediterranean diet can help reduce carbohydrate intake to better control hyperglycemia.[58] Diets such as intermittent fasting and ketogenic diet help reduce calorie consumption which could significantly reduce hyperglycemia.[citation needed]

Carbohydrates are the main cause for hyperglycemia. Non-whole-wheat items should be substituted by whole-wheat items. Although fruits can be nutritious, fruit intake should be limited due to high sugar content.[59]

Epidemiology

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Environmental factors

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Hyperglycemia is lower in higher income groups since there is access to better education, healthcare and resources. Low-middle income groups are more likely to develop hyperglycemia, due in part to a limited access to education and a reduced availability of healthy food options.[60] Living in warmer climates can reduce hyperglycemia due to increased physical activity while people are less active in colder climates.[61]

Population

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Hyperglycemia is one of the main symptoms of diabetes and it has substantially affected the population making it an epidemic due to the population's increased calorie consumption.[62] Healthcare providers are trying to work more closely with people allowing them more freedom with interventions that suit their lifestyle.[63] As physical inactivity and calorie consumption increases it makes individuals more susceptible to developing hyperglycemia.[64] Hyperglycemia is caused by type 1 diabetes and non-whites have a higher susceptibility for it.[65]

Etymology

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The origin of the term is Greek: prefix ὑπέρ- hyper- "over-", γλυκός glycos "sweet wine, must", αἷμα haima "blood", -ία, -εια -ia suffix for abstract nouns of feminine gender.[citation needed]

See also

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References

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  1. ^ a b Biradar, Rajeshwari A.; Singh, Dharmendra P.; Thakur, Harshad; Halli, Shiva S. (July 2020). "Gender differences in the risk factors for high and very high blood glucose levels: A study of Kerala". Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 14 (4): 627–636. doi:10.1016/j.dsx.2020.05.001. PMID 32422447.
  2. ^ a b c Moreira, Fernanda Duarte; Reis, Caio Eduardo Gonçalves; Gallassi, Andrea Donatti; Moreira, Daniel Carneiro; Welker, Alexis Fonseca (2024-10-09). Dardari, Dured (ed.). "Suppression of the postprandial hyperglycemia in patients with type 2 diabetes by a raw medicinal herb powder is weakened when consumed in ordinary hard gelatin capsules: A randomized crossover clinical trial". PLOS ONE. 19 (10): e0311501. doi:10.1371/journal.pone.0311501. ISSN 1932-6203. PMC 11463819. PMID 39383145.
  3. ^ a b Monnier, L.; Colette, C.; Owens, D. (March 2021). "Application of medium-term metrics for assessing glucose homoeostasis: Usefulness, strengths and weaknesses". Diabetes & Metabolism. 47 (2): 101173. doi:10.1016/j.diabet.2020.06.004. PMID 32561428.
  4. ^ Pazos-Couselo, Marcos; Portos-Regueiro, Cristina; González-Rodríguez, María; Manuel García-Lopez, Jose; Alonso-Sampredro, Manuela; Rodríguez-González, Raquel; Fernández-Merino, Carmen; Gude, Francisco (June 2022). "Aging of glucose profiles in an adult population without diabetes". Diabetes Research and Clinical Practice. 188: 109929. doi:10.1016/j.diabres.2022.109929. PMID 35580705.
  5. ^ American Diabetes Association Professional Practice Committee (2022-01-01). "2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2022". Diabetes Care. 45 (Supplement_1): S17–S38. doi:10.2337/dc22-S002. ISSN 0149-5992.
  6. ^ Nakayama, Yuto; Ono, Kumiko; Okagawa, Junya; Urabe, Junji; Yamau, Ryoga; Ishikawa, Akira (2022-04-01). "Home-Based High-Intensity Interval Exercise Improves the Postprandial Glucose Response in Young Adults with Postprandial Hyperglycemia". International Journal of Environmental Research and Public Health. 19 (7): 4227. doi:10.3390/ijerph19074227. ISSN 1660-4601. PMC 8998503. PMID 35409907.
  7. ^ Haschka, Stefanie J; Gar, Christina; Potzel, Anne L; Sacco, Vanessa; Kern-Matschilles, Stefanie; Benz, Irina; Then, Cornelia; Seissler, Jochen; Lechner, Andreas (2022-04-07). "A Normalized Real-Life Glucose Profile After Diet-Induced Remission of Type 2 Diabetes: A Pilot Trial". Cureus. 14 (4). doi:10.7759/cureus.23916. ISSN 2168-8184. PMC 9076033. PMID 35530849.
  8. ^ a b Bergman, Michael; Abdul-Ghani, Muhammad; DeFronzo, Ralph A.; Manco, Melania; Sesti, Giorgio; Fiorentino, Teresa Vanessa; Ceriello, Antonio; Rhee, Mary; Phillips, Lawrence S.; Chung, Stephanie; Cravalho, Celeste; Jagannathan, Ram; Monnier, Louis; Colette, Claude; Owens, David (July 2020). "Review of methods for detecting glycemic disorders". Diabetes Research and Clinical Practice. 165: 108233. doi:10.1016/j.diabres.2020.108233. PMC 7977482. PMID 32497744.
  9. ^ Bergman, Michael; Manco, Melania; Sesti, Giorgio; Dankner, Rachel; Pareek, Manan; Jagannathan, Ram; Chetrit, Angela; Abdul-Ghani, Muhammad; Buysschaert, Martin; Olsen, Michael H.; Nilsson, Peter M.; Medina, José Luis; Roth, Jesse; Groop, Leif; del Prato, Stefano (December 2018). "Petition to replace current OGTT criteria for diagnosing prediabetes with the 1-hour post-load plasma glucose ≥ 155 mg/dl (8.6 mmol/L)". Diabetes Research and Clinical Practice. 146: 18–33. doi:10.1016/j.diabres.2018.09.017. PMID 30273707.
  10. ^ Bergman, Michael (2021-09-07). "The 1-Hour Plasma Glucose: Common Link Across the Glycemic Spectrum". Frontiers in Endocrinology. 12. doi:10.3389/fendo.2021.752329. ISSN 1664-2392. PMC 8453142. PMID 34557166.
  11. ^ a b Chawla, Rajeev; Mukherjee, Jagat Jyoti; Chawla, Manoj; Kanungo, Alok; Shunmugavelu, Meenakshi Sundaram; Das, Ashok Kumar (2021-05-28). "Expert Group Recommendations on the Effective Use of Bolus Insulin in the Management of Type 2 Diabetes Mellitus". Medical Sciences. 9 (2): 38. doi:10.3390/medsci9020038. ISSN 2076-3271. PMC 8162981. PMID 34071359.
  12. ^ Brand-Miller, Jennie C; Stockmann, Karola; Atkinson, Fiona; Petocz, Peter; Denyer, Gareth (January 2009). "Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1000 foods". The American Journal of Clinical Nutrition. 89 (1): 97–105. doi:10.3945/ajcn.2008.26354. PMID 19056599.
  13. ^ Alyass, Akram; Almgren, Peter; Akerlund, Mikael; Dushoff, Jonathan; Isomaa, Bo; Nilsson, Peter; Tuomi, Tiinamaija; Lyssenko, Valeriya; Groop, Leif; Meyre, David (January 2015). "Modelling of OGTT curve identifies 1 h plasma glucose level as a strong predictor of incident type 2 diabetes: results from two prospective cohorts". Diabetologia. 58 (1): 87–97. doi:10.1007/s00125-014-3390-x. ISSN 0012-186X. PMID 25292440.
  14. ^ Cui, Shan-Shan; Duan, Li-Jun; Li, Jun-Feng; Qin, Yong-Zhang; Bao, Su-Qing; Jiang, Xia (November 2021). "The Factors Influencing the Renal Glucose Threshold in Patients with Newly Diagnosed Type 2 Diabetes Mellitus". Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 14: 4497–4503. doi:10.2147/DMSO.S336791. ISSN 1178-7007. PMC 8590450. PMID 34785919.
  15. ^ Hieshima, Kunio; Sugiyama, Seigo; Yoshida, Akira; Kurinami, Noboru; Suzuki, Tomoko; Ijima, Hiroko; Miyamoto, Fumio; Kajiwara, Keizo; Jinnouchi, Katsunori; Jinnouchi, Tomio; Jinnouchi, Hideaki (May 2020). "Elevation of the renal threshold for glucose is associated with insulin resistance and higher glycated hemoglobin levels". Journal of Diabetes Investigation. 11 (3): 617–625. doi:10.1111/jdi.13191. ISSN 2040-1116. PMC 7232275. PMID 31770476.
  16. ^ American Diabetes Association Professional Practice Committee (2022-01-01). "6. Glycemic Targets: Standards of Medical Care in Diabetes—2022". Diabetes Care. 45 (Supplement_1): S83–S96. doi:10.2337/dc22-S006. ISSN 0149-5992. PMID 34964868.
  17. ^ American Diabetes Association (2022-01-01). "Standards of Medical Care in Diabetes—2022 Abridged for Primary Care Providers". Clinical Diabetes. 40 (1): 10–38. doi:10.2337/cd22-as01. ISSN 0891-8929. PMC 8865785. PMID 35221470.
  18. ^ Gyberg, Viveca; De Bacquer, Dirk; Kotseva, Kornelia; De Backer, Guy; Schnell, Oliver; Tuomilehto, Jaakko; Wood, David; Rydén, Lars (December 2016). "Time-saving screening for diabetes in patients with coronary artery disease: a report from EUROASPIRE IV". BMJ Open. 6 (12): e013835. doi:10.1136/bmjopen-2016-013835. ISSN 2044-6055. PMC 5168687. PMID 27932342.
  19. ^ Selvin, Elizabeth; Rawlings, Andreea; Lutsey, Pamela; Maruthur, Nisa; Pankow, James S.; Steffes, Michael; Coresh, Josef (2016-01-01). "Association of 1,5-Anhydroglucitol With Cardiovascular Disease and Mortality". Diabetes. 65 (1): 201–208. doi:10.2337/db15-0607. ISSN 0012-1797. PMC 4686946. PMID 26395741.
  20. ^ a b c d e f g h i j American Diabetes Association (2014). "Diagnosis and Classification of Diabetes Mellitus". Diabetes Care. 37: S81–S90. doi:10.2337/dc14-s081. PMID 24357215.
  21. ^ James, Norman (30 March 2019). "Hyperglycemia Symptoms". EndocrineWeb. Retrieved 24 December 2022.
  22. ^ Pais I, Hallschmid M, Jauch-Chara K, et al. (2007). "Mood and cognitive functions during acute euglycaemia and mild hyperglycaemia in type 2 diabetic patients". Exp. Clin. Endocrinol. Diabetes. 115 (1): 42–46. doi:10.1055/s-2007-957348. PMID 17286234.
  23. ^ Sommerfield AJ, Deary IJ, Frier BM (2004). "Acute hyperglycemia alters mood state and impairs cognitive performance in people with type 2 diabetes". Diabetes Care. 27 (10): 2335–40. doi:10.2337/diacare.27.10.2335. PMID 15451897.
  24. ^ a b Geijselaers, Stefan L.C.; Sep, Simone J.S.; Claessens, Danny; Schram, Miranda T.; Van Boxtel, Martin P.J.; Henry, Ronald M.A.; Verhey, Frans R.J.; Kroon, Abraham A.; Dagnelie, Pieter C.; Schalkwijk, Casper G.; Van Der Kallen, Carla J.H.; Biessels, Geert Jan; Stehouwer, Coen D.A. (2017). "The Role of Hyperglycemia, Insulin Resistance, and Blood Pressure in Diabetes-Associated Differences in Cognitive Performance—The Maastricht Study". Diabetes Care. 40 (11): 1537–1547. doi:10.2337/dc17-0330. PMID 28842522.
  25. ^ Kraemer, Fredric B.; Shen, Wen-Jun (2002). "Hormone-sensitive lipase". Journal of Lipid Research. 43 (10): 1585–1594. doi:10.1194/jlr.R200009-JLR200. ISSN 0022-2275. PMID 12364542.
  26. ^ "Chronic hyperglycemia may lead to cardiac damage". Journal of the American College of Cardiology. 2012-02-03. Archived from the original on 2013-12-27. Retrieved 3 February 2012.
  27. ^ Miller, Miller's Anesthesia, 7th edition, pp. 1716, 2674, 2809.
  28. ^ a b Chávez-Reyes, Jesús; Escárcega-González, Carlos E.; Chavira-Suárez, Erika; León-Buitimea, Angel; Vázquez-León, Priscila; Morones-Ramírez, José R.; Villalón, Carlos M.; Quintanar-Stephano, Andrés; Marichal-Cancino, Bruno A. (2021). "Susceptibility for Some Infectious Diseases in Patients With Diabetes: The Key Role of Glycemia". Frontiers in Public Health. 9. doi:10.3389/fpubh.2021.559595. ISSN 2296-2565. PMC 7921169. PMID 33665182.
  29. ^ Ngo, Minh Dao; Bartlett, Stacey; Ronacher, Katharina (November 2021). "Diabetes-Associated Susceptibility to Tuberculosis: Contribution of Hyperglycemia vs. Dyslipidemia". Microorganisms. 9 (11): 2282. doi:10.3390/microorganisms9112282. ISSN 2076-2607. PMC 8620310. PMID 34835407.
  30. ^ CDC (2023-07-31). "Diabetes and Your Immune System". Centers for Disease Control and Prevention. Retrieved 2024-05-06.
  31. ^ Baccouch, Mahboub (2021-02-17), "A Brief Summary of the Finite Element Method for Differential Equations", Finite Element Methods and Their Applications, IntechOpen, ISBN 978-1-83962-342-4, retrieved 2024-05-06
  32. ^ Duncan AE (2012). "Hyperglycemia and Perioperative Glucose Management". Current Pharmaceutical Design. 18 (38): 6195–6203. doi:10.2174/138161212803832236. PMC 3641560. PMID 22762467.
  33. ^ "Hyperglycemia in diabetes-Hyperglycemia in diabetes - Symptoms & causes". Mayo Clinic. Retrieved 2024-04-06.
  34. ^ "Hyperglycemia: Symptoms, Causes, and Treatments". Yale Medicine. Retrieved 2024-04-06.
  35. ^ Umpierrez, Guillermo E.; Pasquel, Francisco J. (April 2017). "Management of Inpatient Hyperglycemia and Diabetes in Older Adults". Diabetes Care. 40 (4): 509–517. doi:10.2337/dc16-0989. ISSN 0149-5992. PMC 5864102. PMID 28325798.
  36. ^ a b Hage, Mirella; Zantout, Mira S.; Azar, Sami T. (2011-07-12). "Thyroid Disorders and Diabetes Mellitus". Journal of Thyroid Research. 2011: 439463. doi:10.4061/2011/439463. ISSN 2042-0072. PMC 3139205. PMID 21785689.
  37. ^ Scaroni, Carla; Zilio, Marialuisa; Foti, Michelangelo; Boscaro, Marco (2017-06-01). "Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management". Endocrine Reviews. 38 (3): 189–219. doi:10.1210/er.2016-1105. ISSN 0163-769X. PMID 28368467. S2CID 3985558.
  38. ^ Mubarik, Ateeq; Aeddula, Narothama R. (2020), "Chromaffin Cell Cancer", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 30570981, archived from the original on 2022-01-26, retrieved 2020-11-22
  39. ^ Oxford desk reference. Endocrinology. Turner, Helen E., 1967-, Eastell, R. (Richard), Grossman, Ashley (First ed.). Oxford. 2018. ISBN 978-0-19-967283-7. OCLC 1016052167. Archived from the original on 2022-01-26. Retrieved 2020-11-22.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link)
  40. ^ Wewer Albrechtsen, Nicolai J.; Kuhre, Rune E.; Pedersen, Jens; Knop, Filip K.; Holst, Jens J. (November 2016). "The biology of glucagon and the consequences of hyperglucagonemia". Biomarkers in Medicine. 10 (11): 1141–1151. doi:10.2217/bmm-2016-0090. ISSN 1752-0371. PMID 27611762.
  41. ^ "Hyperglycemia in diabetes". Mayo Clinic. Archived from the original on 26 January 2022. Retrieved 22 Sep 2020.
  42. ^ Kim, J. Y.; Bacha, F.; Tfayli, H.; Michaliszyn, S. F.; Yousuf, S.; Arslanian, S. (2019). "Adipose Tissue Insulin Resistance in Youth on the Spectrum From Normal Weight to Obese and From Normal Glucose Tolerance to Impaired Glucose Tolerance to Type 2 Diabetes". Diabetes Care. 42 (2): 265–272. doi:10.2337/dc18-1178. PMC 6341282. PMID 30455334.
  43. ^ Swe MT, Pongchaidecha A, Chatsudthipong V, Chattipakorn N, Lungkaphin A (2019). "Molecular signaling mechanisms of renal gluconeogenesis in nondiabetic and diabetic conditions". Journal of Cellular Physiology. 234 (6): 8134–8151. doi:10.1002/jcp.27598. PMID 30370538. S2CID 53097552.
  44. ^ Sargsyan A, Herman MA (2019). "Regulation of Glucose Production in the Pathogenesis of Type 2 Diabetes". Current Diabetes Reports. 19 (9): 77. doi:10.1007/s11892-019-1195-5. PMC 6834297. PMID 31377934.
  45. ^ a b Lee S, Dong HH (2017). "FoxO integration of insulin signaling with glucose and lipid metabolism". Journal of Endocrinology. 233 (2): R67–R79. doi:10.1530/JOE-17-0002. PMC 5480241. PMID 28213398.
  46. ^ Cetin M, Yetgin S, Kara A, et al. (1994). "Hyperglycemia, ketoacidosis and other complications of L-asparaginase in children with acute lymphoblastic leukemia". J Med. 25 (3–4): 219–29. PMID 7996065.
  47. ^ Luna B, Feinglos MN (2001). "Drug-induced hyperglycemia". JAMA. 286 (16): 1945–48. doi:10.1001/jama.286.16.1945. PMID 11667913.
  48. ^ Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC (2001). "Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview". Stroke. 32 (10): 2426–32. doi:10.1161/hs1001.096194. PMID 11588337.
  49. ^ a b Umpierrez, Guillermo E.; Pasquel, Francisco J. (2017). "Management of Inpatient Hyperglycemia and Diabetes in Older Adults". Diabetes Care. 40 (4): 509–517. doi:10.2337/dc16-0989. PMC 5864102. PMID 28325798.
  50. ^ "diabetes FAQ: general (part 1 of 5)Section - What are mg/dL and mmol/L? How to convert? Glucose? Cholesterol?". www.faqs.org. Archived from the original on 2018-08-28. Retrieved 2007-02-10.
  51. ^ Total Health Life (2005). "High Blood Sugar". Total Health Institute. Archived from the original on August 17, 2013. Retrieved May 4, 2011.
  52. ^ Giugliano D, Marfella R, Coppola L, et al. (1997). "Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia". Circulation. 95 (7): 1783–90. doi:10.1161/01.CIR.95.7.1783. PMID 9107164.
  53. ^ Florvall, Gösta; Basu, Samar; Helmersson, Johanna; Larsson, Anders (2006). "Hemocue Urine Albumin Point-Of-Care Test Shows Strong Agreement With the Results Obtained With a Large Nephelometer". Diabetes Care. 29 (2): 422–423. doi:10.2337/diacare.29.02.06.dc05-1080. PMID 16443900. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  54. ^ Ron Walls; John J. Ratey; Robert I. Simon (2009). Rosen's Emergency Medicine: Expert Consult Premium Edition – Enhanced Online Features and Print (Rosen's Emergency Medicine: Concepts & Clinical Practice (2v.)). St. Louis: Mosby. ISBN 978-0-323-05472-0.
  55. ^ Pearson, Ewan R.; Starkey, Bryan J.; Powell, Roy J.; Gribble, Fiona M.; Clark, Penny M.; Hattersley, Andrew T. (2003). "Genetic cause of hyperglycaemia and response to treatment in diabetes". The Lancet. 362 (9392): 1275–1281. doi:10.1016/s0140-6736(03)14571-0. PMID 14575972. S2CID 34914098.
  56. ^ Aronson, Ronnie; Brown, Ruth E; Li, Aihua; Riddell, Michael C (2019). "Optimal Insulin Correction Factor in Post–High-Intensity Exercise Hyperglycemia in Adults With Type 1 Diabetes: The FIT Study". Diabetes Care. 42 (1): 10–16. doi:10.2337/dc18-1475. PMID 30455336. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  57. ^ "High Blood sugar". Total health institute. 2005. Archived from the original on 2013-08-17.
  58. ^ Mattei, Josiemer; Bigornia, Sherman J; Sotos-Prieto, Mercedes; Scott, Tammy; Gao, Xiang; Tucker, Katherine L (2019). "The Mediterranean Diet and 2-Year Change in Cognitive Function by Status of Type 2 Diabetes and Glycemic Control". Diabetes Care. 42 (8): 1372–1379. doi:10.2337/dc19-0130. PMC 6647047. PMID 31123154.
  59. ^ "Dietary Guidelines 2015-2020". US Department of Health. 2015. Archived from the original on 2020-01-07. Retrieved 2019-12-06.
  60. ^ Ma, Ronald CW; Popkin, Barry M (2017). "Intergenerational diabetes and obesity—A cycle to break?". PLOS ONE. 14 (10): e1002415. doi:10.1371/journal.pmed.1002415. PMC 5663330. PMID 29088227.
  61. ^ Ishii, Hajime; Suzuki, Hodaka; Baba, Tsuneharu; Nakamura, Keiko; Watanabe, Tsuyoshi (2001). "Seasonal Variation of Glycemic Control in Type 2 Diabetic Patients". Diabetes Care. 24 (8): 1503. doi:10.2337/diacare.24.8.1503. PMID 11473100. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  62. ^ American Diabetes Association (2019). "Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2019" (PDF). Diabetes Care. 42 (Suppl 1): S13–S28. doi:10.2337/dc19-S002. PMID 30559228. S2CID 56176183. Archived from the original on 2022-01-26. Retrieved 2019-12-06.
  63. ^ Inzucchi, Silvio E; Bergenstal, Richard M; Buse, John B; Diamant, Michaela; Ferrannini, Ele; Nauck, Michael; Peters, Anne L; Tsapas, Apostolos; Wender, Richard; Matthews, David R (2012). "Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach". Diabetes Care. 35 (6): 1364–1370. doi:10.2337/dc12-0413. PMC 3357214. PMID 22517736.
  64. ^ Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet. 380 (9838): 219–229. doi:10.1016/S0140-6736(12)61031-9. PMC 3645500. PMID 22818936.
  65. ^ Gujral, U. P.; Narayan KMV (2019). "Diabetes in Normal-Weight Individuals: High Susceptibility in Nonwhite Populations". Diabetes Care. 42 (12): 2164–2166. doi:10.2337/dci19-0046. PMC 6868465. PMID 31748211.
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