Blood sugar level/ja

血糖値（赤）と糖低下ホルモン（青）の変動。 インスリン（青）。砂糖を多く含む食事とデンプンを多く含む食事の効果の1つが強調されている。

血糖値、血糖濃度、血中グルコース濃度、または血糖とは、血液中に濃縮されたグルコースの指標である。代謝恒常性の一部として、身体はしっかりと血糖値の調節を行っている。

70 kg（154 lb）のヒトの場合、常時約4gの溶解グルコース（「血中グルコース」とも呼ばれる）が血漿中に維持されている。血液中を循環していないグルコースは、骨格筋と肝臓細胞にグリコーゲンの形で貯蔵されている。絶食者では、ホメオスタシスを維持するために肝臓と骨格筋に貯蔵されているこれらのグリコーゲンから十分な量のグルコースを放出することで、血中グルコースを一定レベルに維持している。グルコースは、腸または肝臓から血流を介して体内の他の組織に輸送される。細胞内へのグルコースの取り込みは、主に膵臓で産生されるホルモンであるインスリンによって調節されている。細胞内に取り込まれたグルコースは、解糖の過程を経てエネルギー源として機能する。

ヒトでは、脳を含む多くの組織で正常な機能を維持するために、グルコースレベルが適切に維持されることが必要である。血中グルコースの持続的な上昇はグルコース毒性を引き起こし、細胞機能障害や糖尿病の合併症としてまとめられる病態の一因となる。

グルコース値は通常、朝、その日の最初の食事の前に最も低くなり、食後1～2時間後に数mmol上昇する。

異常な高血糖の持続は高血糖と呼ばれ、低レベルは低血糖と呼ばれる。糖尿病は、様々な原因による持続的な高血糖を特徴とし、血糖調節不全に関連する最も著名な疾患である。血糖値の検査や測定にはさまざまな方法がある。

アルコール飲酒は、血糖値を初期に急上昇させ、その後低下させる傾向がある。また、ある種の薬物はグルコースレベルを上昇させたり低下させたりする。

Units

There are two ways of measuring blood glucose levels: In the United Kingdom and Commonwealth countries (Australia, Canada, India, etc.) and ex-USSR countries molar concentration, measured in mmol/L (millimoles per litre, or millimolar, abbreviated mM). In the United States, Germany, Japan and many other countries mass concentration is measured in mg/dL (milligrams per decilitre).

グルコースC₆H₁₂O₆の分子量は180なので、2つの単位の差は18分の1であり、グルコース1 mmol/Lは18 mg/dLに相当する。

正常値の範囲

ヒト

正常値範囲は検査機関によって若干異なる場合がある。グルコースホメオスタシスが正常に働いている場合、血糖値は約4.4～6.1 mmol/L（79～110 mg/dL）の狭い範囲に回復する（空腹時血糖検査で測定）。

ヒトの空腹時血糖値の世界平均は約5.5 mmol/L（100 mg/dL）であるが、この値は一日を通して変動する。糖尿病でなく空腹時でない人の血糖値は、6.9 mmol/L（125 mg/dL）以下であるべきである。

非糖尿病患者の正常血糖値（空腹時検査）は3.9～5.6mmol/L（70～100mg/dL）である。

米国糖尿病学会によると、糖尿病患者の空腹時血糖値の目標範囲は、3.9～7.2mmol/L（70～130mg/dL）、食後2時間は10 mmol/L（180 mg/dL）未満とされている（血糖測定器による測定）。

Despite widely variable intervals between meals or the occasional consumption of meals with a substantial carbohydrate load, human blood glucose levels tend to remain within the normal range. However, shortly after eating, the blood glucose level may rise, in non-diabetics, temporarily up to 7.8 mmol/L (140 mg/dL) or slightly more.

The actual amount of glucose in the blood and body fluids is very small. In a healthy adult male of 75 kg (165 lb) with a blood volume of 5 L, a blood glucose level of 5.5 mmol/L (100 mg/dL) amounts to 5 g, equivalent to about a teaspoonful of sugar. Part of the reason why this amount is so small is that, to maintain an influx of glucose into cells, enzymes modify glucose by adding phosphate or other groups to it.

Other animals

In general, ranges of blood sugar in common domestic ruminants are lower than in many monogastric mammals. However this generalization does not extend to wild ruminants or camelids. For serum glucose in mg/dL, reference ranges of 42 to 75 for cows, 44 to 81 for sheep, and 48 to 76 for goats, but 61 to 124 for cats; 62 to 108 for dogs, 62 to 114 for horses, 66 to 116 for pigs, 75 to 155 for rabbits, and 90 to 140 for llamas have been reported. A 90 percent reference interval for serum glucose of 26 to 181 mg/dL has been reported for captured mountain goats (Oreamnos americanus), where no effects of the pursuit and capture on measured levels were evident. For beluga whales, the 25–75 percent range for serum glucose has been estimated to be 94 to 115 mg/dL. For the white rhinoceros, one study has indicated that the 95 percent range is 28 to 140 mg/dL. For harp seals, a serum glucose range of 4.9 to 12.1 mmol/L [i.e. 88 to 218 mg/dL] has been reported; for hooded seals, a range of 7.5 to 15.7 mmol/L [i.e. about 135 to 283 mg/dL] has been reported.

Regulation

Main article: Blood sugar regulation

The body's homeostatic mechanism keeps blood glucose levels within a narrow range. It is composed of several interacting systems, of which hormone regulation is the most important.

There are two types of mutually antagonistic metabolic hormones affecting blood glucose levels:

• catabolic hormones (such as glucagon, cortisol and catecholamines) which increase blood glucose;
• and one anabolic hormone (insulin), which decreases blood glucose.

These hormones are secreted from pancreatic islets (bundles of endocrine tissues), of which there are four types: alpha (A) cells, beta (B) cells, Delta (D) cells and F cells. Glucagon is secreted from alpha cells, while insulin is secreted by beta cells. Together they regulate the blood-glucose levels through negative feedback, a process where the end product of one reaction stimulates the beginning of another reaction. In blood-glucose levels, insulin lowers the concentration of glucose in the blood. The lower blood-glucose level (a product of the insulin secretion) triggers glucagon to be secreted, and repeats the cycle.

In order for blood glucose to be kept stable, modifications to insulin, glucagon, epinephrine and cortisol are made. Each of these hormones has a different responsibility to keep blood glucose regulated; when blood sugar is too high, insulin tells muscles to take up excess glucose for storage in the form of glycogen. Glucagon responds to too low of a blood glucose level; it informs the tissue to release some glucose from the glycogen stores. Epinephrine prepares the muscles and respiratory system for activity in the case of a "fight or flight" response. Lastly, cortisol supplies the body with fuel in times of heavy stress.

Abnormalities

See also: Dysglycemia

High blood sugar

Main article: Hyperglycemia

If blood sugar levels remain too high the body suppresses appetite over the short term. Long-term hyperglycemia causes many health problems including heart disease, cancer, eye, kidney, and nerve damage.

Blood sugar levels above 16.7 mmol/L (300 mg/dL) can cause fatal reactions. Ketones will be very high (a magnitude higher than when eating a very low carbohydrate diet) initiating ketoacidosis. The ADA (American Diabetes Association) recommends seeing a doctor if blood glucose reaches 13.3 mmol/L (240 mg/dL), The most common cause of hyperglycemia is diabetes. When diabetes is the cause, physicians typically recommend an anti-diabetic medication as treatment. From the perspective of the majority of patients, treatment with an old, well-understood diabetes drug such as metformin will be the safest, most effective, least expensive, and most comfortable route to managing the condition. Treatment will vary for the distinct forms of Diabetes and can differ from person to person based on how they are reacting to treatment. Diet changes and exercise implementation may also be part of a treatment plan for diabetes.

Some medications may cause a rise in blood sugars of diabetics, such as steroid medications, including cortisone, hydrocortisone, prednisolone, prednisone, and dexamethasone.

Low blood sugar

Main article: Hypoglycemia

When the blood sugar level is below 70 mg/dL, this is referred to as having low blood sugar. Low blood sugar is very frequent among type 1 diabetics. There are several causes of low blood sugar, including, taking an excessive amount of insulin, not consuming enough carbohydrates, drinking alcohol, spending time at a high elevation, puberty, and menstruation. If blood sugar levels drop too low, a potentially fatal condition called hypoglycemia develops. Symptoms may include lethargy, impaired mental functioning; irritability; shaking, twitching, weakness in arm and leg muscles; pale complexion; sweating; loss of consciousness.

Mechanisms that restore satisfactory blood glucose levels after extreme hypoglycemia (below 2.2 mmol/L or 40 mg/dL) must be quick and effective to prevent extremely serious consequences of insufficient glucose: confusion or unsteadiness and, in the extreme (below 0.8 mmol/L or 15 mg/dL) loss of consciousness and seizures. Without discounting the potentially quite serious conditions and risks due to or oftentimes accompanying hyperglycemia, especially in the long-term (diabetes or pre-diabetes, obesity or overweight, hyperlipidemia, hypertension, etc.), it is still generally more dangerous to have too little glucose – especially if levels are very low – in the blood than too much, at least temporarily, because glucose is so important for metabolism and nutrition and the proper functioning of the body's organs. This is especially the case for those organs that are metabolically active or that require a constant, regulated supply of blood sugar (the liver and brain are examples). Symptomatic hypoglycemia is most likely associated with diabetes and liver disease (especially overnight or postprandial), without treatment or with wrong treatment, possibly in combination with carbohydrate malabsorption, physical over-exertion or drugs. Many other less likely illnesses, like cancer, could also be a reason. Starvation, possibly due to eating disorders, like anorexia, will also eventually lead to hypoglycemia. Hypoglycemic episodes can vary greatly between persons and from time to time, both in severity and swiftness of onset. For severe cases, prompt medical assistance is essential, as damage to brain and other tissues and even death will result from sufficiently low blood-glucose levels.

Glucose measurement

Main articles: Blood glucose monitoring, Continuous glucose monitor, and Glucose meter

In the past to measure blood glucose it was necessary to take a blood sample, as explained below, but since 2015 it has also been possible to use a continuous glucose monitor, which involves an electrode placed under the skin. Both methods, as of 2023, cost hundreds of dollars or euros per year for supplies needed.

Sample source

Glucose testing in a fasting individual shows comparable levels of glucose in arterial, venous, and capillary blood. But following meals, capillary and arterial blood glucose levels can be significantly higher than venous levels. Although these differences vary widely, one study found that following the consumption of 50 grams of glucose, "the mean capillary blood glucose concentration is higher than the mean venous blood glucose concentration by 35%."

Sample type

Glucose is measured in whole blood, plasma or serum. Historically, blood glucose values were given in terms of whole blood, but most laboratories now measure and report plasma or serum glucose levels. Because red blood cells (erythrocytes) have a higher concentration of protein (e.g., hemoglobin) than serum, serum has a higher water content and consequently more dissolved glucose than does whole blood. To convert from whole-blood glucose, multiplication by 1.14 has been shown to generally give the serum/plasma level.

To prevent contamination of the sample with intravenous fluids, particular care should be given to drawing blood samples from the arm opposite the one in which an intravenous line is inserted. Alternatively, blood can be drawn from the same arm with an IV line after the IV has been turned off for at least 5 minutes, and the arm has been elevated to drain infused fluids away from the vein. Inattention can lead to large errors, since as little as 10% contamination with a 5% glucose solution (D5W) will elevate glucose in a sample by 500 mg/dL or more. The actual concentration of glucose in blood is very low, even in the hyperglycemic.

Measurement techniques

Two major methods have been used to measure glucose. The first, still in use in some places, is a chemical method exploiting the nonspecific reducing property of glucose in a reaction with an indicator substance that changes color when reduced. Since other blood compounds also have reducing properties (e.g., urea, which can be abnormally high in uremic patients), this technique can produce erroneous readings in some situations (5–15 mg/dL has been reported). The more recent technique, using enzymes specific to glucose, is less susceptible to this kind of error. The two most common employed enzymes are glucose oxidase and hexokinase. Average blood glucose concentrations can also be measured. This method measures the level of glycated hemoglobin, which is representative of the average blood glucose levels over the last, approximately, 120 days.

In either case, the chemical system is commonly contained on a test strip which is inserted into a meter, and then has a blood sample applied. Test-strip shapes and their exact chemical composition vary between meter systems and cannot be interchanged. Formerly, some test strips were read (after timing and wiping away the blood sample) by visual comparison against a color chart printed on the vial label. Strips of this type are still used for urine glucose readings, but for blood glucose levels they are obsolete. Their error rates were, in any case, much higher. Errors when using test strips were often caused by the age of the strip or exposure to high temperatures or humidity. More precise blood glucose measurements are performed in a medical laboratory, using hexokinase, glucose oxidase, or glucose dehydrogenase enzymes.

Urine glucose readings, however taken, are much less useful. In properly functioning kidneys, glucose does not appear in urine until the renal threshold for glucose has been exceeded. This is substantially above any normal glucose level, and is evidence of an existing severe hyperglycemic condition. However, as urine is stored in the bladder, any glucose in it might have been produced at any time since the last time the bladder was emptied. Since metabolic conditions change rapidly, as a result of any of several factors, this is delayed news and gives no warning of a developing condition. Blood glucose monitoring is far preferable, both clinically and for home monitoring by patients. Healthy urine glucose levels were first standardized and published in 1965 by Hans Renschler.

A noninvasive method of sampling to monitor glucose levels has emerged using an exhaled breath condensate. However this method does need highly sensitive glucose biosensors.

I. Chemical methods
A. Oxidation-reduction reaction
$$\begin{gathered} \mathrm{G}\mathrm{l}\mathrm{u}\mathrm{c}\mathrm{o}\mathrm{s}\mathrm{e}+\mathrm{A}\mathrm{l}\mathrm{k}\mathrm{a}\mathrm{l}\mathrm{i}\mathrm{n}\mathrm{e} \\ \mathrm{c}\mathrm{o}\mathrm{p}\mathrm{p}\mathrm{e}\mathrm{r} \\ \mathrm{t}\mathrm{a}\mathrm{r}\mathrm{t}\mathrm{a}\mathrm{r}\mathrm{a}\mathrm{t}\mathrm{e}\stackrel{\mathrm{R}\mathrm{e}\mathrm{d}\mathrm{u}\mathrm{c}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\to }\mathrm{C}\mathrm{u}\mathrm{p}\mathrm{r}\mathrm{o}\mathrm{u}\mathrm{s} \\ \mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{e} \end{gathered}$$
1. Alkaline copper reduction
Folin-Wu method	$$\begin{gathered} {\mathrm{C}\mathrm{u}}^{2+}+\mathrm{P}\mathrm{h}\mathrm{o}\mathrm{s}\mathrm{p}\mathrm{h}\mathrm{o}\mathrm{m}\mathrm{o}\mathrm{l}\mathrm{y}\mathrm{b}\mathrm{d}\mathrm{i}\mathrm{c} \\ \mathrm{a}\mathrm{c}\mathrm{i}\mathrm{d}\stackrel{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\to }\mathrm{P}\mathrm{h}\mathrm{o}\mathrm{s}\mathrm{p}\mathrm{h}\mathrm{o}\mathrm{m}\mathrm{o}\mathrm{l}\mathrm{y}\mathrm{b}\mathrm{d}\mathrm{e}\mathrm{n}\mathrm{u}\mathrm{m} \\ \mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{e} \end{gathered}$$	Blue end-product
Benedict's method	Modification of Folin–Wu method for qualitative urine glucose.
Nelson–Somogyi method	$$\begin{gathered} {\mathrm{C}\mathrm{u}}^{2+}+\mathrm{A}\mathrm{r}\mathrm{s}\mathrm{e}\mathrm{n}\mathrm{o}\mathrm{m}\mathrm{o}\mathrm{l}\mathrm{y}\mathrm{b}\mathrm{d}\mathrm{i}\mathrm{c} \\ \mathrm{a}\mathrm{c}\mathrm{i}\mathrm{d}\stackrel{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\to }\mathrm{A}\mathrm{r}\mathrm{s}\mathrm{e}\mathrm{n}\mathrm{o}\mathrm{m}\mathrm{o}\mathrm{l}\mathrm{y}\mathrm{b}\mathrm{d}\mathrm{e}\mathrm{n}\mathrm{u}\mathrm{m} \\ \mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{e} \end{gathered}$$	Blue end-product.
Neocuproine method	$$\begin{gathered} {\mathrm{C}\mathrm{u}}^{2+}+\mathrm{N}\mathrm{e}\mathrm{o}\mathrm{c}\mathrm{u}\mathrm{p}\mathrm{r}\mathrm{o}\mathrm{i}\mathrm{n}\mathrm{e}\stackrel{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\to }{\mathrm{C}\mathrm{u}}^{2+}\mathrm{n}\mathrm{e}\mathrm{o}\mathrm{c}\mathrm{u}\mathrm{p}\mathrm{r}\mathrm{o}\mathrm{i}\mathrm{n}\mathrm{e} \\ \mathrm{c}\mathrm{o}\mathrm{m}\mathrm{p}\mathrm{l}\mathrm{e}\mathrm{x} \end{gathered}$$*	Yellow-orange color neocuproine
Shaeffer–Hartmann–Somogyi	Uses the principle of iodine reaction with cuprous byproduct. Excess I2 is then titrated with thiosulfate.
2. Alkaline Ferricyanide reduction
Hagedorn–Jensen	$$\begin{gathered} \mathrm{G}\mathrm{l}\mathrm{u}\mathrm{c}\mathrm{o}\mathrm{s}\mathrm{e}+\mathrm{A}\mathrm{l}\mathrm{k}\mathrm{a}\mathrm{l}\mathrm{i}\mathrm{n}\mathrm{e} \\ \mathrm{f}\mathrm{e}\mathrm{r}\mathrm{r}\mathrm{i}\mathrm{c}\mathrm{y}\mathrm{a}\mathrm{n}\mathrm{i}\mathrm{d}\mathrm{e}⟶\mathrm{F}\mathrm{e}\mathrm{r}\mathrm{r}\mathrm{o}\mathrm{c}\mathrm{y}\mathrm{a}\mathrm{n}\mathrm{i}\mathrm{d}\mathrm{e} \end{gathered}$$	Colorless end product; other reducing substances interfere with reaction.
B. Condensation
Ortho-toluidine method	Uses aromatic amines and hot acetic acid. Forms glycosylamine and Schiff's base which is emerald green in color. This is the most specific method, but the reagent used is toxic.
Anthrone (phenols) method	Forms hydroxymethyl furfural in hot acetic acid
II. Enzymatic methods
A. Glucose oxidase
$$\begin{gathered} \mathrm{G}\mathrm{l}\mathrm{u}\mathrm{c}\mathrm{o}\mathrm{s}\mathrm{e}+{\mathrm{O}}_2\underset{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\overset{\mathrm{g}\mathrm{l}\mathrm{u}\mathrm{c}\mathrm{o}\mathrm{s}\mathrm{e} \\ \mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{s}\mathrm{e}}{\to }}\text{<mrow data-mjx-texclass="ORD">D<mo stretchy="false">−</mo>glucono<mo stretchy="false">−</mo><mn>1</mn><mo>,</mo><mn>5</mn><mo stretchy="false">−</mo>lactone</mrow>}+{\mathrm{H}}_{\mathrm{2}}{\mathrm{O}}_{\mathrm{2}} \end{gathered}$$
Saifer–Gerstenfeld method	$$\begin{gathered} {\mathrm{H}}_{\mathrm{2}}{\mathrm{O}}_{\mathrm{2}}+\text{O}\text{-dianisidine}\underset{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\overset{\mathrm{p}\mathrm{e}\mathrm{r}\mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{s}\mathrm{e}}{\to }}{\mathrm{H}}_{\mathrm{2}}\mathrm{O}+\mathrm{o}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{i}\mathrm{z}\mathrm{e}\mathrm{d} \\ \mathrm{c}\mathrm{h}\mathrm{r}\mathrm{o}\mathrm{m}\mathrm{o}\mathrm{g}\mathrm{e}\mathrm{n} \end{gathered}$$	Inhibited by reducing substances like BUA, bilirubin, glutathione, ascorbic acid.
Trinder method	Uses 4-aminophenazone oxidatively coupled with phenol. Subject to less interference by increases serum levels of creatinine, uric acid or hemoglobin. Inhibited by catalase.
Kodak Ektachem	A dry chemistry method. Uses spectrophotometry to measure the intensity of color through a lower transparent film.
Glucometer	Home monitoring blood glucose assay method. Uses a strip impregnated with a glucose oxidase reagent.
B. Hexokinase
$\begin{array}{rl}& \mathrm{G}\mathrm{l}\mathrm{u}\mathrm{c}\mathrm{o}\mathrm{s}\mathrm{e}+\mathrm{A}\mathrm{T}\mathrm{P}\underset{\mathrm{P}\mathrm{h}\mathrm{o}\mathrm{s}\mathrm{p}\mathrm{h}\mathrm{o}\mathrm{r}\mathrm{y}\mathrm{l}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\overset{\mathrm{H}\mathrm{e}\mathrm{x}\mathrm{o}\mathrm{k}\mathrm{i}\mathrm{n}\mathrm{a}\mathrm{s}\mathrm{e}+{\mathrm{M}\mathrm{g}}^{2+}}{\to }}{\text{<mrow data-mjx-texclass="ORD">G<mo stretchy="false">−</mo><mn>6</mn>PO</mrow>}}_4+\mathrm{A}\mathrm{D}\mathrm{P}\\ & {\text{<mrow data-mjx-texclass="ORD">G<mo stretchy="false">−</mo><mn>6</mn>PO</mrow>}}_4+\mathrm{N}\mathrm{A}\mathrm{D}\mathrm{P}\underset{\mathrm{O}\mathrm{x}\mathrm{i}\mathrm{d}\mathrm{a}\mathrm{t}\mathrm{i}\mathrm{o}\mathrm{n}}{\overset{\text{<mrow data-mjx-texclass="ORD">G<mo stretchy="false">−</mo><mn>6</mn>PD</mrow>}}{\to }}\text{<mrow data-mjx-texclass="ORD"><mn>6</mn><mo stretchy="false">−</mo>Phosphogluconate</mrow>}+\mathrm{N}\mathrm{A}\mathrm{D}\mathrm{P}\mathrm{H}+{\mathrm{H}}^{+}\\ \end{array}$
NADP as cofactor. NADPH (reduced product) is measured in 340 nm. More specific than glucose oxidase method due to G-6PO4, which inhibits interfering substances except when sample is hemolyzed.

Clinical correlation

The fasting blood glucose level, which is measured after a fast of 8 hours, is the most commonly used indication of overall glucose homeostasis, largely because disturbing events such as food intake are avoided. Conditions affecting glucose levels are shown in the table below. Abnormalities in these test results are due to problems in the multiple control mechanism of glucose regulation.

The metabolic response to a carbohydrate challenge is conveniently assessed by a postprandial glucose level drawn 2 hours after a meal or a glucose load. In addition, the glucose tolerance test, consisting of several timed measurements after a standardized amount of oral glucose intake, is used to aid in the diagnosis of diabetes.

Error rates for blood glucose measurements systems vary, depending on laboratories, and on the methods used. Colorimetry techniques can be biased by color changes in test strips (from airborne or finger-borne contamination, perhaps) or interference (e.g., tinting contaminants) with light source or the light sensor. Electrical techniques are less susceptible to these errors, though not to others. In home use, the most important issue is not accuracy, but trend. Thus if a meter / test strip system is consistently wrong by 10%, there will be little consequence, as long as changes (e.g., due to exercise or medication adjustments) are properly tracked. In the US, home use blood test meters must be approved by the federal Food and Drug Administration before they can be sold.

Finally, there are several influences on blood glucose level aside from food intake. Infection, for instance, tends to change blood glucose levels, as does stress either physical or psychological. Exercise, especially if prolonged or long after the most recent meal, will have an effect as well. In the typical person, maintenance of blood glucose at near constant levels will nevertheless be quite effective.

Causes of abnormal glucose levels

Persistent hyperglycemia	Transient hyperglycemia	Persistent hypoglycemia	Transient hypoglycemia
Reference range, fasting blood glucose (FBG): 70–110 mg/dL
Diabetes mellitus	Pheochromocytoma	Insulinoma	Acute alcohol intoxication or ingestion
Adrenal cortical hyperactivity Cushing's syndrome	Severe liver disease	Adrenal cortical insufficiency Addison's disease	Drugs: salicylates, antituberculosis agents
Hyperthyroidism	Acute stress reaction	Hypopituitarism	Severe liver disease
Acromegaly	Shock	Galactosemia	Several glycogen storage diseases
Obesity	Convulsions	Ectopic hormone production from tumors	Hereditary fructose intolerance

See also

• Blood glucose monitoring
• Glycemic index
• Saccharide recognition by boronic acids

References

Further reading

• Henry JB (2001). Clinical diagnosis and Management by Laboratory Methods (20th ed.). Philadelphia: Saunders. ISBN 978-0721688640.
• Levine R (1986). "Monosaccharides in health and disease". Annual Review of Nutrition. 6: 211–24. doi:10.1146/annurev.nu.06.070186.001235. PMID 3524617.
• Röder PV, Wu B, Liu Y, Han W (March 2016). "Pancreatic regulation of glucose homeostasis". Experimental & Molecular Medicine. 48 (3, March): e219. doi:10.1038/emm.2016.6. PMC 4892884. PMID 26964835.

External links

• Media related to Blood sugar level/ja at Wikimedia Commons
• Glucose (blood, serum, plasma): analyte monograph – The Association for Clinical Biochemistry and Laboratory Medicine