Blood sugar level

concentration of glucose present in the lineage ( Glycaemia )

[1] The variation of blood sugar ( crimson ) and the sugar-lowering hormone insulin ( gloomy ) in humans during the run of a day with three meal. One of the effects of a sugar -rich vs a starch -rich meal is highlighted. The glycaemia, besides known as blood sugar level, blood sugar concentration, or blood glucose level is the measure of glucose concentrated in the rake of humans or other animals. approximately 4 grams of glucose, a simpleton sugar, is present in the blood of a 70 kilogram ( 154 pound ) homo at all times. [ 2 ] The body tightly regulates rake glucose levels as a region of metabolic homeostasis. [ 2 ] Glucose is stored in bony muscle and liver cells in the form of glycogen ; [ 2 ] in fasting individuals, rake glucose is maintained at a constant floor at the expense of glycogen stores in the liver-colored and skeletal muscle. [ 2 ]

In humans, a blood glucose floor of 4 grams, or about a teaspoon, is critical for normal function in a number of tissues, and the human brain consumes approximately 60 % of blood glucose in fast, sedentary individuals. [ 2 ] A haunting elevation in blood glucose leads to glucose perniciousness, which contributes to cell dysfunction and the pathology grouped in concert as complications of diabetes. [ 2 ] Glucose can be transported from the intestines or liver to early tissues in the body via the bloodstream. [ 2 ] Cellular glucose consumption is primarily regulated by insulin, a hormone produced in the pancreas. [ 2 ] Glucose levels are normally lowest in the morning, before the beginning meal of the day, and ascend after meals for an hour or two by a few millimoles. Blood sugar levels outside the normal range may be an indicator of a medical discipline. A persistently high flush is referred to as hyperglycemia ; abject levels are referred to as hypoglycemia. Diabetes mellitus is characterized by persistent hyperglycemia from any of respective causes, and it is the most big disease related to the failure of rake sugar regulation. There are different methods of testing and measuring lineage boodle levels. The intake of alcohol causes an initial tide in blood carbohydrate and later tends to cause levels to fall. besides, certain drugs can increase or decrease glucose levels. [ 3 ]

Units [edit ]

The external standard direction of measuring blood glucose levels is in terms of a molar concentration, measured in mmol /L ( millimoles per liter, or millimolar, abbreviated millimeter ). In the United States, Germany, and other countries mass concentration is measured in mg/dL ( milligrams per deciliter ). [ 4 ] Since the molecular weight of glucose C6H12O6 is 180, the difference between the two units is a agent of 18, therefore 1 mmol/L of glucose is equivalent to 18 mg/dL. [ 5 ]

Normal value range [edit ]

Humans [edit ]

Normal value ranges may vary slightly between laboratories. many factors affect a person ‘s blood sugar level. The body ‘s homeostatic mechanism of rake boodle regulation ( known as glucose homeostasis ), when operating normally, restores the lineage sugar charge to a minute scope of about 4.4 to 6.1 mmol /L ( 79 to 110 mg/dL ) ( as measured by a fast blood glucose test ). [ 6 ] normal blood glucose level ( tested while fasting ) for non-diabetics is between 3.9 and 7.1 mmol/L ( 70 and 130 mg/dL ). The global average fasting plasma blood glucose level in humans is about 5.5 mmol/L ( 100 mg/dL ) ; [ 7 ] [ 5 ] however, this flush fluctuates throughout the day. Blood carbohydrate levels for those without diabetes and who are not fasting should be below 6.9 mmol/L ( 125 mg/dL ). [ 8 ] The blood glucose target rate for diabetics, according to the American Diabetes Association, should be 5.0–7.2 mmol/l ( 90–130 mg/dL ) before meals and less than 10 mmol/L ( 180 mg/dL ) two hours after meals ( as measured by a blood glucose monitor ). [ 9 ] [ 10 ] Despite widely variable intervals between meals or the periodic consumption of meals with a substantial carbohydrate load, human blood glucose levels tend to remain within the normal stove. however, shortly after eating, the lineage glucose level may rise, in non-diabetics, temporarily up to 7.8 mmol/L ( 140 mg/dL ) or slenderly more. For people with diabetes maintaining “ tight diabetes control ”, the American Diabetes Association recommends a post-meal glucose level of less than 10 mmol/L ( 180 mg/dL ) and a fast plasma glucose of 3.9 to 7.2 mmol/L ( 70–130 mg/dL ). [ 11 ] The actual total of glucose in the blood and body fluids is identical minor. In a goodly adult male of 75 kg ( 165 pound ) with a lineage volume of 5 L, a blood glucose level of 5.5 mmol/L ( 100 mg/dL ) amounts to 5 g, equivalent to about a teaspoon of carbohydrate. [ 12 ] Part of the reason why this amount is so small is that, to maintain an inflow of glucose into cells, enzymes modify glucose by adding phosphate or early groups to it .

other animals [edit ]

In general, ranges of blood sugar in common domestic ruminants are lower than in many monogastric mammals. [ 13 ] 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. [ 14 ] A 90 percentage reference book interval for serum glucose of 26 to 181 mg/dL has been reported for appropriate batch goats ( Oreamnos americanus ), where no effects of the pursuit and capture on measured levels were discernible. [ 15 ] For beluga whales, the 25–75 percentage range for serum glucose has been estimated to be 94 to 115 mg/dL. [ 16 ] For the white rhinoceros, one study has indicated that the 95 percentage range is 28 to 140 mg/dL. [ 17 ] For harp seals, a serum glucose stove of 4.9 to 12.1 mmol/L [ i.e. 88 to 218 mg/dL ] has been reported ; for hooded seals, a crop of 7.5 to 15.7 mmol/L [ i.e. about 135 to 283 mg/dL ] has been reported. [ 18 ]

regulation [edit ]

The body ‘s homeostatic mechanism keeps lineage glucose levels within a minute scope. It is composed of respective interacting systems, of which hormone regulation is the most crucial. [ citation needed ] There are two types of mutually antagonistic metabolic hormones affecting lineage glucose levels :

  • catabolic hormones (such as glucagon, cortisol and catecholamines) which increase blood glucose;[19]
  • and one anabolic hormone (insulin), which decreases blood glucose.

These hormones are secreted from pancreatic islets ( bundles of hormone 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 conclusion product of one reaction stimulates the begin of another reaction. In blood-glucose levels, insulin lowers the concentration of glucose in the blood. The lower blood-glucose degree ( a product of the insulin secretion ) triggers glucagon to be secreted, and repeats the cycle. [ 20 ] In order for blood glucose to be kept stable, modifications to insulin, glucagon, epinephrine and hydrocortisone are made. Each of these hormones has a different province to keep rake glucose regulated ; when lineage boodle is besides high, insulin tells muscles to take up excess glucose for storage. Glucagon responds to excessively humble of a lineage glucose level ; it informs the tissue to produce more glucose. Epinephrine prepares the muscles and respiratory arrangement for action in the shell of a “ battle and flight ” reaction. last, hydrocortisone supplies the body with fuel in times of heavy stress. [ 21 ]

Abnormalities [edit ]

high rake carbohydrate [edit ]

If blood sugar levels remain besides high the body suppresses appetite over the short-circuit term. long-run hyperglycemia causes many health problems including center disease, cancer, [ 22 ] eye, kidney, and heart damage. [ 23 ] Blood carbohydrate levels above 16.7 mmol/L ( 300 mg/dL ) can cause fatal reactions. Ketones will be very high ( a order of magnitude higher than when eating a very low carbohydrate diet ) initiating ketoacidosis. The Mayo Clinic recommends emergency room treatment above 16.7 mmol/L ( 300 mg/dL ) rake glucose. [ citation needed ] The most common lawsuit of hyperglycemia is diabetes. When diabetes is the campaign, physicians typically recommend an anti-diabetic medicine as treatment. From the perspective of the majority of patients, discussion with an erstwhile, well-understood diabetes drug such as metformin will be the safest, most effective, least expensive, and most comfortable path to managing the stipulate. [ 24 ] Diet changes and exercise execution may besides be separate of a treatment plan for diabetes. Some medications may cause a upgrade in blood sugars of diabetics, such as steroid medications, including cortisone, hydrocortisone, prednisolone, prednisone and dexamethasone. [ 25 ]

abject lineage sugar [edit ]

If blood boodle levels drop besides low, a potentially fateful condition called hypoglycemia train. Symptoms may include languor, impair mental function ; irritability ; shake, twitching, helplessness in arm and leg muscles ; picket complexion ; sweating ; passing of awareness. Mechanisms that restore satisfactory lineage glucose levels after extreme hypoglycemia ( below 2.2 mmol/L or 40 mg/dL ) must be quick and effective to prevent highly good consequences of insufficient glucose : confusion or unsteadiness and, in the extreme point ( below 0.8 mmol/L or 15 mg/dL ) loss of awareness and seizures. Without discounting the potentially quite good conditions and risks due to or oftentimes accompanying hyperglycemia, specially in the long-run ( diabetes or pre-diabetes, fleshiness or fleshy, lipemia, high blood pressure, etc. ), it is calm generally more dangerous to have besides small glucose – specially if levels are very low – in the blood than besides much, at least temporarily, because glucose is therefore authoritative for metabolism and nutrition and the proper function of the body ‘s organs. This is specially the case for those organs that are metabolically active or that require a constant, baffle supply of rake sugar ( the liver-colored and brain are examples ). In healthy individuals, blood glucose-regulating mechanisms are generally quite effective, and symptomatic hypoglycemia is by and large found only in diabetics using insulin or early pharmacological discussion, and in starvation or severe malnutrition or malabsorption ( of versatile causes ), and conditions such as anorexia. [ dubious – discuss ] Hypoglycemic episodes can vary greatly between persons and from time to time, both in austereness and speed of attack. For hard cases, prompt medical aid is necessity, as price to brain and other tissues and even death will result from sufficiently low blood-glucose levels .

Glucose measurement [edit ]

Sample source [edit ]

Glucose testing in a fast individual shows comparable levels of glucose in arterial, venous, and capillary rake. But following meals, capillary and arterial blood glucose levels can be importantly higher than venous levels. Although these differences vary widely, one cogitation 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 %. ” [ 26 ] [ 27 ]

Sample type [edit ]

Glucose is measured in hale blood, plasma or serum. Historically, blood glucose values were given in terms of unharmed rake, but most laboratories now measure and report plasma or serum glucose levels. Because crimson blood cells ( erythrocytes ) have a higher concentration of protein ( for example, hemoglobin ) than serum, serum has a higher urine content and consequently more dissolve glucose than does whole blood. To convert from whole-blood glucose, multiplication by 1.14 [ 28 ] has been shown to generally give the serum/plasma level.

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To prevent contaminant of the sample with intravenous fluids, particular caution should be given to drawing lineage samples from the branch opposite the one in which an intravenous tune is inserted. alternatively, blood can be drawn from the lapp 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 steep fluids away from the vein. inattention can lead to big errors, since vitamin a little as 10 % contamination with a 5 % glucose solution ( D5W ) will elevate glucose in a sample distribution by 500 mg/dL or more. The actual concentration of glucose in blood is very broken, even in the hyperglycemic. [ citation needed ]

measurement techniques [edit ]

Two major methods have been used to measure glucose. The first, hush in use in some places, is a chemical method acting exploiting the nonspecific reducing property of glucose in a reaction with an indicator kernel that changes color when reduced. Since other lineage compounds besides have reducing properties ( for example, urea, which can be abnormally high in azotemic patients ), this proficiency can produce erroneous readings in some situations ( 5–15 mg/dL has been reported ). The more recent proficiency, using enzymes specific to glucose, is less susceptible to this kind of error. The two most common employed enzymes are glucose oxidase and hexokinase. [ 29 ] Average blood glucose concentrations can besides be measured. This method acting measures the floor of glycated hemoglobin, which is spokesperson of the average rake glucose levels over the end, approximately, 120 days. [ 29 ] In either case, the chemical arrangement is normally 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 constitution vary between meter systems and can not be interchanged. Formerly, some test strips were read ( after time and wiping away the blood sample distribution ) by ocular comparison against a color graph printed on the phial label. Strips of this type are hush used for urine glucose readings, but for blood glucose levels they are disused. Their erroneousness rates were, in any font, much higher. Errors when using test strips were much caused by the age of the strip or exposure to high temperatures or humidity. [ 30 ] More precise lineage glucose measurements are performed in a medical lab, using hexokinase, glucose oxidase, or glucose dehydrogenase enzymes. Urine glucose readings, however taken, are much less utilitarian. In properly function kidneys, glucose does not appear in urine until the nephritic doorway for glucose has been exceeded. This is well above any normal glucose level, and is attest of an existing severe hyperglycemic condition. however, as urine is stored in the bladder, any glucose in it might have been produced at any fourth dimension since the last time the bladder was emptied. Since metabolic conditions change quickly, as a solution of any of several factors, this is delayed news program and gives no warning of a develop condition. Blood glucose monitor is far preferable, both clinically and for dwelling monitoring by patients. Healthy urine glucose levels were beginning standardized and published in 1965 [ 31 ] by Hans Renschler. A noninvasive method of sampling to monitor glucose levels has emerged using an exhaled breath condensate. however this method acting does need highly sensitive glucose biosensors. [ 32 ]

I. Chemical methods

A. Oxidation-reduction reaction

G fifty uracil deoxycytidine monophosphate oxygen mho east + A l k a lambert i n e c o phosphorus p einsteinium roentgen t a gas constant thyroxine a roentgen a thymine vitamin e → R east d u hundred deoxythymidine monophosphate one o north C uranium phosphorus radius o uranium second o adam iodine d e { \displaystyle \mathrm { Glucose } +\mathrm { Alkaline\ copper\ tartarate } { \xrightarrow { \mathrm { reduction } } } \mathrm { Cuprous\ oxide } }\mathrm{Glucose} + \mathrm{Alkaline\ copper\ tartarate}\xrightarrow{\mathrm{Reduction}} \mathrm{Cuprous\ oxide}

1. Alkaline copper reduction

Folin-Wu method

C u 2 + + P henry oxygen south phosphorus hydrogen o molarity oxygen lambert y b five hundred i c a deoxycytidine monophosphate one d → O ten one d a triiodothyronine one o north P hydrogen o mho phosphorus heat content o m oxygen liter yttrium barn vitamin d east nitrogen u molarity o x iodine d e { \displaystyle \mathrm { Cu } ^ { 2+ } +\mathrm { Phosphomolybdic\ acid } { \xrightarrow { \mathrm { oxidation } } } \mathrm { Phosphomolybdenum\ oxide } }{\displaystyle \mathrm {Cu} ^{2+}+\mathrm {Phosphomolybdic\ acid} {\xrightarrow {\mathrm {Oxidation} }}\mathrm {Phosphomolybdenum\ oxide} }
Blue end-product

Benedict’s method

  • Modification of Folin–Wu method for qualitative urine glucose.

Nelson–Somogyi method

C uracil 2 + + A radius mho e newton o thousand o l yttrium b vitamin d i c a hundred i d → O x one d a deoxythymidine monophosphate one o n A roentgen randomness e north oxygen megabyte oxygen l yttrium bacillus five hundred e n uranium thousand o ten one d vitamin e { \displaystyle \mathrm { Cu } ^ { 2+ } +\mathrm { Arsenomolybdic\ acidic } { \xrightarrow { \mathrm { oxidation } } } \mathrm { Arsenomolybdenum\ oxide } }{\displaystyle \mathrm {Cu} ^{2+}+\mathrm {Arsenomolybdic\ acid} {\xrightarrow {\mathrm {Oxidation} }}\mathrm {Arsenomolybdenum\ oxide} }
Blue end-product.

Neocuproine method

C u 2 + + N e oxygen c u p r o i n e → O x one d a deoxythymidine monophosphate iodine o north C u 2 + n einsteinium o c u p gas constant o iodine n e c o m phosphorus lambert e x { \displaystyle \mathrm { Cu } ^ { 2+ } +\mathrm { Neocuproine } { \xrightarrow { \mathrm { oxidation } } } \mathrm { Cu } ^ { 2+ } \mathrm { neocuproine\ complex } }{\displaystyle \mathrm {Cu} ^{2+}+\mathrm {Neocuproine} {\xrightarrow {\mathrm {Oxidation} }}\mathrm {Cu} ^{2+}\mathrm {neocuproine\ complex} }
Yellow-orange color neocuproine[33]

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

G lambert uranium coulomb oxygen randomness e + A fifty thousand a lambert iodine n einsteinium fluorine e r roentgen i c y a n one d e ⟶ F einsteinium radius r o coke yttrium a n iodine d e { \displaystyle \mathrm { Glucose } +\mathrm { Alkaline\ ferricyanide } \longrightarrow \mathrm { Ferrocyanide } }\mathrm{Glucose} + \mathrm{Alkaline\ ferricyanide}\longrightarrow \mathrm{Ferrocyanide}
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

G fifty uranium hundred oxygen sulfur vitamin e + O 2 → O x one d a thymine one o normality guanine lambert u c o mho vitamin e o ten one d a mho einsteinium D-glucono-1,5-lactone + H 2 O 2 { \displaystyle \mathrm { Glucose } +\mathrm { O } _ { 2 } { \xrightarrow [ { \mathrm { oxidation } } ] { \mathrm { glucose\ oxidase } } } { \textrm { D-glucono-1,5-lactone } } +\mathrm { H_ { 2 } O_ { 2 } } }\mathrm{Glucose} + \mathrm{O}_{2}\xrightarrow[\mathrm{Oxidation}] {\mathrm{glucose\ oxidase}}\textrm{D-glucono-1,5-lactone} + \mathrm{H_{2}O_{2}}

Saifer–Gerstenfeld method

H 2 O 2 + O -dianisidine → O x iodine d a thymine one o newton phosphorus e radius o adam i d a sulfur e H 2 O + o x i d iodine z e vitamin d deoxycytidine monophosphate h roentgen o megabyte o g east newton { \displaystyle \mathrm { H_ { 2 } O_ { 2 } } + { \textit { O } } { \text { -dianisidine } } { \xrightarrow [ { \mathrm { oxidation } } ] { \mathrm { peroxidase } } } \mathrm { H_ { 2 } O } +\mathrm { oxidized\ chromogen } }\mathrm{H_{2}O_2} + \textit{O}\text{-dianisidine}\xrightarrow[\mathrm{Oxidation}] {\mathrm{peroxidase}} \mathrm{H_2O} + \mathrm{oxidized\ chromogen}
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

G l u c oxygen randomness einsteinium + A T P → P hydrogen oxygen s p hydrogen o r y l a triiodothyronine one o normality H e x o kilobyte one n a second vitamin e + M g 2 + G-6PO 4 + A D P G-6PO 4 + N A D P → O x iodine d a t one o north G-6PD 6-Phosphogluconate + N A D P H + H + { \displaystyle { \begin { alignedat } { 2 } & \mathrm { Glucose } +\mathrm { ATP } { \xrightarrow [ { \mathrm { Phosphorylation } } ] { \mathrm { Hexokinase } +\mathrm { Mg } ^ { 2+ } } } { \textrm { G-6PO } } _ { 4 } +\mathrm { ADP } \\ & { \textrm { G-6PO } } _ { 4 } +\mathrm { NADP } { \xrightarrow [ { \mathrm { oxidation } } ] { \textrm { G-6PD } } } { \textrm { 6-Phosphogluconate } } +\mathrm { NADPH } +\mathrm { H } ^ { + } \\\end { alignedat } } } {\displaystyle {\begin{alignedat}{2}&\mathrm {Glucose} +\mathrm {ATP} {\xrightarrow[{\mathrm {Phosphorylation} }]{\mathrm {Hexokinase} +\mathrm {Mg} ^{2+}}}{\textrm {G-6PO}}_{4}+\mathrm {ADP} \\&{\textrm {G-6PO}}_{4}+\mathrm {NADP} {\xrightarrow[{\mathrm {Oxidation} }]{\textrm {G-6PD}}}{\textrm {6-Phosphogluconate}}+\mathrm {NADPH} +\mathrm {H} ^{+}\\\end{alignedat}}}

  • 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 [edit ]

The fast rake glucose grade, which is measured after a fast of 8 hours, is the most normally use reading of overall glucose homeostasis, largely because disturbing events such as food consumption are avoided. Conditions affecting glucose levels are shown in the board below. Abnormalities in these test results are due to problems in the multiple command mechanism of glucose regulation. [ citation needed ] The metabolic response to a carbohydrate challenge is handily assessed by a postprandial glucose level string 2 hours after a meal or a glucose load. In summation, the glucose tolerance test, consisting of respective timed measurements after a standardize come 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 feel bear contaminant, possibly ) or interference ( for example, tinting contaminants ) with sparkle source or the light detector. electrical techniques are less susceptible to these errors, though not to others. In home plate manipulation, the most important issue is not accuracy, but swerve. frankincense if a meter / test undress system is systematically wrong by 10 %, there will be little consequence, equally long as changes ( for example, due to exercise or medication adjustments ) are by rights tracked. In the US, home function blood test meters must be approved by the federal Food and Drug Administration before they can be sold. finally, there are several influences on lineage glucose grade apart from food intake. Infection, for case, tends to change blood glucose levels, as does stress either physical or psychological. exercise, particularly if prolonged or hanker after the most late meal, will have an effect angstrom well. In the distinctive person, maintenance of blood glucose at near constant levels will however be quite effective. [ clarification needed ]

See besides [edit ]

References [edit ]

farther read [edit ]

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