Insulin resistance: Difference between revisions
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<font face="Gill Sans MT">Diminished effectiveness of [[insulin]] in lowering blood sugar [glucose]<ref name=gluc group=Note/> levels: requiring the use of 200 units or more of insulin per day to prevent [[hyperglycemia]] or [[ketosis]].</font><ref name=meshir/> | <font face="Gill Sans MT">Diminished effectiveness of [[insulin]] in lowering blood sugar [glucose]<ref name=gluc group=Note/> levels: requiring the use of 200 units or more of insulin per day to prevent [[hyperglycemia]] or [[ketosis]].</font><ref name=meshir/> | ||
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Insulin resistance | Insulin resistance consists in part reduced action of insulin on its major target tissue involved in glucose homeostasis—skeletal muscle, adipose tissue, and liver. Insulin resistance manifests as reduced insulin-induced uptake of glucose, largely in skeletal muscle.<ref name=shulman1990/> | ||
In people who have not developed the characteristic [[phenotype]] of [[Diabetes mellitus type 2|type 2 diabetes mellitus]] ([[Diabetes mellitus type 2|T2DM]]), prospective studies reveal insulin resistance as the strongest predictor of T2DM subsequent development. (See<ref name=lillioja1993/> and the references cited therein.) (See also<ref name=martin1992/>). | |||
==Causes of insulin resistance== | ==Causes of insulin resistance== | ||
Revision as of 17:14, 25 February 2013
See Article on insulin, if necessary, to better understand present article.
As described in the 2013 Medical Subject Headings of the National Library of Medicine, insulin resistance consists of
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Diminished effectiveness of insulin in lowering blood sugar [glucose][Note 1] levels: requiring the use of 200 units or more of insulin per day to prevent hyperglycemia or ketosis.[1] |
Insulin resistance consists in part reduced action of insulin on its major target tissue involved in glucose homeostasis—skeletal muscle, adipose tissue, and liver. Insulin resistance manifests as reduced insulin-induced uptake of glucose, largely in skeletal muscle.[2]
In people who have not developed the characteristic phenotype of type 2 diabetes mellitus (T2DM), prospective studies reveal insulin resistance as the strongest predictor of T2DM subsequent development. (See[3] and the references cited therein.) (See also[4]).
Causes of insulin resistance
It can be caused by the presence of insulin antibodies or the abnormalities in insulin receptors (receptor, insulin) on target cell surfaces. It is often associated with obesity; diabetic ketoacidosis; infection; and certain rare conditions.
Methods of detecting and quantifying insulin resistance
Insulin resistance (HOMA-IR) can be measured by:[5]
Notes
- ↑ Glucose belongs to the class of nutrients called carbohydrates, combinations of carbon (C) and water (H2O):
C6H20)6
C6H12O6
Molecular weight (molar mass) of glucose: 180.15588 (~180.2) g/mol, or 180.2 mg/mmol, calculated as the sum of the number of atoms per molecule of glucose times the atomic weights of: carbon (C) * 6, hydrogen (H) * 12, oxygen (O) * 6: (12 * 6) + (1 * 12) + (16 * 6) = ~180.2
The concentration of glucose in blood plasma, usually expressed in U.S. as milligrams/deciliter (mg/dl), where deciliter equals one-tenth of a liter (L), or 100 milliliters (100 ml).
However, the standard unit for plasma glucose: mmol/L.
To convert mg/dl to mmol/L, divide by 18:
- N mg glucose/dL = N mg glucose/100 ml
- N mg glucose/100 ml = N mg glucose/ 0.1 L
- N mg glucose/0.1 L / 180.2 mg glucose/mmol glucose = N mmol glucose/0.1 *180.2 mmol glucose/L
- N mmol glucose/0.1 *180.2 mmol glucose/L = N mmol glucose/L/0.1*180.2
- N mmol glucose/L/0.1*180.2 = (N/18) mmol glucose
Conversely, to convert mmol glucose/L to mg glucose/dl, multiply by 18.
References
- ↑ Insulin Resistance. National Library of Medicine.
- ↑
Shulman GI, Rothman DL, Jue T, Stein P, DeFronzo RA, Shulman RG. (1990) Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy. N Engl J Med 322:223-8.
- The mean glucose uptake was markedly reduced in the diabetic (30±4 mumol per kilogram per minute) as compared with the normal subjects (51±3 mumol per kilogram per minute; P less than 0.005). The mean rate of nonoxidative glucose metabolism was 22±4 mumol per kilogram per minute in the diabetic subjects and 42±4 mumol per kilogram per minute in the normal subjects (P less than 0.005). When these rates are extrapolated to apply to the whole body, the synthesis of muscle glycogen would account for most of the total-body glucose uptake and all of the nonoxidative glucose metabolism in both normal and diabetic subjects. We conclude that muscle glycogen synthesis is the principal pathway of glucose disposal in both normal and diabetic subjects and that defects in muscle glycogen synthesis have a dominant role in the insulin resistance that occurs in persons with NIDDM.
- ↑ Lillioja S, Mott DM, Spraul M, Ferraro R, Foley JE, Ravussin E, Knowler WE, Bennett PH, Bogardus C. (1993) Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians. N. Engl. J. Med. 329:1988–1992.
- ↑
Martin BC, Warram JH, Krolewski AS, Soeldner JS, Kahn CR, Martin BC, Bergman RN. (1992) Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet; 340:925-29.
- The development of type 2 diabetes is preceded by and predicted by defects in both insulin-dependent and insulin-independent glucose uptake; the defects are detectable when the patients are normoglycaemic and in most cases more than a decade before diagnosis of disease.
- ↑ Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC (1985). "Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man". Diabetologia 28: 412–9. PMID 3899825. [e]