Insulin resistance: Difference between revisions

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:<math>\text{HOMA-IR} = \frac{\text{fasting plasma glucose} * \text{fasting insulin}}{22.5}</math>
:<math>\text{HOMA-IR} = \frac{\text{fasting plasma glucose} * \text{fasting insulin}}{22.5}</math>


===HOMA2===
===&nbsp;•&nbsp;HOMA2===
HOMA calculator.<ref name=homacalc/>
HOMA calculator.<ref name=homacalc/>
===&nbsp;•&nbsp;Hyperglycemic clamp===
===&nbsp;•&nbsp;Hyperglycemic clamp===


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<ref name="pmid3899825">
<ref name="pmid3899825">
{{cite journal |author=Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC |title=Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man |journal=Diabetologia |volume=28 |pages=412–9 |year=1985 |pmid=3899825 |doi= |url= |issn=}}
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 28:412-419. PMID 3899825.
</ref>
</ref>
<ref name=meshir>
<ref name=meshir>
[http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?term=Insulin+resistance Insulin Resistance]. National Library of Medicine.
[http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?term=Insulin+resistance Insulin Resistance]. National Library of Medicine.
</ref>
</ref>
<ref name=shulman1990>
<ref name=shulman1990>
Shulman GI, Rothman DL, Jue T, Stein P, DeFronzo RA, Shulman RG. (1990) [http://dx.doi.org/10.1056/NEJM199001253220403 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.  
Shulman GI, Rothman DL, Jue T, Stein P, DeFronzo RA, Shulman RG. (1990) [http://dx.doi.org/10.1056/NEJM199001253220403 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.  
*<font face="Gill Sans MT">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.
*<font face="Gill Sans MT">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.
</ref>
</ref>
<ref name=lillioja1993>
<ref name=lillioja1993>
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.
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.
</ref>
</ref>
<ref name=martin1992>
<ref name=martin1992>
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.
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.
*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.
</ref>
</ref>
<ref name=homacalc>
<ref name=homacalc>
[http://www.dtu.ox.ac.uk/homacalculator/ HOMA Calculator]. [http://www.dtu.ox.ac.uk/ Diabetes Trial Unit]. University of Oxford.
[http://www.dtu.ox.ac.uk/homacalculator/ HOMA Calculator]. [http://www.dtu.ox.ac.uk/ Diabetes Trial Unit]. University of Oxford.

Revision as of 21:38, 25 February 2013

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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

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 of reduced action of insulin on its major target tissues 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

 • Euglycemic hyperinsulinemic clamp

 • HOMA-IR: homeostasis model assessment of insulin resistance

Insulin resistance (HOMA-IR) can be measured by:[5]

 • HOMA2

HOMA calculator.[6]

 • Hyperglycemic clamp

 • Oral glucose tolerance test

 • Intravenous glucose tolerance test

Notes

  1. ↑ 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

  1. ↑ Insulin Resistance. National Library of Medicine.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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 28:412-419. PMID 3899825.
  6. ↑ HOMA Calculator. Diabetes Trial Unit. University of Oxford.

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