Insulin resistance: Difference between revisions

Latest revision as of 11:01, 1 September 2024

Main Article

Discussion

Related Articles ^[?]

Bibliography ^[?]

External Links ^[?]

Citable Version ^[?]

This editable Main Article is under development and subject to a disclaimer.

[edit intro]

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]

Christos Mantzoros, writing in UpToDate, offers:^[2]

Insulin resistance can be broadly defined as a subnormal biological response to normal insulin concentrations. By this definition, it may pertain to many biological actions of insulin in many tissues of the body. Typically, however, in clinical practice, insulin resistance refers to a state in which a given concentration of insulin is associated with a subnormal glucose response [i.e., subnormal reduction in plasma glucose concentration] [cites: Moller DE, Flier JS. Insulin resistance--mechanisms, syndromes, and implications. N Engl J Med 1991; 325:938.].

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.^[3] 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^[4] and the references cited therein.) (See also^[5]).

Metabolic and physiologic consequences of pathologic insulin resistance

The normal action of insulin to increase cellular uptake of glucose from plasma involves the delivery of an intracellular glucose transporter, a protein called GLUT4, to the cell membrane. GLUT4 proteins remain in storage in intracellular vesicles, endosomes, until insulin, through a series of biochemical steps initiated by insulin acting on its cell membrane receptor, stimulates the GLUT4-containing endosomes to deliver the glucose uptake transporter to the cell membrane. In the circumstance of insulin resistance, characterized by abnormally high plasma glucose concentrations, maintaining an adequate delivery of GLUT4 to the cell membrane to facilitate glucose uptake requires abnormally high plasma insulin concentrations. The hyperglycemia that results from insulin resistance helps to achieve those abnormally high plasma insulin concentrations by overstimulation of insulin secretion by cells in the pancreas. Over time, insulin resistant persons experience abnormally high integrated levels of both glucose and insulin in the systemic circulation, accompanied by multi-system glucose and insulin toxicity.

Hyperglycemia toxicity

Hyperinsulinemia toxicity

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.

Role of obesity

Role of Inflammation

Role of lipid metabolism

Role of gastrointestinal microbiota

Role of systemic acid-base status

Role of potassium

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:^[6]

{\text{HOMA-IR}}={\frac {{\text{fasting plasma glucose}}*{\text{fasting insulin}}}{22.5}}

• HOMA2

HOMA calculator.^[7]

• Hyperglycemic clamp

• Oral glucose tolerance test

• Intravenous glucose tolerance test

Notes

↑
Glucose belongs to the class of nutrients called carbohydrates, combinations of carbon (C) and water (H₂O):

C₆(H₂0)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.
↑ Mantzoros C. (2012) Insulin resistance: Definition and clinical spectrum. UpToDate. Topic 1762. Version 4.
↑
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 28:412-419. PMID 3899825.

↑ HOMA Calculator. Diabetes Trial Unit. University of Oxford.

[gluc-1] Glucose belongs to the class of nutrients called carbohydrates, combinations of carbon (C) and water (H₂O):

C₆(H₂0)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.

[2] N mg glucose/dL = N mg glucose/100 ml

[3] N mg glucose/100 ml = N mg glucose/ 0.1 L

[4] N mg glucose/0.1 L / 180.2 mg glucose/mmol glucose = N mmol glucose/0.1 *180.2 mmol glucose/L

[5] N mmol glucose/0.1 *180.2 mmol glucose/L = N mmol glucose/L/0.1*180.2

[6] N mmol glucose/L/0.1*180.2 = (N/18) mmol glucose

[meshir-2] Insulin Resistance. National Library of Medicine.

[mantzorosutd-3] Mantzoros C. (2012) Insulin resistance: Definition and clinical spectrum. UpToDate. Topic 1762. Version 4.

[shulman1990-4] 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.

[10] 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.

[lillioja1993-5] 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.

[martin1992-6] 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.

[13] 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.

[pmid3899825-7] 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.

[homacalc-8] HOMA Calculator. Diabetes Trial Unit. University of Oxford.

[Note 1]

[1]

[2]

[3]

[4]

[5]

[6]

[7]

@@ Line 1: / Line 1: @@
 {{subpages}}
-:See: ''Article on [[insulin]], if necessary, to better understand present article.''
+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
-:<font face="Gill Sans MT">Diminished effectiveness of [[insulin]] in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent [[hyperglycemia]] or [[ketosis]].</font><ref name=meshir>{{MeSH}}</ref>
+{|align="center" style="width:90%;font-size:98%;"
+|
+<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/>
+|}
+Christos Mantzoros, writing in UpToDate, offers:<ref name=mantzorosutd/>
+{|align="center" style="width:90%;font-size:98%;"
+|
+<font face="Gill Sans MT">Insulin resistance can be broadly defined as a subnormal biological response to normal insulin concentrations. By this definition, it may pertain to many biological actions of insulin in many tissues of the body. Typically, however, in clinical practice, insulin resistance refers to a state in which a given concentration of insulin is associated with a subnormal glucose response [i.e., subnormal reduction in plasma glucose concentration] [cites: Moller DE, Flier JS. Insulin resistance--mechanisms, syndromes, and implications. ''N Engl J Med'' 1991; 325:938.].</font>
+|}
-Insulin resistance reflects abnormally reduced insulin-induced uptake of glucose, largely in skeletal muscle.<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.
+Insulin resistance consists in part of reduced action of insulin on its major target tissues involved in glucose homeostasis&mdash;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/>).
-**<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> In people who have not developed the characteristic phenotype of type 2 diabetes mellitus, prospective studies reveal insulin resistance as the strongest predictor of its subsequent development. (See<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.</ref> and the references cited therein.) (See also:<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.
-**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>
+==Metabolic and physiologic consequences of pathologic insulin resistance==
+The normal action of insulin to increase cellular uptake of glucose from plasma involves the delivery of an intracellular glucose transporter, a protein called GLUT4, to the cell membrane. GLUT4 proteins remain in storage in intracellular vesicles, endosomes, until insulin, through a series of biochemical steps initiated by insulin acting on its cell membrane receptor, stimulates the GLUT4-containing endosomes to deliver the glucose uptake transporter to the cell membrane. In the circumstance of insulin resistance, characterized by abnormally high plasma glucose concentrations, maintaining an adequate delivery of GLUT4 to the cell membrane to facilitate glucose uptake requires abnormally high plasma insulin concentrations. The hyperglycemia that results from insulin resistance helps to achieve those abnormally high plasma insulin concentrations by overstimulation of insulin secretion by cells in the pancreas. Over time, insulin resistant persons experience abnormally high integrated levels of both glucose and insulin in the systemic circulation, accompanied by multi-system glucose and insulin toxicity.
+===Hyperglycemia toxicity===
+=== Hyperinsulinemia toxicity===
 ==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.
+===Role of obesity===
+===Role of Inflammation===
+<!--\dat\insulin resistance\Johnson e Olefsky-->
+===Role of lipid metabolism===
+===Role of gastrointestinal microbiota===
+===Role of systemic acid-base status===
+===Role of potassium===
 ==Methods of detecting and quantifying insulin resistance==
-[[Insulin resistance]] (HOMA-IR) can be measured by:<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=}}</ref>
+===•&nbsp;Euglycemic hyperinsulinemic clamp===
+===•&nbsp;HOMA-IR: homeostasis model assessment of insulin resistance===
+[[Insulin resistance]] (HOMA-IR) can be measured by:<ref name="pmid3899825"/>
 :<math>\text{HOMA-IR} = \frac{\text{fasting plasma glucose} * \text{fasting insulin}}{22.5}</math>
+===•&nbsp;HOMA2===
+HOMA calculator.<ref name=homacalc/>
+===•&nbsp;Hyperglycemic clamp===
+===•&nbsp;Oral glucose tolerance test===
+<!--  &nbsp;•&nbsp;  -->
+===•&nbsp;Intravenous glucose tolerance test===
+==Notes==
+{{reflist|group=Note|refs=
+<ref name=gluc group=Note>Glucose belongs to the class of nutrients called carbohydrates, combinations of carbon (C) and water (H<sub>2</sub>O):<br>
+<br>
+C<sub>6</sub>(H<sub>2</sub>0)<sub>6</sub><br>
+C<sub>6</sub>H<sub>12</sub>O<sub>6</sub><br>
+<br>
+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<br>
+<br>
+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).<br>
+<br>
+However, the standard unit for plasma glucose: mmol/L.<br>
+<br>
+To convert mg/dl to mmol/L, divide by 18:<br>
+*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<br>
+<br>
+Conversely, to convert mmol glucose/L to mg glucose/dl, multiply by 18.
+</ref>
+}}
 ==References==
-<references/>
+{{reflist3 test|refs=
+<ref name="pmid3899825">
+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 name=mantzorosutd>
+Mantzoros C. (2012) Insulin resistance: Definition and clinical spectrum. ''UpToDate''. Topic 1762. Version 4.
+</ref>
+<ref name=meshir>
+[http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?term=Insulin+resistance Insulin Resistance]. National Library of Medicine.
+</ref>
+<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.
+*<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 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.
+</ref>
+<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.
+*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 name=homacalc>
+[http://www.dtu.ox.ac.uk/homacalculator/ HOMA Calculator]. [http://www.dtu.ox.ac.uk/ Diabetes Trial Unit]. University of Oxford.
+</ref>
+}}[[Category:Suggestion Bot Tag]]

Insulin resistance: Difference between revisions

Latest revision as of 11:01, 1 September 2024

Contents

Metabolic and physiologic consequences of pathologic insulin resistance

Hyperglycemia toxicity

Hyperinsulinemia toxicity

Causes of insulin resistance

Role of obesity

Role of Inflammation

Role of lipid metabolism

Role of gastrointestinal microbiota

Role of systemic acid-base status

Role of potassium

Methods of detecting and quantifying insulin resistance

• Euglycemic hyperinsulinemic clamp

• HOMA-IR: homeostasis model assessment of insulin resistance

• HOMA2

• Hyperglycemic clamp

• Oral glucose tolerance test

• Intravenous glucose tolerance test

Notes

References

Navigation menu

Insulin resistance: Difference between revisions

Latest revision as of 11:01, 1 September 2024

Metabolic and physiologic consequences of pathologic insulin resistance

Hyperglycemia toxicity

Hyperinsulinemia toxicity

Causes of insulin resistance

Role of obesity

Role of Inflammation

Role of lipid metabolism

Role of gastrointestinal microbiota

Role of systemic acid-base status

Role of potassium

Methods of detecting and quantifying insulin resistance

• Euglycemic hyperinsulinemic clamp

• HOMA-IR: homeostasis model assessment of insulin resistance

• HOMA2

• Hyperglycemic clamp

• Oral glucose tolerance test

• Intravenous glucose tolerance test

Notes

References

Navigation menu

Search