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Autor     Jiaxu Li
Titel    The Dynamic of Glucose-Insulin Endocrine Metabolic Regulatory System
Datum    December 2004
Anmerkung    A Dissertation Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy, ARIZONA STATE UNIVERSITY
URL    https://math.la.asu.edu/~kuang/paper/JiaxuLi.pdf

Literaturverz.   

no
Fußnoten    no
Fragmente    7


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1. INTRODUCTION

1.1. Diabetes Mellitus

Human bodies need to maintain a glucose concentration level in a narrow range (70 - 109 mg/dl or 3.9 - 6.04 mmol/l). If the glucose concentration level is significantly out of the normal range (70 - 110 mg/dl), this person is considered to have hyperglycaemia (140 mg/dl or 7.8 mmol/l after an oral glucose tolerance test, or 100 mg/dl or 5.5 mmol/l after a fasting glucose tolerance test) or hypoglycaemia (less than 40 mg/dl or 2.2 mmol/l). Diabetes mellitus is a disease in the glucose-insulin endocrine metabolic regulatory system, in which the pancreas either does not release insulin or does not properly use insulin to uptake glucose in the plasma (1) (2) which is referred as hyperglycaemia. The consequences are that the body does not metabolize the glucose and builds up hyperglycaemia which eventually damages the regulatory system. Complications of diabetes mellitus include retinopathy, nephropathy, peripheral neuropathy and blindness (3). Diabetes mellitus is one of the worst diseases with respect to size of the affected population. The world wide diabetics affected population is much higher, especially in underdeveloped countries.

Diabetes mellitus is currently classified as type 1 or type 2 diabetes (2). Type 1 diabetes was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. It develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that synthesize the hormone insulin, which regulates blood glucose. This form of diabetes usually strikes children and young adults, although disease onset can occur at any age. Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes. Risk factors for type 1 diabetes include autoimmune, genetic, and environmental factors. Type 2 diabetes is adult onset or non-insulin-dependent diabetes mellitus (NIDDM) as this is due to a deficit in the mass of β cells, reduced insulin secretion (4), and resistance to the action of insulin. The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified (5). About 90% to 95% of all diabetics diagnose type 2 diabetes. Type 2 diabetes is associated with older age, obesity, family history of diabetes, prior history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, native Americans, some Asian Americans, native Hawaiian, and other Pacific Islanders are at particularly high risk for type 2 diabetes. Type 2 diabetes is increasingly being diagnosed [in children and adolescents.]


1. Topp,B, Promislow,K, deVries,G, Miura,RM, Finegood,DT: A model of beta-cell mass, insulin, and glucose kinetics: pathways to diabetes. J.Theor.Biol. 206:605-619, 2000

2. Bergman,RN, Ider,YZ, Bowden,CR, Cobelli,C: Quantitative estimation of insulin sensitivity. Am.J.Physiol 236:E667-E677, 1979

3. Derouich,M, Boutayeb,A: The effect of physical exercise on the dynamics of glucose and insulin. J.Biomech. 35:911-917, 2002

4. Kloppel,G, Lohr,M, Habich,K, Oberholzer,M, Heitz,PU: Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. Surv.Synth.Pathol.Res. 4:110-125, 1985

5. Cerasi,E: Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a divorce possible? Diabetologia 38:992-997, 1995

[Page 1]

CHAPTER 1

Introduction and Physiological Background

1. Diabetes Mellitus

Human bodies need to maintain a glucose concentration level in a narrow range (70 - 109 ml/dl or 3.9 - 6.04 mmol/l). If one’s glucose concentration level is significantly out of the normal range (70 - 110 ml/dl), this person is considered to have a the plasma glucose problem: hyperglycemia (≥140 mg/dl or 7.8 mmol/l after an Oral Glucose Tolerance Test, or ≥100 mg/dl or 5.5 mmol/l after a Fasting Glucose Tolerance Test) or hypoglycemia (less than 40 mg/dl or 2.2 mmol/l) ([89], [96]).

Diabetes mellitus is a disease in the glucose-insulin endocrine metabolic regulatory system, in which the pancreas either does not release insulin or does not properly use insulin to uptake glucose in the plasma ([9], [85]), which is referred as hyperglycemia.

The consequences are that the body does not metabolize the glucose and builds up hyperglycemia which eventually damages the regulatory system. Complications of diabetes mellitus include retinopathy, nephropathy, peripheral neuropathy and blindness ([25]).

Diabetes mellitus is one of the worst diseases with respect to size of the affected population. [...]

[Page 2]

[...] The world wide diabetics population is much higher, especially in underdeveloped countries.

Diabetes mellitus is currently classified as type 1 diabetes or type 2 diabetes ([9], [85]). Type 1 diabetes was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. It develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin, which regulates blood glucose. This form of diabetes usually strikes children and young adults, although disease onset can occur at any age. Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes. Risk factors for type 1 diabetes include autoimmune, genetic, and environmental factors. Type 2 diabetes is adult onset or non-insulin-dependent diabetes mellitus (NIDDM) as this is due to a deficit in the mass of β cells, reduced insulin secretion [53], and resistance to the action of insulin [32]. The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified [17]. About 90% to 95% of all diabetics diagnose type 2 diabetes. Type 2 diabetes is associated with older age, obesity, family history of diabetes, prior history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, Native Americans, some Asian Americans, Native Hawaiian, and other Pacific Islanders are at particularly high risk for type 2 diabetes. Type 2 diabetes is increasingly being diagnosed in children and adolescents ([93]).


[9] R. N. Bergman, D. T. Finegood, S. E. Kahn, The evolution of beta-cell dysfunction and insulin resistance in type 2 diabetes, Eur. J. Clin. Invest., 32 (2002), (Suppl. 3), 35–45.

[10] R. N. Bergman, Y. Z. Ider, C. R. Bowden and C. Cobelli, Quantitative estimation of insulin sensitivity, Am. J. Physiol., 236 (1979), E667–E677.

[17] E. Cerasi, Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a dovorce Possible?, Diabetologia 38, 992–997.

[25] M. Derouich, A. Boutayeb, The effect of physical exercise on the dynamics of glucose and insulin, J. Biomechanics, 35 (2002), 911–917.

[32] The report of the Expert Committee on the diagnosis and classification of diabetes mellitus, Diabetes Care, 20 (1997), 1183–1197.

[53] G. Kloppel, M. Lohr, K. Habich, M. Oberholzer and P. U. Heitz, Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited, Surv. Synth. Path. Res. 4, 110–125.

[85] B. Topp, K. Promislow, G. De Vries, R. M. Miura and D. T. Finegood, A Model of β-cell mass, insulin, and glucose kinetics: pathways to diabetes, J. Theor. Biol. 206 (2000), 605–619.

[89] http://arbl.cvmbs.colostate.edu/hbooks /pathphys/endocrine/pancreas/index.html

[93] http://www.diabetes.org

[96] http://www.endocrineweb.com/insulin.html

Anmerkungen

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(Graf Isolan), SleepyHollow02

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In addition to type 1 and type 2 diabetes, gestational diabetes is a form of glucose intolerance that is diagnosed in some women during pregnancy (1).

Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and native Americans. It is also more common among obese women and women with a family history of diabetes. During pregnancy, gestational diabetes requires treatment to normalize maternal blood glucose levels to avoid complications in the infant. After pregnancy, 5% to 10% of women with gestational diabetes are found to have type 2 diabetes. Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the next 5-10 years. Other specific types of diabetes result from specific genetic conditions such as maturity-onset diabetes of youth, surgery, drugs, malnutrition, infections, and other illnesses. Such types of diabetes may account for 1% to 5% of all diagnosed cases of diabetes. The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified (5). Due to the large population of diabetes patients in the world and the big health expenses, many researchers are motivated to study the glucose-insulin endocrine metabolic regulatory system so that we can better understand how the mechanism functions (6;7) , what causes the dysfunctions of the system, how to detect the onset of the either type of diabetes including the so called prediabetes , (2;7) (8) and eventually provide more reasonable, more effective, more efficient and more economic treatments to diabetics.

1.2 Glucose-insulin endocrine metabolic regulatory system

Metabolism is the process of extracting useful energy from chemical bounds. A metabolic pathway is a sequence of enzymatic reactions that take place in order to transfer chemical energy from one form to another. The chemical adenosine-triphosphate (ATP) is a common carrier of energy in a cell. There are two different ways to form ATP by adding one inorganic phosphate group to the adenosine-diphosphate (ADP), or adding two inorganic phosphate groups to the adenosine-monophosphate (AMP). The process of inorganic phosphate group addition is referred to phosphorylation. Due to the fact that the three phosphate groups in ATP carry negative charges, it requires lots of energy to overcome the natural repulsion of like-charged phosphates when additional groups are added to AMP. So considerable amount of energy is released during the hydrolysis of ATP to ADP. In the glucose-insulin endocrine metabolic regulatory system, the two pancreatic endocrine hormones, insulin and glucagon, are the primary dynamic factors that regulate the system. Glucose stimulates insulin secretion from β-cells by activating two pathways that require [metabolism of the sugar: the triggering and the amplifying pathway (9) .]


1. Topp,B, Promislow,K, deVries,G, Miura,RM, Finegood,DT: A model of beta-cell mass, insulin, and glucose kinetics: pathways to diabetes. J.Theor.Biol. 206:605-619, 2000

2. Bergman,RN, Ider,YZ, Bowden,CR, Cobelli,C: Quantitative estimation of insulin sensitivity. Am.J.Physiol 236:E667-E677, 1979

5. Cerasi,E: Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a divorce possible? Diabetologia 38:992-997, 1995

6. Porksen,N: The in vivo regulation of pulsatile insulin secretion. Diabetologia 45:3-20, 2002

7. Bergman,RN, Finegood,DT, Kahn,SE: The evolution of beta-cell dysfunction and insulin resistance in type 2 diabetes. Eur.J.Clin.Invest 32 Suppl 3:35-45, 2002

8. Toffolo,G, Bergman,RN, Finegood,DT, Bowden,CR, Cobelli,C: Quantitative estimation of beta cell sensitivity to glucose in the intact organism: a minimal model of insulin kinetics in the dog. Diabetes 29:979-990, 1980

9. Henquin,JC: Triggering and amplifying pathways of regulation of insulin secretion by glucose. Diabetes 49:1751-1760, 2000

In addition to Type 1 and Type 2 diabetes, gestational diabetes is a form of glucose intolerance that is diagnosed in some women during pregnancy ([9], [85], [97]). Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and Native Americans. It is also more common among obese women and

[page 3]

women with a family history of diabetes. During pregnancy, gestational diabetes re- quires treatment to normalize maternal blood glucose levels to avoid complications in the infant. After pregnancy, 5% to 10% of women with gestational diabetes are found to have type 2 diabetes. Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the next 5-10 years. Other specific types of dia- betes result from specific genetic conditions (such as maturity-onset diabetes of youth), surgery, drugs, malnutrition, infections, and other illnesses. Such types of diabetes may account for 1% to 5% of all diagnosed cases of diabetes ([97]).

The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified ([17]).

Due to the large population of diabetes patients in the world and the big health expenses, many researchers are motivated to study the glucose-insulin endocrine metabolic regulatory system so that we can better understand how the mechanism functions ([79], [84], [85], [67], [74], [31], [85], [4] and their references), what cause the dysfunctions of the system ([9] and its rich references), how to detect the onset of the either type of diabetes including the so called prediabetes ([10], [83], [8], [97], [23], [57], [6], [63] and their references), and eventually provide more reasonable, more effective, more efficient and more economic treatments to diabetics.

[page 4]

2. Glucose-Insulin Endocrine Metabolic Regulatory System

Metabolism is the process of extracting useful energy from chemical bounds. A metabolic pathway is a sequence of enzymatic reactions that take place in order to transfer chemical energy from one form to another. The chemical adenosine triphos-phate (ATP) is a common carrier of energy in a cell. There are two different ways to form ATP:

1. adding one inorganic phosphate group (HPO2− 4 ) to the adenosine diphosphate (ADP), or

2. adding two inorganic phosphate groups to the adenosine monophosphate (AMP).

The process of inorganic phosphate group addition is referred to phosphorylation. Due to the fact that the three phosphate groups in ATP carry negative charges, it requires lots of energy to overcome the natural repulsion of like-charged phosphates when addi- tional groups are added to AMP. So considerable amount of energy is released during the hydrolysis of ATP to ADP ([51], [89] and [91]).

In the glucose-insulin endocrine metabolic regulatory system, the two pancre- atic endocrine hormones, insulin and glucagon, are the primary dynamic factors that regulate the system.

[page 11]

Glucose stimulates insulin secretion from β-cells by activating two pathways that require metabolism of the sugar as follows ([47]).


[9] R. N. Bergman, D. T. Finegood, S. E. Kahn, The evolution of beta- cell dysfunction and insulin resistance in type 2 diabetes, Eur. J. Clin. Invest., 32 (2002), (Suppl. 3), 35–45.

[10] R. N. Bergman, Y. Z. Ider, C. R. Bowden and C. Cobelli, Quantitative estimation of insulin sensitivity, Am. J. Physiol., 236 (1979), E667–E677.

[17] E. Cerasi, Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a dovorce Possible?, Diabetologia 38, 992–997.

[47] J. C. Henquin, Triggering and amplifying pathways of regulation of in- sulin secretion by glucose, Diabetes, 49:17511760, 2000.

[83] G. Toffolo, R. N. Bergman, D. T. Finegood, C. R. Bowden, C. Cobelli, Quantitative estimation of beta cell sensitivity to glucose in the intact organism: a minimal model of insulin kinetics in the dog, Diabetes, 29 (1980), No. 12, 979–990.

[85] B. Topp, K. Promislow, G. De Vries, R. M. Miura and D. T. Finegood, A Model of β-cell mass, insulin, and glucose kinetics: pathways to diabetes, J. Theor. Biol. 206 (2000), 605–619.

Anmerkungen

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Note: not all references to the literature of the source have been documented.

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In the triggering pathway, the facilitative glucose transporter GLUT2 transports the glucose into the β cell. It causes the rise in the ratio of ATP/ADP which leads ATP-sensitive K+ channels (KATP channels) in the plasma membrane to close. The decreased K+ permeability leads to membrane depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx, and the eventual rise of the cytosolic Ca2+ concentration ([Ca2+]c) that triggers exocytosis of insulin containing vesicles. This pathway is also called KATP channel-dependent pathway. Please see Figure 1 for an illustration. The amplifying pathway which is a KATP channel-independent pathway, simply increases the efficiency of the Ca2+ on exocytosis when the concentration of Ca2+ has been elevated. Triggering Pathway The GLUT2 transports the glucose into the β cell. It causes the rise in the ratio of ATP/ADP which causes ATP-sensitive K+ channels (KATP channels) in the plasma membrane to close. The decreased K+ permeability leads to membrane depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx, and the eventual rise of the cytosolic Ca2+ concentration ([Ca2+]c) that triggers exocytosis. This pathway is also called KATP channel-dependent pathway. See Figure 1.3.2 for an illustration.

Amplifying Pathway The KATP channel-independent pathway simply increases the efficiency of the Ca2+ on exocytosis when the concentration of Ca2+ has been elevated.

Anmerkungen

The two described figures are not identical.

The source is not mentioned.

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(Hindemith) LieschenMueller

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Figure 1. Pancreatic beta cells secrete insulin when glucose concentration levels are elevated.

The facilitated glucose transporter GLUT2 transports the glucose into the cell where it is phosphorylated by glucokinase. The glucose metabolism causes ATP-sensitive K+ channels to close, the membrane to depolarize and the Ca2+ channels to open. This triggers a cascade of protein phosphorylations leading to insulin exocytosis.

The insulin receptor is a transmembrane glycoprotein that belongs to the large class of tyrosine kinase receptors. Two α subunits and two β subunits make up the insulin receptor. The β subunits pass through the cellular membrane and are linked by disulfide bonds (10) .


10. Ackermann,AM, Gannon,M: Molecular regulation of pancreatic beta-cell mass development, maintenance, and expansion. J.Mol.Endocrinol. 38:193-206, 2007

Figure 1.3.2. The β cells secrete insulin when glucose concentration level elevated

The facilitated GLUT2 transport the glucose into the β cell and the glucose is phosphorylated by glucokinase. The ratio of ATP:ADP is elevated. The glucose metabolism causes ATP-sensitive K+ channels to close, the membrane to depolarize and the Ca2+ channels to open. This triggers a cascade of protein phosphorylations and leads to insulin exocytosis [68]. (The figure is partially adapted from [68].)

[page 13]

3.4. Insulin Receptors. In molecular biology, the insulin receptor is a transmembrane glycoprotein that is activated by insulin. It belongs to the large class of tyrosine kinase receptors. Two α subunits and two β subunits make up the insulin receptor. The β subunits pass through the cellular membrane and are linked by disulfide bonds ([90]).


[68] V. Poitout, An integrated view of β-cell dysfunction in type-II diabetes, Annu. Rev. Med. 1996. 47:6983.

[89] http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/pancreas/index.html

Anmerkungen

The source is not given.

The two figures with nearly identical captions are in fact quite different.

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(Hindemith), PlagProf:-)

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The insulin receptors are embedded in the plasma membrane of myocytes and adipocytes (11). The binding of insulin to the receptors is the initial step in a signal transduction pathway, triggering the consumption and metabolism of glucose. Bound by insulin , the insulin receptor phosphorylates several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) that activate Phosphatidylinositol 3-kinase (PI-3-K) leading to an increase in the facilitative glucose transporters (GLUT4 and GLUT1) molecules in the outer membrane of muscle cells and adipocytes, and therefore to an increase in the uptake of glucose from blood into muscle and adipose tissue. Figure 2 elucidates this signaling pathway (12).

[FIGURE]

Figure 2. Insulin signals cells to utilize glucose. Insulin binds to its receptors on the membrane of the cells and induces phosphorylation of several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) which activate Phosphatidylinositol 3-kinase (PI-3-K) thereby leading to an increase in glucose transporter (GLUT1 and GLUT4) molecules in the plasma membrane. GLUT1 and GLUT4 transport the glucose into the cells efficiently.

The kinetics of insulin receptor binding is complex. The number of insulin receptors of each cell changes opposite to the circulating insulin concentration level. Increased insulin circulating level reduces the number of insulin receptors per cell and the decreased [circulating level of insulin triggers the number of receptors to increase (13).]


11. Sesti,G: Pathophysiology of insulin resistance. Best.Pract.Res.Clin.Endocrinol.Metab 20:665-679, 2006

12. Wardzala,LJ, Jeanrenaud,B: Potential mechanism of insulin action on glucose transport in the isolated rat diaphragm. Apparent translocation of intracellular transport units to the plasma membrane. J.Biol.Chem. 256:7090-7093, 1981

13. Grunberger,G, Ryan,J, Gorden,P: Sulfonylureas do not affect insulin binding or glycemic control in insulin-dependent diabetics. Diabetes 31:890-896, 1982

The insulin receptors are embedded in the plasma membrane of hepatocytes and myocytes. The binding of insulin to the receptors is the initial step in a signal

[page 14]

transduction pathway, triggering the consumption and metabolism of glucose ([89], [86]). Bound by insulin, the insulin receptor phosphorylates from ATP to several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) containing signaling molecules, activates Phosphatidylinositol 3-kinase (PI-3-K) and leads to an increase in glucose transporter (GLUT4) molecules ([98]) in the outer membrane of muscle cells and adipocytes, and therefore to an increase in the uptake of glucose from blood into muscle and adipose tissue ([89]). GLUT4 will transport the glucose to the cells efficiently. Figure 1.3.3 elucidates this signaling pathway.

[...]

However, the kinetics of insulin receptor binding are complex. The number of insulin receptors of each cell changes opposite to the circulating insulin concentration level. Increased insulin circulating level reduces the number of insulin receptors per cell and the decreased circulating level of insulin triggers the number of receptors to increase.

[page 15]

[FIGURE]

Figure 1.3.3. Insulin signals cells to utilize glucose

Insulin binds to its receptors on the membrane of the cells and phosphorylates several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) containing signaling molecules, activates Phosphatidylinositol 3-kinase (PI-3-K) and leads to an increase in glucose transporter (GLUT4) molecules. This leads to an increase in glucose transporter (GLUT4) molecules. GLUT4 will transport the glucose to the cells efficiently.


[86] S.Wanant and M. J. Quon, Insulin Receptor Binding Kinetics: Modeling and Simulation Studies, J. Theor. Bio., 205 (2000), 355-364.

[89] http://arbl.cvmbs.colostate.edu/hbooks/ pathphys/endocrine/pancreas/index.html

[98] E. Y. Skolnik, Insulin receptor signaling pathways, http://www.med.nyu.edu/research/skolne01.html

Anmerkungen

The source is not given.

The two figures are not identical.

Sichter
(Hindemith), LieschenMueller

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The number of receptors is increased during starvation and decreased in obesity and acromegaly (14). The affinity of the receptor for the second insulin molecule is significantly lower than for the first bound molecule. This may explain the negative cooperative interactions observed at high insulin concentrations. That is, as the concentration of insulin increases and more receptors become occupied, the affinity of the receptors for insulin decreases (15). Conversely, at low insulin concentrations, positive cooperation has been recorded. That is, the binding of insulin to its receptor at low insulin concentrations seems to enhance further binding.

The alpha cells in the pancreas release glucagon, a protein hormone that has important effects in the regulation of carbohydrate metabolism. Glucagon mobilizes glucose, fatty acids and amino acids from storage into the blood. When the glucose concentration level in the plasma is low, the liver converts glucagon to glucose. Both insulin and glucagon are important in the regulation of carbohydrate, protein and lipid metabolism.


14. Pav,J, Marek,J, Sramkova,J: [The effect of acromegaly treatment on glucose tolerance]. Cas.Lek.Cesk. 125:1451-1454, 1986

15. Niessen,M, Jaschinski,F, Item,F, McNamara,MP, Spinas,GA, Trub,T: Insulin receptor substrates 1 and 2 but not Shc can activate the insulin receptor independent of insulin and induce proliferation in CHO-IR cells. Exp.Cell Res. 313:805-815, 2007

[page 14]

The number of receptors is increased during starvation and decreased in obesity and acromegaly. But, the receptor affinity is decreased by excess glucocorticoids. The affinity of the receptor for the second insulin molecule is significantly lower than for the first bound molecule. This may explain the negative cooperative interactions observed at high insulin concentrations. That is, as the concentration of insulin increases and more receptors become occupied, the affinity of the receptors for insulin decreases. Conversely, at low insulin concentrations, positive cooperation has been recorded. That

[page 15]

is, the binding of insulin to its receptor at low insulin concentrations seems to enhance further binding (([89]), [86]).

[page 9]

The α cells release glucagon, a protein hormone that has important effects in the regulation of carbohydrate metabolism. Glucagon is a catabolic hormone, that is, it mobilizes glucose, fatty acids and amino acids from storage into the blood. When the glucose concentration level in the plasma is low, the liver will convert the glucagon to glucose.

Both insulin and glucagon are important in the regulation of carbohydrate, protein and lipid metabolism.


[86] S.Wanant and M. J. Quon, Insulin Receptor Binding Kinetics: Modeling and Simulation Studies, J. Theor. Bio., 205 (2000), 355-364.

[89] http://arbl.cvmbs.colostate.edu/hbooks/ pathphys/endocrine/pancreas/index.html

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith), LieschenMueller

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[FIGURE]

Figure 3. Glucose- insulin endocrine metabolic regulatory system. The dashed lines indicate that exercises and fasting consume glucose and lower the glucose concentration, which signals the pancreas to release glucagon in the liver converts glycogen to glucose. The solid lines indicate that the glucose infusion elevates the plasma glucose concentration level which signals the pancreas to secrete insulin and decrease plasma glucose.

[FIGURE]

Figure 1.2.1. Glucose-Insulin Regulatory System

The dashed lines indicate that exercises and fasting consume glucose and lower the glucose concentration, which signals the pancreas to release glucagon and the liver converts the glucagon and glycogen to glucose. The solid lines indicate that the glucose infusion elevate the plasma glucose concentration level which signals the pancreas to secrete insulin and consume the glucose. (This figure is adapted from [96].)


[96] http://www.endocrineweb.com/insulin.html

Anmerkungen

The two figures are similar, but not identical.

Neither the source Li (2004) is mentioned, or the original source [1], from where Li has taken some inspiration.

The figure caption cannot be found in the original source.

Sichter
(Hindemith) LieschenMueller

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