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Role of Serum and Glucocoritcoid [sic] inducible Kinase SGK1 in the regulation of glucose transport

von Dr. Sankarganesh Jeyaraj

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[1.] Sj/Fragment 002 01 - Diskussion
Zuletzt bearbeitet: 2015-05-30 19:12:37 Hindemith
Fragment, Gesichtet, KomplettPlagiat, Li 2004, SMWFragment, Schutzlevel sysop, Sj

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KomplettPlagiat
Bearbeiter
Graf Isolan, Hindemith
Gesichtet
Untersuchte Arbeit:
Seite: 2, Zeilen: 2 ff. (entire page)
Quelle: Li 2004
Seite(n): 2, 3, 4, 11, Zeilen: 2:21 ff.; 3: 1 ff.; 4: 1 ff.; 11: 2 ff.
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.

Sichter
(Graf Isolan), (Hindemith), SleepyHollow02



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