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==Pathophysiology== | ==Pathophysiology== | ||
* The cause of the [[metabolic syndrome]] is unknown. | * The cause of the [[metabolic syndrome]] is unknown. | ||
* The pathophysiology is extremely complex and has only been partially elucidated. | * The pathophysiology is extremely complex and has only been partially elucidated. | ||
* Most patients are older, obese, sedentary, and have a degree of [[insulin resistance]]. | * Most patients are older, obese, sedentary, and have a degree of [[insulin resistance]]. | ||
* The most important factors in order are 1) aging, 2) genetics and 3) lifestyle (i.e., decreased physical activity and excess caloric intake). | * The most important factors in order are 1) aging, 2) genetics and 3) lifestyle (i.e., decreased physical activity and excess caloric intake). | ||
* There is debate regarding whether obesity or insulin resistance is the ''cause'' of the metabolic syndrome or if it is a by-product of a more far-reaching metabolic derangement <ref name="pmid18356555">{{cite journal| author=Després JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E et al.| title=Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. | journal=Arterioscler Thromb Vasc Biol | year= 2008 | volume= 28 | issue= 6 | pages= 1039-49 | pmid=18356555 | doi=10.1161/ATVBAHA.107.159228 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18356555 }} </ref> | * There is debate regarding whether obesity or insulin resistance is the ''cause'' of the metabolic syndrome or if it is a by-product of a more far-reaching metabolic derangement <ref name="pmid18356555">{{cite journal| author=Després JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E et al.| title=Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. | journal=Arterioscler Thromb Vasc Biol | year= 2008 | volume= 28 | issue= 6 | pages= 1039-49 | pmid=18356555 | doi=10.1161/ATVBAHA.107.159228 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18356555 }} </ref> | ||
* Systemic [[inflammation]]: a number of inflammatory markers (including [[C-reactive protein]]) are often increased, as are [[fibrinogen]], [[interleukin 6]] (IL−6), [[Tumor necrosis factor-alpha]] (TNFα) and others. | * Systemic [[inflammation]]: a number of inflammatory markers (including [[C-reactive protein]]) are often increased, as are [[fibrinogen]], [[interleukin 6]] (IL−6), [[Tumor necrosis factor-alpha]] (TNFα) and others. | ||
* Some have pointed to [[oxidative stress]] due to a variety of causes including dietary [[fructose]] mediated increased uric acid levels.<ref>{{cite journal | author=Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ | title=A causal role for uric acid in fructose-induced metabolic syndrome | journal=Am J Phys Renal Phys | year=2006 | volume=290 | issue=3 | pages= F625–F631 | id=PMID 16234313}}</ref><ref>{{cite journal | author=Hallfrisch J | title=Metabolic effects of dietary fructose | journal=FASEB J | year=1990 | volume=4 | issue=9 | pages= 2652–2660 | id=PMID 2189777}}</ref><ref>{{cite journal | author=Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ | title=Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch | journal= Am J Clin Nutr | year=1989 | volume=49 | issue=5 | pages= 832–839 | id=PMID 2497634}}</ref> | * Some have pointed to [[oxidative stress]] due to a variety of causes including dietary [[fructose]] mediated increased uric acid levels.<ref>{{cite journal | author=Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ | title=A causal role for uric acid in fructose-induced metabolic syndrome | journal=Am J Phys Renal Phys | year=2006 | volume=290 | issue=3 | pages= F625–F631 | id=PMID 16234313}}</ref><ref>{{cite journal | author=Hallfrisch J | title=Metabolic effects of dietary fructose | journal=FASEB J | year=1990 | volume=4 | issue=9 | pages= 2652–2660 | id=PMID 2189777}}</ref><ref>{{cite journal | author=Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ | title=Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch | journal= Am J Clin Nutr | year=1989 | volume=49 | issue=5 | pages= 832–839 | id=PMID 2497634}}</ref> | ||
* Commonly, there is development of [[visceral fat]] followed by the [[adipocyte]]s (fat [[Cell (biology)|cell]]s) of the visceral fat increasing [[blood plasma|plasma]] levels of TNFα and altering levels of a number of other substances (e.g., adiponectin, resistin, PAI-1). | * Commonly, there is development of [[visceral fat]] followed by the [[adipocyte]]s (fat [[Cell (biology)|cell]]s) of the visceral fat increasing [[blood plasma|plasma]] levels of TNFα and altering levels of a number of other substances (e.g., adiponectin, resistin, PAI-1). | ||
* TNFα has been shown to not only cause the production of inflammatory [[cytokine]]s, but may also trigger cell signaling by interaction with a TNFα [[Receptor (biochemistry)|receptor]] that may lead to insulin resistance. | * TNFα has been shown to not only cause the production of inflammatory [[cytokine]]s, but may also trigger cell signaling by interaction with a TNFα [[Receptor (biochemistry)|receptor]] that may lead to insulin resistance. | ||
* An experiment with rats that were fed a diet one-third of which was [[sucrose]] has been proposed as a model for the development of the metabolic syndrome. The sucrose first elevated blood levels of [[triglyceride]]s, which induced [[visceral]] fat and ultimately resulted in insulin resistance <ref>{{cite journal | author=Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. | title=Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats | journal=Exp Biol Med | year=2004 | volume=229 | issue=6 | pages= 486–493 | url=http://www.ebmonline.org/cgi/content/full/229/6/486 | id=PMID 15169967}}</ref>. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome. | * An experiment with rats that were fed a diet one-third of which was [[sucrose]] has been proposed as a model for the development of the metabolic syndrome. The sucrose first elevated blood levels of [[triglyceride]]s, which induced [[visceral]] fat and ultimately resulted in insulin resistance <ref>{{cite journal | author=Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. | title=Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats | journal=Exp Biol Med | year=2004 | volume=229 | issue=6 | pages= 486–493 | url=http://www.ebmonline.org/cgi/content/full/229/6/486 | id=PMID 15169967}}</ref>. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome. | ||
==Associated | ==Associated Disorders== | ||
*[[Polycystic ovarian syndrome]] | *[[Polycystic ovarian syndrome]] | ||
*[[Hemochromatosis]](iron overload) | *[[Hemochromatosis]](iron overload) | ||
==References== | ==References== | ||
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[[Category:Metabolic disorders]] | [[Category:Metabolic disorders]] | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] | ||
[[Category:Syndromes]] | [[Category:Syndromes]] | ||
[[Category: | [[Category:Disease]] | ||
Revision as of 19:14, 29 April 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Overview
Metabolic syndrome are characterized by a cluster of conditions that greatly increases the risk of a person to develop heart diseases, diabetes and stroke. By definition one is said to have a metabolic syndrome if they have 3 of the following 5 conditions: high blood pressure (>130/85), abnormal fasting blood glucose > 100 mg/dl, increased weight around the waist (women > 35 inches, male > 40 inches), triglycerides > 150 mg/dl and a low HDL (female < 50, male < 40).
Pathophysiology
- The cause of the metabolic syndrome is unknown.
- The pathophysiology is extremely complex and has only been partially elucidated.
- Most patients are older, obese, sedentary, and have a degree of insulin resistance.
- The most important factors in order are 1) aging, 2) genetics and 3) lifestyle (i.e., decreased physical activity and excess caloric intake).
- There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if it is a by-product of a more far-reaching metabolic derangement [1]
- Systemic inflammation: a number of inflammatory markers (including C-reactive protein) are often increased, as are fibrinogen, interleukin 6 (IL−6), Tumor necrosis factor-alpha (TNFα) and others.
- Some have pointed to oxidative stress due to a variety of causes including dietary fructose mediated increased uric acid levels.[2][3][4]
- Commonly, there is development of visceral fat followed by the adipocytes (fat cells) of the visceral fat increasing plasma levels of TNFα and altering levels of a number of other substances (e.g., adiponectin, resistin, PAI-1).
- TNFα has been shown to not only cause the production of inflammatory cytokines, but may also trigger cell signaling by interaction with a TNFα receptor that may lead to insulin resistance.
- An experiment with rats that were fed a diet one-third of which was sucrose has been proposed as a model for the development of the metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance [5]. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome.
Associated Disorders
- Polycystic ovarian syndrome
- Hemochromatosis(iron overload)
References
- ↑ Després JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E; et al. (2008). "Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk". Arterioscler Thromb Vasc Biol. 28 (6): 1039–49. doi:10.1161/ATVBAHA.107.159228. PMID 18356555.
- ↑ Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ (2006). "A causal role for uric acid in fructose-induced metabolic syndrome". Am J Phys Renal Phys. 290 (3): F625&ndash, F631. PMID 16234313.
- ↑ Hallfrisch J (1990). "Metabolic effects of dietary fructose". FASEB J. 4 (9): 2652&ndash, 2660. PMID 2189777.
- ↑ Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ (1989). "Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch". Am J Clin Nutr. 49 (5): 832&ndash, 839. PMID 2497634.
- ↑ Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. (2004). "Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats". Exp Biol Med. 229 (6): 486&ndash, 493. PMID 15169967.