Metabolic syndrome pathophysiology: Difference between revisions
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===Associated Disorders=== | ===Associated Disorders=== | ||
*[[Polycystic ovarian syndrome]] | *[[Polycystic ovarian syndrome]] | ||
*[[Hemochromatosis]](iron overload) | *[[Hemochromatosis]] (iron overload) | ||
==References== | ==References== | ||
Revision as of 16:36, 2 May 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.