Metabolic Syndrome - Serum & Plasma

Detect, Assess, Guide...

Obesity will be among the greatest influences on morbidity and mortality in the coming decades. A major contributor to obesity is "Metabolic Syndrome," defined by a combination of clinical and laboratory parameters, including:

• Central obesity (Increased waist to hip ratio due to excessive fat tissue in and around the abdomen)
• Raised blood pressure (130/85 mmHg or higher)
• Dyslipidemia (Mainly high triglycerides and low HDL)
• Insulin resistance (Hyperinsulinemia)
• Proinflammatory state (Elevated plasma AA/EPA ratio)

Metabolic Syndrome has widely replaced earlier references to "Syndrome X," although a more descriptive term might be Insulin Insensitivity Syndrome. The most direct cause of Metabolic Syndrome is declining responsiveness to insulin, leading to increased pancreatic insulin output to maintain normal blood glucose. The characteristic laboratory pattern is normal fasting serum glucose with elevated fasting insulin. Increased circulating insulin also stimulates the biosynthesis of fatty acids and cholesterol, raising serum levels of these lipids.

Elevated levels of the nitric oxide inhibitor ADMA* (asymmetric dimethylarginine) is one of the most sensitive markers of insulin insensitivity. There is a clear relationship between the loss of insulin sensitivity and the rise of plasma ADMA levels. Dietary modifications of antioxidant vitamins and folic acid have been shown to successfully lower ADMA levels.

Balancing eicosanoid precursor fatty acids also helps to reverse metabolic syndrome. Any increase in inflammatory tendencies can exacerbate the effects of insulin insensitivity. When the plasma ratio of arachidonic acid (AA) to eicosapentaenoic acid (EPA) is high, the response of every tissue to inflammatory signals is exaggerated. This pro-inflammatory response tends to raise ADMA levels, propagating a vicious, feed-forward cycle. Such a cycle can be broken by fish oil supplements to raise EPA levels and lower the AA/EPA Ratio.

Factors contributing to Metabolic Syndrome are:

• Lifestyle, including high dietary carbohydrate (especially simple sugars) and physical inactivity that leads to low lean body mass
• Individual genetics
• Nitric oxide inhibition and eicosanoid imbalance leading to insulin insensitivity

The Metabolic Syndrome* Profile:

• Detects insulin insensitivity and dyslipidemic sequelae
  • Insulin
  • Glucose
  • HDL cholesterol
  • Triglycerides
• Assesses underlying factors of nitric oxide and eicosanoid cell response regulators
• ADMA
• Arachidonic acid (AA)
• Eicosapentaenoic acid (EPA)
• AA/EPA ratio
• Guides interventions to restore and monitor metabolic function

*Some analytes may not be reported in New York profiles. Please see Clinician Info and CPT codes for details

*ADMA not reported in New York

Test name:	0146 - Metabolic Syndrome Profile
Description:	Metabolic Syndrome is characterized by a group of metabolic risk factors that include: central obesity, dyslipidemia, elevated blood pressure, insulin resistance or glucose intolerance, increased tendency to clot, and inflammation. The Metametrix Metabolic Syndrome Profile compiles several laboratory markers of the metabolic syndrome together, allowing for a more comprehensive evaluation. The cutting-edge marker, ADMA*, accentuates the innovative combination of analytes within this profile, allowing clinicians to have an unprecedented view into endothelial function.
Method:	LC/MS-MS, GC/MS, Spectrophotometry, Chemiluminescence Assay
Turnaround time:	8-12 days, 10 days average
Analytes:	HDL Cholesterol Triglycerides Glucose Insulin ADMA (Asymmetric Dimethylarginine)* AA/EPA Ratio *Not reported in New York profiles

83718 - HDL Cholesterol 84478 - Triglycerides 82947 - Glucose 83525 - Insulin 82131 - Amino acids, 2-5, quantitative* 82726 x2 - Fatty acids, x2 *Not reported in New York

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	References Metabolic Syndrome
	Association of total cholesterol/ high-density lipoprotein cholesterol ratio with proximal coronary atherosclerosis detected by multislice computed tomography. Nair D, Carrigan TP, Curtin RJ, Prev Cardiol. 2009 Winter;12(1):19-26. Fish oil and the management of hypertriglyceridemia. Mattar M, Obeid O. Nutr Health. 2009;20(1):41-9. Human C-reactive protein and the metabolic syndrome. Devaraj S, Singh U, Jialal I. Curr Opin Lipidol. 2009 Apr 14. C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham Offspring Study. Rutter MK, Meigs JB, Sullivan LM, D'Agostino RB Sr, Wilson PW. Circulation. 2004 Jul 27;110(4):380-5. Epub 2004 Jul 19. The impact of age, body mass index, and fish intake on the EPA and DHA content of human erythrocytes. Sands SA, Reid KJ, Windsor SL, Harris WS. Lipids. 2005 Apr;40(4):343-7. Tissue n-3 and n-6 fatty acids and risk for coronary heart disease events. Harris WS, Poston WC, Haddock CK. Atherosclerosis. 2007 Jul;193(1):1-10. Epub 2007 May 15. Blood omega-3 and trans fatty acids in middle-aged acute coronary syndrome patients. Harris WS, Reid KJ, Sands SA, Spertus JA. Am J Cardiol. 2007 Jan 15;99(2):154-8. ocSum Asymmetric dimethylarginine causes hypertension and cardiac dysfunction in humans and is actively metabolized by dimethylarginine dimethylaminohydrolase. Achan V, Broadhead M, Malaki M, et al. Arterioscler Thromb Vasc Biol. Aug 1 2003;23(8):1455-1459. Mild-to-moderate hypertriglyceridemia in young men is associated with endothelial dysfunction and increased plasma concentrations of asymmetric dimethylarginine. Lundman P, Eriksson MJ, Stuhlinger M, Cooke JP, Hamsten A, Tornvall P. J Am Coll Cardiol. Jul 2001;38(1):111-116. Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor. Stuhlinger MC, Abbasi F, Chu JW, et al. Jama. Mar 20 2002;287(11):1420-1426.