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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.
*ADMA not reported in New York |
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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
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Clinician Info
| Test name: |
0146 - Metabolic Syndrome Profile
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| 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.
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| Method: |
LC/MS-MS, GC/MS, Spectrophotometry, Chemiluminescence Assay |
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| Turnaround time: |
8-12 days, 10 days average |
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Analytes:
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HDL Cholesterol
Triglycerides
Glucose
Insulin
ADMA (Asymmetric Dimethylarginine)*
AA/EPA Ratio
*Not reported in New York profiles
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CPT codes:
| 83718 |
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| HDL Cholesterol |
| 84478 |
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| Triglycerides |
| 82947 |
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| Glucose |
| 83525 |
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| Insulin |
| 82131 |
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| Amino acids, 2-5, quantitative* |
| 82726 x2 |
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| Fatty acids, x2 |
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| *Not reported in New York |
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Biochemical evidence for impaired nitric oxide synthesis in patients with peripheral arterial occlusive disease
Boger RH, Bode-Boger SM, Thiele W, Junker W, Alexander K, Frolich JC [see comments]. Circulation. 1997;95(8):2068-2074.
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.
Plasma asymmetric dimethylarginine and hyperemic myocardial blood flow in young subjects with borderline hypertension or familial hypercholesterolemia.
Paiva H, Laakso J, Laine H, Laaksonen R, Knuuti J, Raitakari OT. J Am Coll Cardiol. Oct 2 2002;40(7):1241-1247.
Oral L-arginine improves endothelial function in healthy individuals older than 70 years.
Bode-Boger SM, Muke J, Surdacki A, Brabant G, Boger RH, Frolich JC. Vasc Med. May 2003;8(2):77-81.
Asymmetrical dimethylarginine (ADMA) in critically ill patients: high plasma ADMA concentration is an independent risk factor of ICU mortality.
Nijveldt RJ, Teerlink T, Van Der Hoven B, et al. Clin Nutr. Feb 2003;22(1):23-30.
Increased levels of asymmetric dimethylarginine in populations at risk for atherosclerotic disease.
Eid HM, Eritsland J, Larsen J, Arnesen H, Seljeflot I. Effects of pravastatin. Atherosclerosis. Feb 2003;166(2):279-284.
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.
Dietary composition as a determinant of plasma asymmetric dimethylarginine in subjects with mild hypercholesterolemia.
Paiva H, Lehtimaki T, Laakso J, et al. Metabolism. Aug 2004;53(8):1072-1075.
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.
Plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, is elevated in hyperthyroid patients.
Hermenegildo C, Medina P, Peiro M, et al. J Clin Endocrinol Metab. Dec 2002;87(12):5636-5640.
Does ADMA cause endothelial dysfunction?
Cooke JP. Arterioscler Thromb Vasc Biol. 2000;20(9):2032-2037.
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