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Lipid Profile (Triglycerides) 

  • Author: Blake Morris, MD; Chief Editor: Eric B Staros, MD  more...
 
Updated: Feb 11, 2014
 

Reference Range

Triglycerides are lipid compounds composed of a glycerol esterified to 3 fatty acid chains of varying length and composition. These fatty acid chains can be saturated or unsaturated, and the chemical composition of each chain is different. Each chain consists of carbon and hydrogen atoms with varying single or double-bonded chains, depending on the degree of saturation or unsaturation. Triglycerides are formed of mixed chains, and the structural comparison between the chains is heterogenous in nature.

Serum triglyceride levels and classifications are as follows[1] :

  • Less than 100 mg/dL - Optimal
  • 101-150 mg/dL - Normal
  • 150-199 mg/dL - Borderline
  • 200-499 mg/dL - High
  • 500 mg/dL or higher - Very high
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Interpretation

Normal values of triglycerides (TG) are less than 150mg/dL. Unusually low levels of triglycerides can be present in disease states, producing syndromes of malabsorption in addition to patients who carry genes for familial hypobetalipoproteinemia.[2, 3]

Elevated triglycerides are determined based upon serum laboratory values being greater than 149mg/dL. Levels greater than 149 mg/dL constitute hypertriglyceridemia, and severity of TG is further classified by serum values falling within classification value ranges. Analysis of the significance of hypertriglyceridemia should take into account coexisting dyslipidemias. Hypertriglyceridemia is indicative of insulin resistance when present with low high-density lipoprotein (HDL) and elevated low-density lipoprotein (LDL), while elevated triglyceride is a clinical risk factor for coronary artery disease (CAD), especially when low HDL is present.[4, 5] Additionally, TG of 150 mg/dL or greater is one criterion for metabolic syndrome and can aid in the diagnosis when present with 2 additional criteria.[6, 7]

Very high levels of triglycerides are defined by serum levels of 500mg/dL or greater and can be concerning for development of pancreatitis.[4] If pancreatitis is likely or potentially threatening and levels of triglycerides are found to be 1000 mg/dL or greater, immediate institution of lipid lowering therapy should begin.[1, 6, 8]

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Collection and Panels

Triglycerides

See the list below:

  • Patient preparation - Fasting specimen
  • Specimen - Blood
  • Collection method - Routine venipuncture
  • Container - Light-green tube, gold tube
  • Anticoagulant - Lithium heparin (light green), clotting factors (gold)
  • Storage/transport temperature - Refrigerated
  • Stability (after separation) - Ambient: 72 h; Refrigerated: 1 week; Frozen: 3 months

Panels

Serum triglyceride is typically part of the following panels:

  • Lipid panel
  • Lipid profile
  • Cardiac prevention panel
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Background

Description

Triglycerides are lipid compounds composed of a glycerol esterified to 3 fatty acid chains of varying length and composition. These fatty acid chains can be saturated or unsaturated, and the chemical composition of each chain is different. Each chain consists of carbon and hydrogen atoms with varying single or double-bonded chains, depending on the degree of saturation or unsaturation. Triglycerides are formed of mixed chains, and the structural comparison between the chains is heterogenous in nature.

Triglyceride is the most abundant dietary lipid compound found throughout the diet and is the method with which energy is stored in the body. Initial digestion of dietary triglycerides takes place with pancreatic lipase, which hydrolyzes one fatty acid chain at a time to form 2 free fatty acid (FFA) chains and one 2-monoglyceride (2MG) compound per each triglyceride. Bile salts are released in the duodenum in response to cholecystokinin release occurring in the presence of lipid compounds within the ingesta. Bile salts aid in forming lipid micelles, which create a hydrophilic surface with a hydrophobic core of lipid molecules, including FFA.

Absorption of lipid compounds into the enterocyte for biochemical usage occurs through diffusion across the cellular membrane and also through lipid transporters that are located on the luminal side of the enterocyte. Once in the enterocyte, FFA chains and 2MG compounds are transported to the endoplasmic reticulum, where they are reformed into triglycerides and packaged into chylomicrons in the golgi apparatus to receive chylomicron specific apolipoproteins, namely apo B48, which is a marker for TG chylomicron. These newly formed chylomicrons are then released from the enterocyte and transported to circulation by the lymphatic system.[9]

Once in the circulation, the triglyceride-rich chylomicrons pass through the vasculature, where they undergo a complex process of protein exchange mediated by HDL and, based upon this protein exchange process, are either received in the liver for further metabolism and packaging or undergo delipidation at the vascular endothelial surface by lipoprotein lipase (LPL).[9] The largest proportion of chylomicrons containing dietary triglycerides undergo hepatic uptake, where triglycerides are packaged into very-low dense lipoprotein (VLDL) for transport to peripheral tissues.

VLDL is the major carrier of triglycerides and FFA in serum and is synthesized within the hepatocyte, while a smaller percentage of FFA travels in a unesterified form, which is complexed to albumin for transport.[10] Once the VLDL is release into serum, it travels to peripheral tissues where it undergoes a delipidation cascade, and triglyceride is removed by LPL at multiple LPL receptor sites along the endothelium.[9] Following delipidation, a VLDL remnant (IDL) is formed, which has released the bulk of triglyceride originally packaged and is cleared by the liver or transformed to LDL by serum protein exchange process.

Triglyceride is the major high-energy compound for energy storage supplying 9 Kcal/g of FFA. Those lipids that are intended for storage are recognized by and are removed from VLDL by LPL as well as storage specific transmembrane proteins that aid in a process of lipid droplet formation within adipocytes and muscle tissue for use later as an energy source.[9, 11] Liberation of triglycerides from lipid stores begins under metabolic stressors when circulating systemic nutrient supply is not sufficient to meet metabolic energy demand.

Regulation of enzymes needed for lipolysis occur through cyclic adenosine monophosphate (cAMP)–mediated and cAMP-independent pathways that activate adipose triglyceride lipase, hormone-sensitive lipase, and monoacylglycerol lipase, which hydrolyzes the ester bonds of stored triglyceride producing glycerol and FFA chains.[12] Glycerol undergoes cellular removal through transcellular aquaporins, and FFAs are either moved to serum, esterified or metabolized into signaling molecules.[12]

Once FFA has been liberated from adipocytes for use in energy production they are transported and received by cells for metabolism and mobilized to intracellular mitochondria and peroxisomes for use. These lipid compounds undergo fatty acid oxidation, providing acetyl-CoA for hepatic ketogenesis and substrates for energy production through oxidative phosphorylation.[10]

Triglycerides and FFA have been implicated in playing a role in atherosclerotic disease formation. High triglyceride is a marker for elevated levels of atherogenic lipoproteins that contain triglyceride and FFA.[13] As mentioned previously, elevation of triglycerides can indicate insulin resistance in the setting of low levels of HDL and elevated LDL.[4, 13] Patients with this lipid profile typically have elevated VLDLs, small LDL and HDL particles, and have elevated levels of circulating chylomicrons and places patients at risk for coronary heart disease.[13] Hypertriglyceridemia is a clinical risk factor for coronary artery disease (CAD), especially when low HDL is present, and should be considered a continued risk factor despite adequate control of LDL cholesterol.[4, 5, 13]

Indications/Applications

The USPSTF recommends lipid screening in both men and women who are at increased risk for coronary heart disease, men aged 35 years and older, or women aged 45 years and older.[14] AHRQ has similar recommendations to start routine screening at age 35 years or in those patients who have heart disease risk factors and aged 20-35 years.[15] Currently, no guidelines support routine screening of lipids in young adults aged 20-35 years without risks of coronary heart disease. Likewise, supporting evidence of routine lipid screening in children is lacking, and, therefore, no recommendation exists. The NCEP Report of the Expert Panel on Blood Cholesterol levels in Children and Adolescents recommends screening lipid panels as routine health care in children of families in which premature heart disease is evident or familial dyslipidemias are established.[16]

Secondary causes for hypertriglyceridemia can be a source for abnormal triglyceride on screening lipid panel, and clinical investigation should aim at discovering suspected secondary causes and treating appropriately. Possible etiologies of secondary hypertriglyceridemia include disease states such as uncontrolled diabetes, nephrotic syndrome, end-stage renal disease, hypothyroidism, and HIV.[17]

Common substances and medications that may be responsible for elevation of triglycerides include but are not limited to ethanol, corticosteroids, noncardioselective beta-blockers, thiazide diuretics, bile-binding resins, oral estrogens, progestins, and tamoxifen, as well as antiretroviral therapy.[17, 18] Patients on medications or ingesting substances known to raise triglycerides who are at risk for developing secondary hypertriglyceridemia in the setting of CAD, diabetes, disease states secondarily elevating triglycerides, or other coronary artery disease–equivalent states should receive routine screening. Additionally, surveillance lipid profiles should be considered at appropriate intervals with attention to removal of secondary causes of hypertriglyceridemia or institution of triglyceride-lowering therapy as needed.

Very-high levels of triglyceride can place patients at risk for the development of pancreatitis and work-up of a new diagnosis of pancreatitis should include a baseline lipid panel to investigate triglyceride levels.[1] Patients who present with extraordinarily high lipids levels or patients that have pancreatitis due to hypertriglyceridemia should have institution of triglyceride-lowering therapy, investigation of factors causing secondary hypertiglyceridemia, and consideration of concomitant familial dyslipidemia.[6, 8]

Considerations

Recently published ACC/AHA cholesterol guidelines have not provided guideline specifics pertaining to triglycerides, but a 2011 scientific statement describes the screening processes of special populations[1, 19] beyond the scope of this article. The clinical applicability of the lipid panel for analyzing triglyceride levels rests on the clinician's understanding of patient risk factors and use of those risk factors as guides to screening patients for hypertriglyceridemia and other dyslipidemias.

Once lipid-lowering therapy has been initiated, surveillance of lipid levels should continue until lipid levels are at recommended goal levels based upon the patient’s risk factor profile, with yearly checks thereafter. Continued surveillance of lipid panels should persist if any adjustments in therapy occur or if poor compliance to therapy is suspected. Screening lipid panel can show falsely positive high-triglyceride levels and occurs in patients who have consumed a meal high in lipidcompounds and have not fasted for 8 hours prior to venipuncture. Also, patients who have recently consumed ethanol can have elevation of triglycerides that may not necessarily be indicative of baseline levels.

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Contributor Information and Disclosures
Author

Blake Morris, MD Chief Medical Resident, Department of Internal Medicine, University of Oklahoma College of Medicine

Blake Morris, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Oklahoma State Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011 May 24. 123(20):2292-333. [Medline].

  2. Klapproth JA, Yang VW. Malabsorption work up. Medscape Reference. Available at http://emedicine.medscape.com/article/180785-workup. Accessed: 3/25/12.

  3. Singh VN, Citkowitz E. Low LDL Cholesterol (Hypobetalipoproteinemia). Medscape Reference. Available at http://emedicine.medscape.com/article/121975-workup. Accessed: 3/29/12.

  4. Solano MP, Goldberg RB. Lipid management in type 2 diabetes. Clin Diab. 2006. 24:27-32.

  5. Abdel-Maksoud MF, Hokanson JE. The complex role of triglycerides in cardiovascular disease. Semin Vasc Med. 2002. 2:325-333.

  6. Grundy SM, Cleeman JI, Danies SR, et al. Diagnosis and management of the metabolic syndrome: An American Heart Association/National Heart, Lung and Blood Institute scientific statement. Circulation. 2005. 112(17):2735-2752.

  7. Wang SS, Subhi Y, Pearlman JD, Talavera F. Metabolic Syndrome. Medscape Reference. Available at http://emedicine.medscape.com/article/165124-overview. Accessed: 3/29/12.

  8. Fletcher B, Berra K, Ades P, et al. Managing abnormal blood lipids:a collaborative approach. Circulation. 2005. 112(20):3184-3209.

  9. Fielding CJ, Fielding PE. Oxidation of fatty acids in eukaryotes. Vance DE, Vance JE. Biochemistry of Lipids, Lipoproteins and Membranes. 5th ed. The Netherlands: Elselvier; 2008. 131-154.

  10. Horst S. Oxidation of fatty acids in eukaryotes. Vance DE, Vance JE. Biochemistry of Lipids, Lipoproteins and Membranes. 5th ed. The Netherlands: Elselvier; 2008. 533-554.

  11. Gross D, Zhan C, Silver DL. Direct binding of triglyceride to fat storage-inducing transmembrane proteins 1 and 2 is important for lipid droplet formation. PNAS. 2011. 108(49):19581-86.

  12. Hertzel AV, Thompson BR, Wiczer BM, Bernlohr DA. Lipid metabolism in adipose tissue. Vance DE, Vance JE. Biochemistry of Lipids, Lipoproteins and Membranes. 5th ed. The Netherlands: Elselvier; 2008.

  13. Talayero BG, Sacks FM. The role of triglycerides in atherosclerosis. Curr Cardiol Rep. 2001. 13(6):277-304.

  14. U.S. Preventive Services Task Force. Screening for Lipid Disorders in Adults, Topic Page. June 2008. Available at http://www.uspreventiveservicestaskforce.org/uspstf/uspschol.htm. Accessed: January 2, 2014.

  15. [Guideline] Agency for Healthcare Reasearch and Quality. Screening and Management of Lipids. Available at http://guideline.gov/content.aspx?id=14421. Accessed: January 2, 2014.

  16. [Guideline] NCEP: Highlights of the report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescent. Pediatrics. 1992. 89:495-501.

  17. Brunzell JD. Hypertriglyceridemia. N Engl J Med. 2001. 357(10):1009-15.

  18. Yuan G, Al-Shali KZ, Hegele RA. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ. 2007. 176(8):1113-1120.

  19. [Guideline] Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Nov 12. [Medline].

 
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