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At a Glance

Why Get Tested?

To determine if you have a leptin deficiency that is contributing to obesity; to identify increased leptin; on a research basis to help understand leptin’s roles in the body and its ties to obesity

When To Get Tested?

When a child has severe obesity that may be due to a very rare inherited leptin deficiency; sometimes to help evaluate obesity; when participating in a research study

Sample Required?

A blood sample drawn from a vein in your arm

Test Preparation Needed?


You may be able to find your test results on your laboratory’s website or patient portal. However, you are currently at Testing.com. You may have been directed here by your lab’s website in order to provide you with background information about the test(s) you had performed. You will need to return to your lab’s website or portal, or contact your healthcare practitioner in order to obtain your test results.

Testing.com is an award-winning patient education website offering information on laboratory tests. The content on the site, which has been reviewed by laboratory scientists and other medical professionals, provides general explanations of what results might mean for each test listed on the site, such as what a high or low value might suggest to your healthcare practitioner about your health or medical condition.

The reference ranges for your tests can be found on your laboratory report. They are typically found to the right of your results.

If you do not have your lab report, consult your healthcare provider or the laboratory that performed the test(s) to obtain the reference range.

Laboratory test results are not meaningful by themselves. Their meaning comes from comparison to reference ranges. Reference ranges are the values expected for a healthy person. They are sometimes called “normal” values. By comparing your test results with reference values, you and your healthcare provider can see if any of your test results fall outside the range of expected values. Values that are outside expected ranges can provide clues to help identify possible conditions or diseases.

While accuracy of laboratory testing has significantly evolved over the past few decades, some lab-to-lab variability can occur due to differences in testing equipment, chemical reagents, and techniques. This is a reason why so few reference ranges are provided on this site. It is important to know that you must use the range supplied by the laboratory that performed your test to evaluate whether your results are “within normal limits.”

For more information, please read the article Reference Ranges and What They Mean.

What is being tested?

Leptin is a hormone that helps regulate appetite by signaling hunger satisfaction (satiety). This test measures the amount of leptin in the blood to detect a deficiency that may be contributing to obesity.

Leptin is produced primarily by fat cells (adipocytes) and to a lesser degree by other tissues, including the placenta in pregnant women. It is transported in the blood receptors in the hypothalamus in the brain. When sufficient food has been consumed, it tells the body that it is no longer hungry. In a normal feedback response, a low level of leptin triggers hunger and an increase in food consumption. As the level of leptin rises from an increase in fat cells, hunger diminishes and food consumption drops off.

Insufficient leptin can cause persistent hunger as the body attempts to protect itself from perceived underfeeding (starvation). Very rare inherited leptin deficiencies can cause severe obesity through constant hunger and constant eating that starts in early childhood. Leptin replacement therapy has been shown to be successful in treating some of those affected.

Obesity is most commonly associated with elevated leptin levels. This is thought to be due to a resistance to leptin that is similar to the insulin resistance often seen with obesity. People who are affected are resistant to the action of leptin—they continue to experience hunger even after consuming sufficient food. The body continues to produce more leptin in an attempt to compensate and in response to the perceived hunger. However, about 10% of those who are obese are estimated to have some degree of leptin deficiency.

There is significant interest in better understanding leptin’s ties to obesity. Obesity is a major health concern in the U.S. because it increases the risk of many conditions, such as high blood pressure (hypertension), dyslipidemias (high cholesterol and/or high triglycerides), type 2 diabetes, joint problems, sleep apnea, coronary heart disease, stroke, and some cancers. The rate of obesity has increased steadily over the last 20 years in all age ranges and, according to the Centers for Disease Control and Prevention, more than one-third of adults and 17% of children and teens in this country are currently classified as obese. Classification is based on body mass index or BMI. (See Common Questions below).

A recent study found that in some people a leptin level might be more accurate than the traditional body mass index in gauging how much excess fat a person is carrying. In general, the higher the level of leptin in the bloodstream, the more fat tissue a person has. In the study, this was especially true with older women and in those with large muscles or dense bones where the results of the BMI score could be misleading.

Research is ongoing to evaluate leptin’s roles in the body and the links between leptin and obesity, and between leptin and successful weight loss. There is also continued interest in determining whether a leptin-based treatment might be useful for those who are obese and leptin-deficient.

Common Questions

How is it used?

The leptin test is not ordered routinely and its usefulness in medical settings is yet to be fully established. Most testing is still performed in a research setting as the role of leptin is further investigated.

In clinical settings, the leptin test is most likely to be ordered on an obese child, especially if there is a family history of early-onset obesity. It may sometimes be ordered on an obese person who has symptoms of frequent, persistent hunger to detect a leptin deficiency or excess.

On occasion, the test may be used along with other tests, such as a lipid profile, thyroid panel, glucose, insulin, and/or A1c, to evaluate the health status of an obese person and to detect underlying conditions that may be contributing to or complicating their condition.

When is it ordered?

Leptin is primarily ordered during clinical studies, when it is performed to further investigate the role of leptin.

Leptin testing is not frequently ordered outside of a research setting, but it may sometimes be ordered when a child has been classified as obese, especially when there is a family history of early-onset obesity. (For classifications, see Common Questions below.)

Some doctors may order a leptin test when evaluating an obese person to determine whether they may have a leptin deficiency or an excess (to detect leptin resistance).

What does the test result mean?

In the obese, decreased leptin levels may indicate some degree of deficiency, while increased concentrations are thought to be associated with resistance to the effects of leptin. Most obese people will have increased levels, but about 10% may have some degree of leptin deficiency.

Very rarely, significantly decreased leptin levels may indicate an inherited leptin deficiency linked to severe obesity.

Leptin secretion follows a circadian pattern, meaning that the concentration in blood will vary throughout a 24-hour time period (higher at night than during the day).

Is there anything else I should know?

Women normally have higher leptin levels than men. Leptin concentrations are also increased during pregnancy and may be significantly increased in women with gestational diabetes or preeclampsia. The test is not, however, used to monitor these conditions.

The usefulness of leptin results in a medical setting, especially in evaluating excess or and deficient amounts of the hormone, is yet to be fully established. For instance, someone with a rare inherited deficiency may benefit from leptin replacement therapy, but there is not yet sufficient data to determine whether or not a person with a mild deficiency would also benefit from a targeted treatment.

Some of the other topics that have been or are being studied in association with leptin include its:

  • Contribution to inflammation and atherosclerosis or, conversely, its protection from atherosclerosis
  • Increase with gestational diabetes and with pre-eclampsia during pregnancy
  • Role in fertility
  • Association with depression, stress, and anxiety
  • Role in maintaining glucose levels and its interaction with insulin
  • Association between leptin levels, weight loss, and hunger

Should everyone who is overweight have a leptin test performed?

Leptin testing is not routinely performed and is not indicated for most people. If someone is obese and has persistent hunger, or has a young child who is severely obese, then leptin testing may be considered.

How are classifications of body weight determined?

Classification is currently based on body mass index, or BMI.

For youth, weight and height as well as age and sex are considered in determining their BMI percentile. An overweight youth is one whose BMI is between the 85th percentile and the 94th percentile on standardized growth charts. An obese youth is one who is at or above the 95th percentile on standardized growth charts or has a BMI of greater than or equal to 30 kg/m2, whichever is lower.

For adults, BMI is calculated as:

BMI = (Weight in pounds) / (height in inches squared) x 703

BMI                 Classification

Less than 18.5     Underweight

18.5 – 24.9         Normal weight

25.0 – 29.9         Overweight

30 and above      Obese


Can leptin testing be performed in my doctor's office?

No. Leptin testing is not performed in doctors’ offices and is not offered by most laboratories. The test will probably need to be sent to a reference laboratory.

What can I do to lower or increase leptin levels?

Leptin levels will often decrease when an obese person loses weight and increase when a person becomes obese, but they do not otherwise respond to lifestyle changes.

How is leptin deficiency treated?

In those with very rare inherited leptin deficiencies, replacement therapy has been successful in addressing obesity. However, there are insufficient data at this time to support its routine use for other leptin deficiencies.

Are there other adipokines besides leptin?

Although leptin was the first adipocyte cytokine (or “adipokine”) identified, many others have been discovered. The two that have been most extensively investigated are resistin, which increases insulin resistance, and adiponectin, which lowers it. Resistin is increased and adiponectin is decreased in obesity. They also have opposite effects on inflammation; resistin increases inflammation, while adiponectin decreases it. Another recently discovered adipokine is visfatin, which is elevated in type 2 diabetes and may play a role in elevating insulin levels. Several other adipokines are aplin, chemerin, and omentin, all of which appear to be anti-inflammatory.

View Sources

Sources Used in Current Review

Deck, C. et. al.(2017 April 7). Assessing the Functional Role of Leptin in Energy Homeostasis and the Stress Response in Vertebrates. Front Endocrinol (Lausanne). 2017; 8: 63. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384446/. Accessed on 05/01/17.

Londraville, R. et. al. (2017 April 10). On the Molecular Evolution of Leptin, Leptin Receptor, and Endospanin. Front Endocrinol (Lausanne). 2017; 8: 58. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385356/. Accessed on 05/01/17.

Kruljac, I. et. al. (2016). Changes in Metabolic Hormones After Bariatric Surgery and Their Predictive Impact on Weight Loss. Medscape Clinical Endocrinology from Clin Endocrinol. 2016;85(6):852-860. Available online at http://www.medscape.com/viewarticle/872569. Accessed on 05/01/17.

(© 2017). What Does Leptin Do? Hormone Health Network. Available online at http://www.hormone.org/hormones-and-health/what-do-hormones-do/cortisol/leptin. Accessed on 05/01/17.

Lee, C. et. al. (2015). Obesity, Adipokines and Cancer: An Update. Medscape Clinical Endocrinology from Clin Endocrinol. 2015;83(2):147-156. Available online at http://www.medscape.com/viewarticle/848555_1. Accessed on 05/01/17.

McCall, B. (2016 November 17). Medscape Conference News. Low Vitamin B12 and Leptin: Link to Metabolic Risk in Next Generation? Available online at http://www.medscape.com/viewarticle/872008. Accessed on 05/01/17.

Chawla, J. and Park, Y. (2016 June 29 Updated). Endocrine System Anatomy. Medscape Drugs and Diseases, Anatomy. Available online at http://emedicine.medscape.com/article/1948709-overview#showall. Accessed on 05/01/17.

Sources Used in Previous Reviews

Hamdy, O. (Updated 2013 January 24). Obesity. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/123702-overview#showall. Accessed February 2013.

(© 1995-2013). Leptin. Mayo Clinic Mayo Medical Laboratories [On-line information]. Available online at http://www.mayomedicallaboratories.com/test-catalog/Overview/91339. Accessed February 2013.

Miehle, K. et. al. (2012). Leptin, Adiponectin and Other Adipokines in Gestational Diabetes Mellitus and Pre-eclampsia. Medscape from Clin Endocrinol. 2012;76(1):2-11 [On-line information]. Available online at http://www.medscape.com/viewarticle/755467. Accessed February 2013.

Lawson, E. (2012). Leptin Levels are Associated With Decreased Depressive Symptoms in Women Across the Weight Spectrum, Independent of Body Fat. Medscape from Clin Endocrinol. 2012;76(4):520-525 [On-line information]. Available online at http://www.medscape.com/viewarticle/760937. Accessed February 2013.

Schwarz, S. and Windle, M. (Updated 2012 December 12). Obesity in Children. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/985333-overview. Accessed February 2013.

Chawla, J. and Youngsook P. (Updated 2012 October 3). Endocrine System Anatomy. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/1948709-overview#showall. Accessed February 2013.

Ahima, R. (2008 July 1). Revisiting leptin’s role in obesity and weight loss. J Clin Invest. V 118 (7):2380–2383. [On-line information]. Available online at http://www.jci.org/articles/view/36284. Accessed February 2013.

Koh, K. et. al. (2008). Contemporary Reviews in Cardiovascular Medicine, Leptin and Cardiovascular Disease, Response to Therapeutic Interventions [On-line information]. Circulation v 117: 3238-3249. [On-line information]. Available online at http://circ.ahajournals.org/content/117/25/3238.full. Accessed February 2013.

Ahmet Ursavas, A. et. al. (2010 July – September). Ghrelin, leptin, adiponectin, and resistin levels in sleep apnea syndrome: Role of obesity. Ann Thorac Med. 2010 Jul-Sep; 5(3): 161–165 [On-line information]. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930655/. Accessed February 2013.

Scheer, F. (2009 March 17). Adverse metabolic and cardiovascular consequences of circadian misalignment. PNAS v 106 (11) 4453-4458 [On-line information]. Available online at http://www.pnas.org/content/106/11/4453.long. Accessed February 2013.

Carlson, J. et. al. (2009 August 11). Pre- and post- prandial appetite hormone levels in normal weight and severely obese women. Nutrition & Metabolism v 6 (32) [On-line information]. Available online at http://www.nutritionandmetabolism.com/content/6/1/32. Accessed February 2013.

Farooqi, S. and O’Rahilly, S. (2006 December 1). Genetics of Obesity in Humans. Endocrine Reviews v 27 (7) 710-718. [On-line information]. Available online at http://edrv.endojournals.org/content/27/7/710.full. Accessed February 2013.

Franks, P. et. al. (2007 May). Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity. Journal of Applied Physiology c 102 (5) 1921-1926. [On-line information]. Available online at http://jap.physiology.org/content/102/5/1921.full. Accessed February 2013.

Stella L. Volpe, S. et. al. (2008 April). Effect of Diet and Exercise on Body Composition, Energy Intake and Leptin Levels in Overweight Women and Men. J Am Coll Nutr v 27 (2) 195-208 [On-line information]. Available online at http://www.jacn.org/content/27/2/195.full. Accessed February 2013.

Chiesa, C. et. al. (2008) Ghrelin, Leptin, IGF-1, IGFBP-3, and Insulin Concentrations at Birth: Is There a Relationship with Fetal Growth and Neonatal Anthropometry? Clinical Chemistry v 54 (3) 550–558 [On-line information]. Available online at http://www.clinchem.org/content/54/3/550.full. Accessed February 2013.

Henson, M. and Castracane, V. (2006 February 1). Leptin in Pregnancy: An Update. Biology of Reproduction v 74 (2) 218-229 [On-line information]. Available online at http://www.biolreprod.org/content/74/2/218.full. Accessed February 2013.

S17 Choquet, H. and Meyre, D. (2011 May) Genetics of Obesity: What have we Learned? Curr Genomics v 12(3): 169–179. [On-line information]. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137002/. Accessed February 2013.

Considine, R, et al. Serum Immunoreactive-Leptin Concentrations in Normal-Weight and Obese Humans. N Engl J Med 1996; 334:292-295. Available online at http://www.nejm.org/doi/full/10.1056/NEJM199602013340503#t=articleTop. Accessed February 2013.

Nirav R. Shah, Eric R. Braverman. Measuring Adiposity in Patients: The Utility of Body Mass Index (BMI), Percent Body Fat, and Leptin. PLoS One. Published April 2, 2012. Available online at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033308. Accessed February 2013.


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