Expected Turnaround Time
4 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum or plasma
Volume
0.5 mL
Minimum Volume
0.2 mL (Note: This volume does not allow for repeat testing.)
Container
Red-top tube, gel-barrier tube, or lavender-top (EDTA) tube
Collection
Transfer serum or plasma from cells and transfer to a plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
Temperature | Period |
|---|---|
Room temperature | 14 days |
Refrigerated | 30 days |
Frozen | 21 days |
Freeze/thaw cycles | Stable x3 |
Causes for Rejection
Gross lipemia; gross hemolysis
Test Details
Use
Measurement of leptin levels in serum or plasma
Limitations
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.
Obesity is not generally caused by leptin deficiency, neither mutations of the leptin gene or the leptin receptor gene are frequent in humans, but leptin levels are commonly higher in subjects with obesity, and insensitivity to endogenous leptin is a hallmark of most cases of human obesity.1
Methodology
Enzyme immunoassay (EIA)
Reference Interval
See tables.2
BMI | Tanner Stage 1−2 | Tanner Stage 3−4 | Tanner Stage 5 |
|---|---|---|---|
11 | 0.3−1.5 | 0.4−1.3 | 0.7−2.7 |
12 | 0.4−1.9 | 0.5−1.6 | 0.8−3.2 |
13 | 0.5−2.4 | 0.7−2.1 | 0.9−3.7 |
14 | 0.6−3.1 | 0.8−2.6 | 1.0−4.3 |
15 | 0.8−3.9 | 1.1−3.3 | 1.2−5.0 |
16 | 1.1−5.0 | 1.3−4.2 | 1.4−5.8 |
17 | 1.4−6.5 | 1.7−5.3 | 1.6−6.7 |
18 | 1.7−8.3 | 2.1−6.7 | 1.9−7.8 |
19 | 2.2−10.7 | 2.7−8.5 | 2.2−9.1 |
20 | 2.9−13.7 | 3.4−10.7 | 2.6−10.5 |
21 | 3.7−17.6 | 4.3−13.6 | 3.0−12.3 |
22 | 4.7−22.6 | 5.5−17.2 | 3.5−14.2 |
23 | 6.0−29.0 | 6.9−21.8 | 4.0−16.6 |
24 | 7.8−37.2 | 8.8−27.6 | 4.7−19.3 |
25 | 10.0−47.8 | 11.1−34.9 | 5.5−22.4 |
26 | 12.8−61.4 | 14.0−44.2 | 6.4−26.0 |
27 | 16.4−78.8 | 17.7−56.0 | 7.4−30.3 |
28 | 21.5−101.0 | 22.5−70.9 | 8.6−35.2 |
29 | 27.0−130.0 | 28.4−89.7 | 10.0−40.9 |
30 | 36.0−114.0 | 11.6−47.6 | |
31 | 45.6−144.0 | 13.5−55.3 | |
32 | 57.7−144.0 | 15.7−64.4 | |
33 | 18.3−74.9 | ||
34 | 21.2−87.0 | ||
35 | 24.7−101.0 | ||
36 | 28.7−118.0 | ||
37 | 33.4−137.0 |
BMI | Tanner Stage 1−2 | Tanner Stage 3−4 | Tanner Stage 5 |
|---|---|---|---|
11 | 0.1−0.7 | 0.1−0.6 | 0.1−0.5 |
12 | 0.2−0.9 | 0.1−0.7 | 0.1−0.5 |
13 | 0.2−1.2 | 0.1−0.9 | 0.1−0.6 |
14 | 0.3−1.6 | 0.1−1.1 | 0.1−0.7 |
15 | 0.4−2.0 | 0.1−1.3 | 0.1−0.8 |
16 | 0.5−2.7 | 0.2−1.6 | 0.1−1.0 |
17 | 0.6−3.5 | 0.2−2.0 | 0.1−1.1 |
18 | 0.8−4.6 | 0.2−2.5 | 0.2−1.3 |
19 | 1.0−6.0 | 0.3−3.0 | 0.2−1.5 |
20 | 1.4−7.9 | 0.3−3.7 | 0.2−1.7 |
21 | 1.8−10.4 | 0.4−4.6 | 0.2−2.0 |
22 | 2.3−13.6 | 0.5−5.6 | 0.3−2.3 |
23 | 3.1−17.8 | 0.6−6.9 | 0.3−2.7 |
24 | 4.0−23.3 | 0.8−8.5 | 0.4−3.1 |
25 | 5.2−30.6 | 1.0−10.5 | 0.4−3.6 |
26 | 6.9−40.1 | 1.2−12.9 | 0.5−4.2 |
27 | 9.0−52.5 | 1.5−15.8 | 0.6−4.8 |
28 | 11.8−68.9 | 1.8−19.4 | 0.6−5.6 |
29 | 15.5−90.3 | 2.2−23.9 | 0.7−6.5 |
30 | 20.3−118.0 | 2.7−29.4 | 0.9−7.5 |
31 | 3.3−36.2 | 1.0−8.7 | |
32 | 4.1−44.5 | 1.2−10.0 | |
33 | 5.0−54.7 | 1.3−11.6 | |
34 | 6.2−67.2 | 1.5−13.4 | |
35 | 7.6−82.6 | 1.8−15.6 | |
36 | 9.4−101.0 | 2.1−18.0 | |
37 | 11.5−124.0 | 2.4−20.8 | |
38 | 2.8−24.1 | ||
39 | 3.2−27.9 | ||
40 | 3.7−32.3 |
BMI | Range | BMI | Range |
|---|---|---|---|
11 | 0.7−3.6 | 24 | 4.4−24.2 |
12 | 0.8−4.2 | 25 | 5.1−28.0 |
13 | 0.9−4.8 | 26 | 5.9−32.4 |
14 | 1.0−5.6 | 27 | 6.8−37.5 |
15 | 1.2−6.5 | 28 | 7.9−43.5 |
16 | 1.4−7.5 | 29 | 9.1−50.4 |
17 | 1.6−8.7 | 30 | 10.6−58.3 |
18 | 1.8−10.0 | 31 | 12.2−67.5 |
19 | 2.1−11.6 | 32 | 14.1−78.2 |
20 | 2.4−13.4 | 33 | 16.4−90.5 |
21 | 2.8−15.6 | 34 | 19.0−105.0 |
22 | 3.3−18.0 | 35 | 22.0−121.0 |
23 | 3.8−20.9 | 36 | 25.4−141.0 |
BMI | Range | BMI | Range |
|---|---|---|---|
11 | 0.1−0.4 | 25 | 1.1−9.6 |
12 | 0.1−0.6 | 26 | 1.3−12.0 |
13 | 0.1−0.7 | 27 | 1.6−14.9 |
14 | 0.1−0.9 | 28 | 2.0−18.6 |
15 | 0.1−1.1 | 29 | 2.5−23.2 |
16 | 0.2−1.3 | 30 | 3.2−28.9 |
17 | 0.2−1.7 | 31 | 3.9−36.0 |
18 | 0.2−2.1 | 32 | 4.9−44.9 |
19 | 0.3−2.6 | 33 | 6.1−55.8 |
20 | 0.4−3.2 | 34 | 7.6−69.6 |
21 | 0.4−4.0 | 35 | 9.5−86.7 |
22 | 0.5−5.0 | 36 | 11.8−108.0 |
23 | 0.8−6.2 | 37 | 14.8−135.0 |
24 | 0.9−7.7 |
Additional Information
Leptin is a 16-kilodalton protein that was first identified when it was cloned in 1994.3,4 Humans and mice with defects in the gene that codes for leptin, referred to as the obese or OB gene, tend to become morbidly obese.4 Obese mice with the ob/ob defect lose weight when treated with exogenous leptin.4 Leptin is primarily produced by the adipose tissue in proportion to the size of fat stores.4-7 Besides adipose tissue, leptin is also produced by other tissues, such as the stomach, placenta, and mammary gland.5
Leptin secreted by adipose tissue regulates energy homeostasis, neuroendocrine function, metabolism, immune function and other systems through its effects on the central nervous system and peripheral tissues.8-10 Increased leptin levels stimulate the central nervous system to reduce appetite and increase energy expenditure.4,5,7 Leptin is thought to play an important role in the body's response to food deprivation or starvation.7,8,11,12
Rare homozygous mutations in the leptin (LEP) gene can cause complete leptin deficiency that results in hyperphagia and severe early-onset obesity.13-15 Patients heterozygous for these mutations show partial leptin deficiency and increased body weight.16,17 Leptin administration has been shown to restore metabolic and neuroendocrine abnormalities in individuals with leptin-deficient states, including patients with congenital leptin deficiency generalized lipodystrophy, hypothalamic amenorrhea and lipoatrophy.13-15
Hyperleptinemia and resistance to reducing body mass are two characteristics of typical obesity.18,19 Strong positive associations exist between plasma leptin levels and body fat percentage.6 In obesity the efficacy of the anorexic effect of leptin is decreased with leptin resistance developing due to a defect in intracellular signaling associated with the leptin receptor or decreases in leptin transport across the blood–brain barrier.20 A decrease in tissue sensitivity to leptin leads is characterized by reduced satiety, overconsumption of nutrients, and increased total body mass and the development of metabolic disorders, such as insulin resistance and dyslipidemia.6,20,21
A role for leptin has been implicated in the control of angiogenesis, hematopoiesis, immunity and bone formation, and a number of other functions.4 Leptin is thought to play a role in normal sexual development and in reproduction.11,22 Humans and mice with genetic absence of leptin fail to complete puberty and increased leptin levels in mice lead to early puberty.11 Studies also suggest that leptin levels affect fertility in females and may be involved in the development of normal pregnancy.11,22 During pregnancy, the placenta produces leptin, and maternal circulating levels during the second and third trimesters are approximately twice the level of the non-pregnant state.11,22
Footnotes
1. Considine RV, Sinha MK, Heiman ML, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996 Feb 1;334(5):292-295.8532024
2. Blum WF, Juul A. Reference ranges of leptin levels according to body mass index, gender and development stage. In: Blum WF, Kiess WF, Rascher W, eds. Leptin−The Voice of Adipose Tissue. Heidelberg, Germany: Johann Ambrosius Barth Verlag;1997:319-326.
3. Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994 Dec 1; 372(6505):425-432.7984236
4. Trayhurn P, Hoggard N, Mercer JG, Rayner DV. Leptin: Fundamental aspects. Int J Obes Relat Metab Disord. 1999 Feb; 23(Suppl 1):22-28.10193858
5. Picó C, Palou M, Pomar CA, Rodríguez AM, Palou A. Leptin as a key regulator of the adipose organ. Rev Endocr Metab Disord. 2022 Feb;23(1):13-30.34523036
6. Perakakis N, Farr OM, Mantzoros CS. Leptin in Leanness and Obesity: JACC State-of-the-Art Review. J Am Coll Cardiol. 2021 Feb 16;77(6):745-760.33573745
7. Van Gaal LF, Wauters MA, Mertens IL, Considine RV, De Leeuw IH. Clinical endocrinology of human leptin. Int J Obes Relat Metab Disord. 1999 Feb; 23(Suppl 1):29-36.10193859
8. Friedman JM. Leptin and the endocrine control of energy balance. Nat Metab. 2019 Aug;1(8):754-764.32694767
9. Papathanasiou AE, Nolen-Doerr E, Farr OM, Mantzoros CS. Geoffrey Harris Prize Lecture 2018: Novel pathways regulating neuroendocrine function, energy homeostasis and metabolism in humans. Eur J Endocrinol. 2019 Feb 1;180(2):R59-R71.30475221
10. Park HK, Ahima RS. Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. Metabolism. 2015 Jan;64(1):24-34.25199978
11. Reitman ML, Bi S, Marcus-Samuels B, Gavrilova O. Leptin and its role in pregnancy and fetal development−An overview. Biochem Soc Trans. 2001 May; 29(Pt 2):68-72.11356129
12. Ahima RS, Prabakaran D, Mantzoros C, et al. Role of leptin in the neuroendocrine response to fasting. Nature. 1996 Jul 18;382(6588):250-252.8717038
13. Yaghootkar H, Zhang Y, Spracklen CN, et al. Genetic Studies of Leptin Concentrations Implicate Leptin in the Regulation of Early Adiposity. Diabetes. 2020 Dec;69(12):2806-2818.32917775
14. Farooqi IS, Matarese G, Lord GM, et al. Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. J Clin Invest. 2002 Oct;110(8):1093-1103.12393845
15. Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature. 1997 Jun 26;387(6636):903-908.9202122
16. Farooqi IS, Keogh JM, Kamath S, et al. Partial leptin deficiency and human adiposity. Nature. 2001 Nov 1;414(6859):34-35.11689931
17. Wabitsch M, Funcke JB, Lennerz B, et al. Biologically inactive leptin and early-onset extreme obesity. N Engl J Med. 2015 Jan 1;372(1):48-54.25551525
18. Izquierdo AG, Crujeiras AB, Casanueva FF, Carreira MC. Leptin, Obesity, and Leptin Resistance: Where Are We 25 Years Later? Nutrients. 2019 Nov 8;11(11):2704.31717265
19. Farr OM, Gavrieli A, Mantzoros CS. Leptin applications in 2015: what have we learned about leptin and obesity? Curr Opin Endocrinol Diabetes Obes. 2015 Oct;22(5):353-359.26313897
20. Gruzdeva O, Borodkina D, Uchasova E, Dyleva Y, Barbarash O. Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab Syndr Obes. 2019 Jan 25;12:191-198.30774404
21. Obradovic M, Sudar-Milovanovic E, Soskic S, et al. Leptin and Obesity: Role and Clinical Implication. Front Endocrinol (Lausanne). 2021 May 18;12:585887.34084149
22. Hoggard N, Haggarty P, Thomas L, Lea RG. Leptin expression in placental and fetal tissues: Does leptin have a functional role? Biochem Soc Trans. 2001 May; 29(Pt 2):57-63.11356127
LOINC® Map
| Order Code | Order Code Name | Order Loinc | Result Code | Result Code Name | UofM | Result LOINC |
|---|---|---|---|---|---|---|
| 146712 | Leptin, Serum | 21365-2 | 146713 | Leptin, Serum | ng/mL | 21365-2 |
© 2021 Laboratory Corporation of America® Holdings and Lexi-Comp Inc. All Rights Reserved.
CPT Statement/Profile Statement
The LOINC® codes are copyright © 1994-2021, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee. Permission is granted in perpetuity, without payment of license fees or royalties, to use, copy, or distribute the LOINC® codes for any commercial or non-commercial purpose, subject to the terms under the license agreement found at https://loinc.org/license/. Additional information regarding LOINC® codes can be found at LOINC.org, including the LOINC Manual, which can be downloaded at LOINC.org/downloads/files/LOINCManual.pdf