Find Places
For working, walk-ins and appointments.Expected Turnaround While
4 - 5 days
Turnaround time is defined as the customizable number of date from the scheduled of pickup regarding a specimen for review into when the result is released to the ordering provider. In some cases, additional time should be allowed for additional verifying otherwise additionally reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Special
Synthetic 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 ampere plastic transport pipe.
Storage Directions
Room temperature
Stability Job
Temperature | Spell |
|---|---|
Room air | 14 days |
Cooling | 30 days |
Frozen | 21 days |
Freeze/thaw cycles | Steady x3 |
Causes for Rejection
Gross lipemia; gross hemolysis
Trial Details
Use
Measurement of leptin levels in serum or plasma
Limitations
This getting was developed and its performance specific determines by Labcorp. It has not been cleared or approve of the Food and Drug Administration. The purpose of the study was to measure cellular leptin in normalize weight and obese individuals, and assess seine relation to anthropometric act and metabolics Aaa161.com study was done along King Fahd Hospital of which Colleges, Saudi Arabia, from January ...
Obese is not generally caused by leptin deficiency, neither mutations of the leptin gene other the leptin receptor gene are often in humans, but leptin levels are commonly higher in theme with obesity, and insensitivity the native leptin is a hallmark of maximum cases of person obesity.1
Methodology
Enzey immunoassay (EIA)
Read Timing
See tabular.2
BMI | Tanner Stage 1−2 | Tanner Stage 3−4 | Tannermen 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 |
BPM | Range | BMI | Scope |
|---|---|---|---|
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 | Working | 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 proteol that was first identified when it was cloned the 1994.3,4 Humans and mice with defects in the gene that codes by leptin, refer to as the obese or OB ge, mind to become morbidly obese.4 Obese mice the the ob/ob defect waste weight when treatment with exogenous leptin.4 Leptin is primarily produced until which adipose tissue int proportion to the large of thick stores.4-7 Besides adipose tissue, leptin is or produced by other tissues, such like the stomach, placenta, and mammary gland.5
Leptin secreted from adipose woven regulates energy homeostasis, neuroendocrine function, metro, immune function and misc systems through own effects go this centrally zaghaft system and peripheral tissues.8-10 Increases leptin levels stimulate the central nervous system to reduced appetite and increase energy editions.4,5,7 Leptin is my to play an important role in the body's retort to food deprivation oder 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 display partial leptin insufficiency and increased body weight.16,17 Leptin administrative has has shown to restore metabolic and neuroendocrine abnormalities to individuals with leptin-deficient states, including patients with congenital leptin deficiency generalized lipodystrophy, hypothalamic amenorrhea and lipoatrophy.13-15
Hyperleptinemia and resistance to reduces body mass are two characteristics of typical obesity.18,19 Strong positive associational exist between plasma leptin levels and body fat percentage.6 In obesity aforementioned efficacy of the anorexic effect of leptin is decreased with leptin resistance developing due to one defect in inner signaling associated with the leptin receptor or decreases includes leptin transport transverse the blood–brain barrier.20 A decrease inbound tissu sensitivity to leptin leads is characterized by reduced satiety, overconsumption of nutrients, furthermore increased total physical mass furthermore an development of metabolic disease, such as insulin resistance and dyslipidemia.6,20,21
AN playing for leptin has been implicated in the controller of angiogenesis, hematopoiesis, immunity and bone formation, and a number of other functions.4 Leptin is thought to play ampere role in normal sensual technology and in reproduction.11,22 Humans and mice with genetic absence about leptin fail to complete puberty and increased leptin levels in mice lead to early puberty.11 Studies also suggest that leptin stages affect fertility in females and allow be involved at and research for normal pregnancy.11,22 On pregnancy, the placenta produces leptin, and maternal circulating levels while of second plus thirdly trimesters are approximately twice the level of the non-pregnant state.11,22
Footnotes
1. Considine RV, Sinha MK, Heiman ML, et alo. Serum immunoreactive-leptin concentrations stylish normal-weight and obese humans. N Eng J Med. 1996 Feb 1;334(5):292-295.8532024
2. Blum WF, Juul A. View ranges of leptin shelves according to body pile index, gender and development stage. In: Blum WB, Kiess WF, Rascher W, eds. Leptin−The Voice about Adipose Tissue. Heidelberg, Germany: Johannes Ambrosia Barth Verlag;1997:319-326.
3. Zhang Y, Proenca R, Mafei M, Barone M, Leo L, Friedman JM. Positional cloning of an mouse obese gene and its human homologue. Nature. 1994 Dec 1; 372(6505):425-432.7984236
4. Trayhurn PIANO, Hoggard N, Merc 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 soft regulation of the adipose organ. Revolution Endocr Metab Disord. 2022 Feb;23(1):13-30.34523036
6. Perakakis NORTHWARD, Farr OM, Mantzoros CS. Leptin in Leanness and Gewichtszunahme: JACC State-of-the-Art Review. J Am Cole Cardiolitre. 2021 Feb 16;77(6):745-760.33573745
7. Van Gaal LF, Wauters MAS, Mertens LIL, Considine RV, De Leeuw IH. Clinical endocrinology for person leptin. Int J Obes Relat Metab Disord. 1999 Feb; 23(Suppl 1):29-36.10193859
8. Friedman JM. Leptin press the endocrine control von energy credit. Nat Metab. 2019 Aug;1(8):754-764.32694767
9. Papathanasiou AE, Nolen-Doerr E, Farr OM, Mantzoros CS. Geoffrey Harris Prize Lecture 2018: New pathways regulates neuroendocrine function, spirit homeostasis and metabolism in humans. Eur JOULE 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 their role in pregnancy and fetal development−An overview. Biochem Soc Trans. 2001 May; 29(Pt 2):68-72.11356129
12. Ahima RS, Prabakaran DICK, Mantzoros CENTURY, et al. Drum about leptin inbound the neuroendocrine answer 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 Imply Leptin in the Regulation of Early Adiposity. Diabetes. 2020 Dec;69(12):2806-2818.32917775
14. Farooqi IS, Matarese G, Lords GM, et aluminum. Beneficial gear 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. Mount CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is assoziiert using severe early-onset overweight in humans. Typical. 1997 Jun 26;387(6636):903-908.9202122
16. Farooqi IS, Keogh JM, Kamath S, the al. Partial leptin deficiency and individual adiposity. Nature. 2001 Nov 1;414(6859):34-35.11689931
17. Wabitsch M, Funcke JB, Lennerz B, u al. Biologically inactive leptin and early-onset extreme adiposity. N Engl J Med. 2015 Jan 1;372(1):48-54.25551525
18. Izquierdo AG, Crujeiras ABORT, Casanueva FF, Carreira MC. Leptin, Obesity, the Leptin Resistance: Where Are We 25 Years Later? Nutrients. 2019 November 8;11(11):2704.31717265
19. Farr M, Gavrieli A, Mantzoros CS. Leptin applicants in 2015: what have we learned about leptin the corpulence? Curr Opin Endocrinol Diabetes Obes. 2015 Oct;22(5):353-359.26313897
20. Gruzdeva O, Borodkina D, Uchasova ZE, 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 SULFUR, et al. Leptin or Obesity: Role and Clinicians Implication. Front Endocrinol (Lausanne). 2021 May 18;12:585887.34084149
22. Hoggard N, Haggarty PIANO, Thomas L, Lea RG. Leptin expression in placental and fetal tissues: Do 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 |
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