rec Leptin (human)
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rec Leptin (human)

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Leptin is an adipose tissue-derived protein encoded by an obesity gene and is involved in controlling food intake, energy expenditure and reproduction, as well as playing a role in immune regulation, inflammation, and hematopoiesis.

Category
Others
Catalog number
BAT-014492
Synonyms
rec Obesity Factor (human); OB gene product; OB Protein; Obesity Protein; OBS; Obesity factor; Leptin (human), (recombinant)
Appearance
Lyophilized Solid
Storage
Store at -20°C
Solubility
Soluble in Water
1. Leptin and its receptor are expressed in the testis and in the epididymis of young and adult pigs
Vittoria Rago, Saveria Aquila, Carmela Guido, Amalia Carpino Anat Rec (Hoboken). 2009 May;292(5):736-45. doi: 10.1002/ar.20880.
Recent studies indicated that leptin, a 16 kDa hormone, is a regulatory signal in human and rodent male reproduction. This work was designed to investigate the expression of leptin and its receptor in testes and epididymides from immature and mature pigs. Immunolocalization revealed that leptin and its receptor were confined only in the interstitial compartment of immature testes, whereas both proteins were detected in Leydig cells and within seminiferous tubules of mature gonads. The immunostaining of epididymal tissues showed that leptin was absent in the epithelial cells of immature pigs but it was present in all the three regions of mature epididymides, although with a minor signal in the cauda. Conversely, leptin receptor was observed in all the epithelial cells of both immature and mature epididymides. Western blot analysis of tissue extracts detected a 16 kDa band for leptin and five/six isoforms, ranging from 120 to 40 kDa, for leptin receptor. In conclusion, this work has identified, for the first time, leptin and leptin receptor in the testis and in the epididymis of the pig showing a differential cell-type expression pattern of the two proteins in young and adult animals. Therefore, our findings suggest a possible involvement of leptin in endocrine or autocrine/paracrine control of porcine male reproductive structures.
2. Sympathetic nervous system regulation of liver repair
Jude A Oben, Anna Mae Diehl Anat Rec A Discov Mol Cell Evol Biol. 2004 Sep;280(1):874-83. doi: 10.1002/ar.a.20081.
This chapter reviews recent evidence that the sympathetic nervous system (SNS) regulates liver repair by modulating the phenotypes of hepatic stellate cells (HSCs), the liver's principal fibrogenic cells, and hepatic epithelial progenitors, i.e., oval cells. SNS nerve fibers touch HSCs and these cells express adrenoceptors, suggesting that HSCs may be targets for SNS neurotransmitters. HSCs also contain catecholamine biosynthetic enzymes, release norepinephrine (NE), and are growth-inhibited by adrenoceptor antagonists. In addition, HSCs from mice with reduced levels of NE grow poorly in culture and exhibit inhibited activation during liver injury. Finally, growth and injury-related fibrogenic responses are rescued by adrenoceptor agonists. Thus, certain SNS inhibitors (SNSIs) protect experimental animals from cirrhosis. Conversely, SNSIs enhance the hepatic accumulation of oval cells (OCs) in injured livers. This response is associated with improved liver injury. Because SNSIs do not affect the expression of cytokines, growth factors, or growth factor receptors that are known to regulate OCs, and OCs express adrenoceptors, it is conceivable that catecholamines influence OCs by direct interaction with OC adrenoceptors. Given evidence that the SNS regulates the viability and activation of HSCs and OCs differentially, SNSIs may be novel therapies to improve the repair of damaged livers.
3. Investigation of serum levels of orexin-A, transforming growth factor β, and leptin in patients with multiple sclerosis
Sepideh Moharami, Alireza Nourazarian, Masoud Nikanfar, Delara Laghousi, Behrouz Shademan, Omid Joodi Khanghah, Fatemeh Khaki-Khatibi J Clin Lab Anal. 2022 Jan;36(1):e24170. doi: 10.1002/jcla.24170. Epub 2021 Dec 11.
Background: Multiple sclerosis (MS) is a chronic inflammatory and autoimmune disease affecting various inflammatory and nutritional parameters. Therefore, this study aimed to investigate the relationship between the Body Mass Index (BMI) of MS patients and the serum levels of leptin, orexin-A, and Transforming Growth Factor β (TGF-β). Methods: This cross-sectional study included 25 patients suffering from MS and 40 healthy individuals as the case and control groups, respectively. The serum levels of leptin, orexin-A, and TGF-β were assessed in the participants using the Enzyme-Linked Immunosorbent Assay methods. Moreover, data were analyzed using the descriptive statistical indices, t-test, chi-square test, and linear regression test. Results: According to our results, the participants' mean age was 38.04 ± 7.53 and 40.23 ± 5.88 in the case and control groups, respectively. Also, the groups were not significantly different in gender, age, alcohol consumption, and smoking (p > 0.05). It was found that the mean serum levels of orexin-A and TGF-β were significantly lower in the MS patients compared to the control group, while the mean serum leptin levels were significantly higher (42.8 vs. 18.9 ng/ml, p < 0.001). Moreover, there was no significant relationship between the BMI of the MS patients and their serum levels of orexin-A, TGF-β, and leptin (p > 0.05). Conclusions: In conclusion, we found significantly lower levels of orexin-A and TGF-β and a significantly higher level of leptin in the MS patients compared to the control group. In addition, there was no significant relationship between the BMI and the serum levels of orexin-A, TGF-β, and leptin in MS patients.
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