Leptin 22-56

Leptin 22-56 (Peptide) – Product Details

Leptin is a hormone involved in the regulation of energy balance and appetite. The specific sequence “22-56” refers to a fragment or segment of the leptin peptide, often used in research contexts.

• CAS Number: 177404-21-6
• Molar Mass: 2004.3 g·mol⁻¹
• Chemical Formula: C₈₇H₁₃₈N₂₂O₂₈S₂
• IUPAC Name: VPIQKVQDDTKTLIKTIVTRINDISHTQSVSSKQ

What is Leptin 22-56?

Leptin (22-56), is a biologically active fragment of leptin, mediated via several isoforms of receptors (Ob-Rs). Leptin, a crucial peptide hormone, emerges from the synthesis in white adipose tissue, with its genetic coding located on chromosome 7q31.3. Comprising 146 amino acids, the mature protein resembles proinflammatory cytokines such as interleukin 6. Its concentration in the bloodstream directly correlates with adipose tissue volume. Leptin orchestrates its physiological actions by binding to leptin receptors (LR) distributed across various tissues, including neuronal, hepatic, pancreatic, cardiac, and perivascular intestinal tissues. The LR, a glycoprotein 130 family member, primarily engages the JAK-STAT pathway. This activation prompts critical second messenger pathways, mediated by the LR’s isoform-b, influencing normal leptin functions.

Leptin’s principal field of influence is the brain, particularly the brainstem and hypothalamus, where it regulates satiety, reward, aversion, and neuroendocrine axes. Specific nuclei, including the ARC nucleus, play pivotal roles in mediating leptin’s effects on appetite and energy homeostasis. Functioning as a marker of long-term energy stores, leptin dynamically adjusts food intake and energy expenditure, acting as a vital regulator in the intricate balance between energy surplus and deficit states. [R]

How Does Leptin 22-56 Work?

Leptin, a peptide hormone released by adipose tissue, plays a pivotal role in various physiological processes beyond its classical functions in appetite regulation and energy homeostasis. Synthesized by white adipose tissue, leptin acts by binding to leptin receptors (LR) present in various tissues, including the brain, liver, pancreas, heart, and intestine. The LR, belonging to the glycoprotein 130 family of cytokine receptors, primarily activates the JAK-STAT signaling pathway, influencing critical second messenger pathways. Leptin’s main site of action is the brain, particularly in the brainstem and hypothalamus, where it modulates satiety, reward, aversion, and various neuroendocrine axes. In the hypothalamus, leptin affects nuclei involved in appetite regulation, such as the ARC nucleus, stimulating POMC-containing neurons and inhibiting AgRP/NPY-containing neurons, ultimately reducing appetite. Overall, leptin serves as a marker of long-term energy stores, with its levels influencing the body’s transition between energy deficit and surplus states, regulating food intake and energy expenditure. [R]

Leptin affects several physiological states by interacting with routes in peripheral tissues and the central nervous system. Leptin is a hormone that is synthesized in many different organs and has functions beyond regulating energy expenditure. It contributes to puberty and metabolic signaling, operates as a growth factor in various cell types, and interacts with hormones such as glucocorticoids, insulin, glucagon, and growth hormone. The identification of several isotypes of the leptin receptor in different bodily tissues emphasizes the complexity of its interactions, which can be direct or centrally mediated. [R]

 

Leptin 22-56 Potential Applications

Below are other research-based benefits Leptin 22-56  may bring:

Leptin for Obesity Research

Leptin, which was discovered in 1994, has shown potential in reversing obesity caused by congenital leptin insufficiency and lipodystrophy. However, its research on typical obesity is limited. Leptin administration in subjects alone does not stimulate weight loss in cases with typical obesity characterized by high levels of leptin and leptin tolerance. Ongoing studies, however, are looking into novel mechanisms of leptin resistance, and the creation of novel methods and medication regimens gives hope for enhancing leptin’s safety and effectiveness in the treatment of obesity. Although leptin might not be a stand-alone treatment for obesity in general, it has the potential to work with other therapies to help people maintain their weight loss. [R]

Leptin for Osteoarthritis Research

Osteoarthritis (OA), a disorder frequently associated with obesity, has been related to leptin, a hormone involved in controlling energy balance. Researchers looked at how leptin affected human OA cartilage in this investigation. The results show that leptin raises the expression of certain proteins (iNOS and COX-2) and the synthesis of compounds linked to inflammation, either by itself or in conjunction with the proinflammatory cytokine IL-1. Leptin’s actions seem to be mediated by certain signaling pathways. Interestingly, there appears to be a correlation between the production of other inflammatory factors and the inhibition of leptin-induced nitric oxide (NO) synthesis. These findings provide credibility to the idea that leptin may boost the synthesis of proinflammatory factors in OA cartilage, which may raise the risk of osteoarthritis linked to obesity. [R]

Leptin for Bone Growth Research

A major factor in pediatric obesity is the hormone leptin, which is produced by fat cells and often causes rapid growth despite low growth hormone levels. A study, that examined how leptin affects skeletal growth centers, showed that leptin is specifically bound to chondrocytes, or cartilage cells, within these growth centers. The introduction of leptin led to an expansion of the chondroprogenitor zone, where cartilage cells originate, promoting both cell division and proliferation. By boosting the quantity of the IGF-I receptor and its messenger RNA, leptin also had an impact on the insulin-like growth factor (IGF) system, which is essential for the growth of bones. According to the research, leptin directly affects growth centers by functioning as a skeletal growth factor. [R]

Leptin for Blood Vessel Growth Research

Recent studies have shown that leptin functions as a growth signal through its receptor (Ob-R) in endothelial cells, encouraging angiogenesis (the development of new blood vessels) in vascular circumstances that are both normal and under stress, such as atherosclerosis. The researchers examined the expression of key proteins related to the development of atherosclerosis, or artery hardening. They observed heightened levels of Ob-R in areas that underwent revascularization within human atherosclerotic lesions. Additionally, there was an increased presence of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), primarily within the endothelium lining and macrophages/foam cells. Using animal models, studies demonstrated that leptin stimulates angiogenic activity. Leptin was found to promote the growth of endothelial cells and affect the production of matrix remodeling-related proteins such as TIMPs and MMPs. This implies that leptin, with its variety of actions, such as stimulating blood vessel cell proliferation, is involved in controlling the remodeling of tissue architecture. [R]

Leptin for Anorexia Nervosa Research

A study explores the mental and behavioral effects of starvation, often associated with reduced leptin levels, a hormone linked to regulating body weight. Starvation-induced changes in leptin secretion, stemming from continuous fat loss, trigger various adaptive functions. Leptin receptors are found in different tissues, influencing not only the hypothalamus-pituitary-end organ pathways but also peripheral and central systems like the gastrointestinal tract and reward system. Examining congenital leptin deficiency, a condition paralleling starvation provides insights into potential mental symptom treatment with leptin. Experiments on rodent models highlight the behavioral impact of hypoleptinemia, while evidence from lipodystrophies underscores its role. The review discusses recent findings on the positive effects of leptin administration in anorexia nervosa, suggesting that leptin may have significant mental health benefits during states of starvation. [R]

Leptin for Fertility Research

In women who maintain a healthy weight, having sufficient levels of leptin facilitates the onset of ovulation and menstruation. Infertility may result from low leptin levels brought on by abnormally low body fat levels. Additionally, some preliminary studies indicate that women who are overweight or obese may have less success with reproductive treatments if they have abnormally high leptin levels. In conclusion, leptin facilitates the communication of fat status to the areas of the brain responsible for reproduction. It seems that maintaining healthy fat stores and leptin levels is necessary for women to naturally ovulate and become pregnant. [R]

Leptin for Diabetes Mellitus

Leptin also helps regulate blood sugar levels and insulin sensitivity. Appropriate leptin signaling is important for maintaining a healthy weight and preventing obesity and type 2 diabetes. Research suggests that increasing leptin sensitivity through pharmaceutical or lifestyle interventions could have future potential therapeutic benefits. Studies have shown that administering synthetic leptin to obese diabetic test subjects reverses insulin resistance and hyperglycemia and strategies that boost endogenous leptin levels or improve leptin sensitivity could potentially help treat diabetes and other metabolic conditions. More research is still needed, but modulating leptin signaling pathways holds potential as a novel therapeutic avenue for obesity, diabetes, and related metabolic disorders. [R]

Leptin for Alzheimer’s Disease

Previous studies have demonstrated that the hormone leptin, which is generated by fat cells, may have positive effects on biomarkers linked to Alzheimer’s disease. The effects of leptin administration were investigated in a recent study using an 8-week transgenic animal model of Alzheimer’s disease. Comparing the brain and blood of the leptin-treated transgenic animal subject to the untreated transgenic controls, the former demonstrated noticeably reduced levels of amyloid-beta, a protein that causes plaques in the Alzheimer’s brain.

Phosphorylated tau, another protein linked to Alzheimer’s disease that causes tangles in the brain, was similarly decreased by leptin. Furthermore, animals administered with leptin exhibited reduced levels of a precursor protein implicated in the synthesis of amyloid-beta and less amyloid plaque accumulation in the hippocampus area of the brain. Crucially, inflammatory indicators in the blood did not seem to be activated by leptin.

In addition to these improvements in Alzheimer ‘s-related biomarkers, after 4–8 weeks of therapy, the leptin-treated animal subjects performed much better than the saline-treated controls on tests of recognition memory and contextual/cued fear conditioning. Based on these preclinical results, leptin can be a potential therapeutic target for Alzheimer’s disease by interacting with several pathways and proteins linked to the disease. Although further research is required, it may be possible to treat Alzheimer’s and other neurodegenerative illnesses by altering leptin and its signaling pathways. [R]

Leptin for Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a complex condition causing joint inflammation, chronic pain, disability, and increased mortality. Current research indicates that leptin plays a significant role in both the development and potential treatment of RA, as shown in laboratory and animal studies. While the exact mechanisms of leptin in RA need further exploration, existing data strongly support its crucial involvement in immune responses and autoimmune diseases. [R]

Leptin directly influences both innate and adaptive immunity, and early clinical findings suggest a possible therapeutic role in RA by modulating leptin signaling at the molecular and genetic levels. Blocking key signal pathways of leptin and inhibiting its activity, including the use of leptin antagonists, show promise as potential therapies for RA, despite potential risks. Leptin exhibits a dual role, displaying both anti-inflammatory and proinflammatory responses. Thus, gaining a deeper understanding of leptin’s mechanisms holds potential benefits for future advancements in RA treatment. [R]

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Conclusion

LEPTIN 22-56, a biologically active fragment of the leptin hormone, demonstrates a multifaceted impact on various health aspects. Research highlights its potential benefits in obesity, osteoarthritis, bone growth, blood vessel development, anorexia nervosa, fertility, diabetes mellitus, Alzheimer’s disease, and rheumatoid arthritis. Notably, Leptin shows potential in addressing obesity-related issues, such as leptin resistance and lipodystrophy, and exhibits positive effects on bone and blood vessel growth. Additionally, it plays a role in mental health, fertility, diabetes management, and neurodegenerative disorders, suggesting its diverse therapeutic potential across a range of health conditions. Further exploration and clinical studies are warranted to fully harness the health benefits of Leptin.

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Strength	2mg

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