Abdominal distress and shifts in bowel habits are hallmarks of Irritable Bowel Syndrome (IBS), a chronic gastrointestinal condition. The Rome Criteria, a symptom-based categorization method, is used to analyze IBS, the most prevailing disorder seen by gastroenterologists; the most recent version, Rome IV, was issued only recently. Approximately 12% prevalence has been observed.
Forty to sixty percent of research models of IBS are believed to exhibit concurrent psychiatric dysfunction, including perceived moroseness or anxious behavior. In addition, models of IBS appear to frequently somatize symptoms more than those with similar gastrointestinal issues but no IBS.
Curative solutions for IBS have not yet been developed. It is now suggested that several factors may at play in the commencement and sustainment of IBS symptoms, making effective management challenging. Methods center on alleviating symptoms, although the standard of care in pharmacological solutions are considered inadequate.
Researchers are working to better understand the neurohormonal basis of IBS after reports of biological dysregulation in IBS models. The specific pathways leading to the development of irritable bowel syndrome (IBS) symptoms remain unclear despite progress in the knowledge of the pathophysiology of the condition.
Inflammatory Bowel Disease
The most common inflammatory bowel illnesses are ulcerative colitis and Crohn’s disease. Crohn’s disorder and ulcerative colitis are inflammatory bowel diseases (IBDs); however, whereas the former is considered to cause inflammation only in the colon, the latter may affect any portion of the digestive system. Inflammatory bowel disease has a mysterious origin.
Bacterial contamination, immune system changes, and genetic contentions are only a few of the elements believed to have a role in the development of this class of disorders. An augmented risk of inflammatory bowel disease (IBD) due to the overproduction of proinflammatory cytokines, for instance, is linked to mutations in the NOD2 gene. It suggests that environmental variables may be more influential than genetic predisposition regarding immune-mediated disorders.
KPV Peptide
Studies suggest that, to a large extent, -MSH, a neurohormone, may modulate the immune response in certain cell types. It is hypothesized to exert powerful anti-inflammatory actions by interacting with melanocortin receptors in the skin. The three-terminal amino acids lysine, proline, and valine (KPV) are speculated to be responsible for -MSH’s anti-inflammatory effect.
Despite missing the parent hormone’s MC-R-binding sequence motif, KPV has been proposed to potentially suppress inflammation. This is due to the assumption that peptides (like KPV) may serve as hormones and communicate between tissues through the circulatory system and biological messengers. It is suggested that KPV’s possible anti-inflammatory properties may be mediated via IL-1 suppression.
Research suggests that KPV may lack the melanotropic effects of -MSH and therefore may possibly not result in pigmentation. It is speculated to be more durable chemically and may come in a smaller package than -MSH. Due to its possible anti-inflammatory properties, KPV has been researched primarily within the context of inflammatory skin disorders. KPV is hydrophilic, is believed to weigh 383.49 Da, and has an isoelectric point (pI) of 14.
BPC-157 Peptide
Body protection compound (BPC) 157 is a penta-decapeptide with a partial BPC sequence identified from stomach fluid. Studies suggest that it may not be water soluble nor able to be digested by enzymes; thus, it may potentially be quite stable. Through various animal experiments, researchers speculated that BPC 157 may accelerate the recovery of damaged skin, mucosa, cornea, muscle, tendon, ligament, and bone. It is unclear how penta-decapeptide BPC 157 may speed up the healing process. Growth factor upregulation, a proangiogenic impact, and nitric oxide (NO) production modification are all hypothesized mechanisms involved. BPC 157 may control the actions of collagen fragments linked to bone morphogenic proteins.
VIP Peptide
VIP, or vasoactive intestinal peptide, comprises 28 amino acids originally isolated from swine duodenum and described in 1970. Research suggests that VIP may be highly conserved across species, sharing at least 85% sequence similarity with fish, frogs,(and all mammals except guinea pigs and chickens).
VIP was first identified and recognized for its perceived vasodilatory potential. Findings imply that VIP may be widespread, and may act as a neurotransmitter and neuroendocrine releasing factor in the brain, spinal cord, periphery, gastrointestinal tract, respiratory, reproductive, and cardiovascular systems. These modifications are in various normal and abnormal processes, including growth, development, and regulating neuronal, epithelial, and endocrine cell function. Carcinogenesis, immunological responses, and circadian rhythms are just a few of the processes VIP is hypothesized to impact.
Visit corepeptides.com for more educational articles on research peptides.
References
[i] Iwasaki M, Akiba Y, Kaunitz JD. Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system. F1000Res. 2019 Sep 12;8:F1000 Faculty Rev-1629. doi: 10.12688/f1000research.18039.1. PMID: 31559013; PMCID: PMC6743256.
[ii] Seo S, Miyake H, Alganabi M, Janssen Lok M, O’Connell JS, Lee C, Li B, Pierro A. Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis. J Pediatr Surg. 2019 Dec;54(12):2520-2523. doi: 10.1016/j.jpedsurg.2019.08.038. Epub 2019 Aug 30. PMID: 31668399.
[iii] Fakhoury M, Negrulj R, Mooranian A, Al-Salami H. Inflammatory bowel disease: clinical aspects and treatments. J Inflamm Res. 2014 Jun 23;7:113-20. doi: 10.2147/JIR.S65979. PMID: 25075198; PMCID: PMC4106026.
[iv] Weaver KR, Melkus GD, Henderson WA. Irritable Bowel Syndrome. Am J Nurs. 2017 Jun;117(6):48-55. doi: 10.1097/01.NAJ.0000520253.57459.01. PMID: 28541989; PMCID: PMC5453305.
[v] Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Bohm M, Luger TA, Domschke W, Kucharzik T. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008 Mar;14(3):324-31. doi: 10.1002/ibd.20334. PMID: 18092346.
[vi] Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008 Jan;134(1):166-78. doi: 10.1053/j.gastro.2007.10.026. Epub 2007 Oct 17. PMID: 18061177; PMCID: PMC2431115.