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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 3
2015 pubmed 49 citations

Cathelicidin Antimicrobial Peptide: A Novel Regulator of Islet Function, Islet Regeneration, and Selected Gut Bacteria.

Pound. Lynley D LD; Patrick. Christopher C; Eberhard. Chandra E CE; Mottawea. Walid W; Wang. Gen-Sheng GS; Abujamel. Turki T; Vandenbeek. Roxanne R; Stintzi. Alain A; Scott. Fraser W FW

Key Findings

  • LL‑37 is naturally present in pancreatic beta cells of rats, mice, and humans.
  • Adding LL‑37 to isolated rat islets increases calcium signaling and stimulates insulin and glucagon secretion.
  • Daily LL‑37 treatment in diabetic‑prone rats enhances beta‑cell regeneration and improves the composition of gut microbiota.

Practical Outcomes

  • LL‑37 could become a future strategy to support glucose regulation and gut health, but at present there are no human dosage guidelines or approved formulations. Enthusiasts should view this as a promising research direction rather than an immediate protocol to try.

Summary

The study shows that the natural peptide LL‑37, also called cathelicidin, is made in pancreas beta cells and can boost insulin and glucagon release, help new beta cells grow, and shift gut bacteria toward a healthier mix in diabetic‑prone rats. While promising for blood‑sugar control and gut health, it’s still early‑stage animal work and not yet a ready‑to‑use supplement for people.

Abstract

Cathelicidin antimicrobial peptide (CAMP) is a naturally occurring secreted peptide that is expressed in several organs with pleiotropic roles in immunomodulation, wound healing, and cell growth. We previously demonstrated that gut Camp expression is upregulated when type 1 diabetes-prone rats are protected from diabetes development. Unexpectedly, we have also identified novel CAMP expression in the pancreatic β-cells of rats, mice, and humans. CAMP was present even in sterile rat embryo islets, germ-free adult rat islets, and neogenic tubular complexes. Camp gene expression was downregulated in young BBdp rat islets before the onset of insulitis compared with control BBc rats. CAMP treatment of dispersed islets resulted in a significant increase in intracellular calcium mobilization, an effect that was both delayed and blunted in the absence of extracellular calcium. Additionally, CAMP treatment promoted insulin and glucagon secretion from isolated rat islets. Thus, CAMP is a promoter of islet paracrine signaling that enhances islet function and glucoregulation. Finally, daily treatment with the CAMP/LL-37 peptide in vivo in BBdp rats resulted in enhanced β-cell neogenesis and upregulation of potentially beneficial gut microbes. In particular, CAMP/LL-37 treatment shifted the abundance of specific bacterial populations, mitigating the gut dysbiosis observed in the BBdp rat. Taken together, these findings indicate a novel functional role for CAMP/LL-37 in islet biology and modification of gut microbiota.

Study Information

Provider

pubmed

Year

2015

Date

2015-09-14T00:00:00.000Z

DOI

10.2337/db15-0788

Citations

49

References

48