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The Tohoku journal of experimental medicine1978; 124(1); 57-64; doi: 10.1620/tjem.124.57

Somatostatin-containing cells in the rat and horse pancreatic islets.

Abstract: Somatostatin-, glucagon- and insulin-containing cells in the rat and horse pancreatic islets were investigated by an indirect immunofluorescent technique using antibodies to insulin, glucagon and somatostatin. In the rat pancreatic islets, insulin-containing cells were located centrally, and glucagon and somatostatin or somatostatin-like substance (SLS)-containing cells were peripherally disposed and glucagon-containing cells were situated more peripherally as compared with distribution of somatostatin-containing cells. On the other hand, in the horse pancreatic islets, insulin-containing cells were found in the peripheral area and glucagon and somatostatin-containing cells were distributed centrally. Insulincontaining cells were most numerous among the three types of cells in the islets of both the rat and horse. Somatostatin or SLS-containing cells in the horse were about equal in number to the glucagon-containing cells while those in the rat seemed to be smaller in number than the glucagon-containing cells. The present study clearly demonstrates that the somatostatin and glucagoncontaining cells are located, in relation to the bloodstream, on the upstream side of the insulin-containing cells in the islets of Langerhans of both the rat and the horse though these two animal species are known to have completely reverse bloodstream pattern in the islets. According to the mechanism of glucagon and insulin secretions from the islets, we proposed the hypothesis that the somatostatin-containing cells regulate the neighbouring glucagon and insulincontaining cells by an intercellular transport mechanism which provides somatostatin through the junctional complex, while other insulin-containing cells which are too remote from the somatostatin containing cells to be affected by such a mechanism are regulated by a fraction of somatostatin released and carried down by the bloodstream.
Publication Date: 1978-01-01 PubMed ID: 345522DOI: 10.1620/tjem.124.57Google Scholar: Lookup
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Summary

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The research paper investigates the distribution of somatostatin, glucagon, and insulin-containing cells in the pancreatic islets of both rats and horses and hypothesizes that somatostatin regulates the neighboring glucagon and insulin cells through an intercellular transport mechanism.

Distribution of Insulin, Glucagon and Somatostatin Cells

  • The study used an indirect immunofluorescent technique with the help of antibodies to insulin, glucagon, and somatostatin to explore the distribution of cells containing these substances in rat and horse pancreatic islets.
  • In rat pancreatic islets, insulin-containing cells were centrally situated, while those containing glucagon and somatostatin/somatostatin-like substance (SLS) were locate on the periphery. Among these peripheral cells, the glucagon-containing cells were more peripheral than the somatostatin-containing cells.
  • In contrast, horse pancreatic islets had a different arrangement: insulin-containing cells were on the periphery, whereas glucagon and somatostatin-containing cells were centrally located.
  • Across both species, insulin-containing cells were the most populous within the pancreatic islets.
  • Somatostatin or SLS-containing cells were about equally as numerous as glucagon-containing cells in horses, while in rats, these cells were less numerous than those containing glucagon.

Somatostatin’s Role in Regulating Other Cells

  • The study demonstrated that regardless of the differences in bloodstream patterns between rats and horses, the somatostatin- and glucagon-containing cells were positioned upstream of the insulin-containing cells in the islets of Langerhans—cell clusters in the pancreas.
  • The authors proposed a hypothesis regarding the regulatory role of somatostatin in the pancreas. They suggest that somatostatin-containing cells regulate the adjacent glucagon and insulin-containing cells through an intercellular transport mechanism that supplies somatostatin via the junctional complex—a specialized cell connection point.
  • Furthermore, insulin-containing cells that are too far away from the somatostatin-containing cells to be influenced by this mechanism are suggested to be regulated by the fraction of somatostatin that is released and carried downstream by the bloodstream.

By exploring the distinct distribution of these cells in different animals and proposing mechanisms for hormonal regulation within the pancreatic islets, the study encourages further research to improve our understanding of pancreatic functions and the pathogenesis of diseases like diabetes.

Cite This Article

APA
Ito S, Yamada Y, Hayashi M, Matsubara Y. (1978). Somatostatin-containing cells in the rat and horse pancreatic islets. Tohoku J Exp Med, 124(1), 57-64. https://doi.org/10.1620/tjem.124.57

Publication

ISSN: 0040-8727
NlmUniqueID: 0417355
Country: Japan
Language: English
Volume: 124
Issue: 1
Pages: 57-64

Researcher Affiliations

Ito, S
    Yamada, Y
      Hayashi, M
        Matsubara, Y

          MeSH Terms

          • Animals
          • Fluorescent Antibody Technique
          • Glucagon / analysis
          • Horses / anatomy & histology
          • Islets of Langerhans / cytology
          • Male
          • Rats / anatomy & histology
          • Somatostatin / analysis

          Citations

          This article has been cited 3 times.
          1. Dybala MP, Butterfield JK, Hendren-Santiago BK, Hara M. Pancreatic Islets and Gestalt Principles.. Diabetes 2020 Sep;69(9):1864-1874.
            doi: 10.2337/db20-0304pubmed: 32669392google scholar: lookup
          2. Steiner DJ, Kim A, Miller K, Hara M. Pancreatic islet plasticity: interspecies comparison of islet architecture and composition.. Islets 2010 May-Jun;2(3):135-45.
            doi: 10.4161/isl.2.3.11815pubmed: 20657742google scholar: lookup
          3. Elayat AA, el-Naggar MM, Tahir M. An immunocytochemical and morphometric study of the rat pancreatic islets.. J Anat 1995 Jun;186 ( Pt 3)(Pt 3):629-37.
            pubmed: 7559135