PUBLICATION

The protective effects of human milk derived peptides on the pancreatic islet biology

Authors

Singh, A., Enjapoori, A.K., Gibert, Y., Dwyer, K.M.

ID

ZDB-PUB-200724-4

Date

2020

Source

Biology Open 9(8): (Journal)

Registered Authors

Gibert, Yann

Keywords

Beta cell, Bovine beta casomorphin, Human beta casomorphin, Pancreas, Regeneration, Type 1 diabetes, Zebrafish

MeSH Terms

Humans
Somatostatin/metabolism
Receptors, Opioid, mu/metabolism
Endorphins/pharmacology
Insulin/metabolism
Islets of Langerhans/drug effects
Islets of Langerhans/physiology*
Zebrafish
Peptides/pharmacology*
Regeneration/drug effects
Cattle
Milk, Human/chemistry*
Glucagon/metabolism
Animals

(all 14)

PubMed

32694188 Full text @ Biol. Open

Abstract

Several epidemiological studies support the protective role of breast-feeding in reducing the risk for type 1 diabetes. Human breast milk is the perfect nutrition for infants and contains many complex proteins, lipids and carbohydrates. In this study, we examined the physiological effects of human milk-derived opioid peptides, beta casomorphins (BCM), and compared them with bovine milk-derived opioid peptides on pancreatic hormone regulation and β-cell regeneration. Exposure of wild-type zebrafish embryos to 50 µg/mL of human BCM -5 and -7 from 3 days post fertilisation until 6 days post fertilisation resulted in an increased insulin domain of expression while exposure to bovine BCM -5 and -7 significantly reduced the insulin domain of expression as analysed by whole-mount in-situ hybridisation. These changes may be accounted for by reduced insulin expression or β-cell number and were mitigated by the µ-opioid receptor antagonist, naloxone. The effect of BCM on β-cell regeneration was assessed following ablation of β-cells in Tg (ins: CFP-NTR) zebrafish from 3 days post fertilisation to 4 days post fertilisation, followed by exposure of bovine and human BCM -5 and -7 (50 µg/mL) from 4 days post fertilisation until 7 days post fertilisation. The regenerative capacity of β-cells was not impeded following exposure to human BCM -5 and -7, whereas the capacity of β-cells to regenerate following bovine BCM -5 and -7 exposure was reduced. Our data suggests that human BCM -5 and -7 may promote β-cell development and enable the regeneration of β-cells, while the bovine milk derived peptides, BCM -5 and -7 play an opposite role. These data may provide some biological explanation for the protective effect of breastfeeding on the development of Type 1 Diabetes.

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