Glucose homeostasis dependency on acini–islet–acinar (AIA) axis communication : a new possible pathophysiological hypothesis regarding diabetes mellitus
(2018) In Nutrition and Diabetes 8(1).- Abstract
Studies have highlighted the existence of two intra-pancreatic axes of communication: one involved in the regulation of enzyme production by insulin—the insular–acinar axis; and another involved in the regulation of insulin release by pancreatic enzymes—the acini–insular axis. Previous studies by our laboratory show that pancreatic enzymes can affect blood glucose homeostasis and insulin secretion independently of their digestive functions, both from the gut lumen and probably from the blood. As a result we would like to introduce here the concept of acini–islet–acinar (AIA) axis communication (feedback), which could play an important role in the development of obesity and diabetes type 2. The AIA feedback links the endocrine and... (More)
Studies have highlighted the existence of two intra-pancreatic axes of communication: one involved in the regulation of enzyme production by insulin—the insular–acinar axis; and another involved in the regulation of insulin release by pancreatic enzymes—the acini–insular axis. Previous studies by our laboratory show that pancreatic enzymes can affect blood glucose homeostasis and insulin secretion independently of their digestive functions, both from the gut lumen and probably from the blood. As a result we would like to introduce here the concept of acini–islet–acinar (AIA) axis communication (feedback), which could play an important role in the development of obesity and diabetes type 2. The AIA feedback links the endocrine and exocrine parts of the pancreas and emphasizes the essential role that the pancreas plays, as a single organ, in the regulation of glucose homeostasis by amylase most probably in gut epithelium and by insulin and glucagon in peripheral blood.
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- author
- Pierzynowski, Stefan G. LU ; Gregory, Peter C. ; Filip, Rafał ; Woliński, Jarosław and Pierzynowska, Kateryna Goncharova
- organization
- publishing date
- 2018
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nutrition and Diabetes
- volume
- 8
- issue
- 1
- article number
- 55
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:30293998
- scopus:85054465418
- ISSN
- 2044-4052
- DOI
- 10.1038/s41387-018-0062-9
- language
- English
- LU publication?
- yes
- id
- 0d8210f1-788d-4195-bf00-e1ea4d6eac3c
- date added to LUP
- 2018-10-29 13:47:50
- date last changed
- 2024-04-01 12:20:45
@article{0d8210f1-788d-4195-bf00-e1ea4d6eac3c,
abstract = {{<p>Studies have highlighted the existence of two intra-pancreatic axes of communication: one involved in the regulation of enzyme production by insulin—the insular–acinar axis; and another involved in the regulation of insulin release by pancreatic enzymes—the acini–insular axis. Previous studies by our laboratory show that pancreatic enzymes can affect blood glucose homeostasis and insulin secretion independently of their digestive functions, both from the gut lumen and probably from the blood. As a result we would like to introduce here the concept of acini–islet–acinar (AIA) axis communication (feedback), which could play an important role in the development of obesity and diabetes type 2. The AIA feedback links the endocrine and exocrine parts of the pancreas and emphasizes the essential role that the pancreas plays, as a single organ, in the regulation of glucose homeostasis by amylase most probably in gut epithelium and by insulin and glucagon in peripheral blood.</p>}},
author = {{Pierzynowski, Stefan G. and Gregory, Peter C. and Filip, Rafał and Woliński, Jarosław and Pierzynowska, Kateryna Goncharova}},
issn = {{2044-4052}},
language = {{eng}},
number = {{1}},
publisher = {{Nature Publishing Group}},
series = {{Nutrition and Diabetes}},
title = {{Glucose homeostasis dependency on acini–islet–acinar (AIA) axis communication : a new possible pathophysiological hypothesis regarding diabetes mellitus}},
url = {{http://dx.doi.org/10.1038/s41387-018-0062-9}},
doi = {{10.1038/s41387-018-0062-9}},
volume = {{8}},
year = {{2018}},
}