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Effects of Dietary Intake on Pancreas

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (15 October 2019) | Viewed by 18825

Special Issue Editors


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Guest Editor
Gastroenterology Unit IRCCS “Casa Sollievo della Sofferenza” Hospital, San Giovanni Rotondo (FG) Italy
Interests: Gene Expression; Gastroenterology; Pancreatic Diseases; Liver Diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The literature reports substantial evidence of the role of nutrition in pancreatic disease. Often this evidence is inconclusive due to confounding factors. Studies are needed to better clarify the interaction between dietary factors and pancreatic disease.

The pancreas is an organ of the digestive system with both endocrine and exocrine functions, which are involved in the control of blood sugar levels and metabolism within the body, and the digestion of substances by breaking down carbohydrates, proteins, and lipids in ingested food entering the duodenum from the stomach, respectively. Playing a vital role in the digestive system, it appears clear that the pancreas can be perturbed by dietary intake leading to pancreatic diseases. Nutritional status, nutraceuticals, active metabolites, pre and probiotics, additives, and preservatives can also have potential protective or harmful effects on pancreatic function and disease. The objective of this proposed Special Issue on “Effects of Dietary Intake on Pancreas” is to publish selected papers (reviews and/or clinical or experimental studies) dealing with specific aspects of nutrition that could play a role in pancreatic function, both in normal subjects and in patients with pancreatic disease. Moreover, we are also interested in the results of nutritional intervention for pancreatic cancer to understand the possible positive impact of nutrients in combination with the current therapies. This will pave the way for the development of novel nutritional intervention that can influence the survival rates and/or the quality of life of the patients.

Dr. Valerio Pazienza
Prof. Marco Falasca
Guest Editors

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Keywords

  • Nutrition, microbiota, and pancreatic disease
  • Nutritional status
  • The impact of nutrition of genes
  • Nutrition integrative therapy
  • Pancreatic cancer
  • Prebiotics, probiotics, and postbiotics

Published Papers (4 papers)

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Research

15 pages, 4161 KiB  
Article
Targeting Mitochondrial Calcium Uptake with the Natural Flavonol Kaempferol, to Promote Metabolism/Secretion Coupling in Pancreatic β-cells
by Flavien Bermont, Aurelie Hermant, Romy Benninga, Christian Chabert, Guillaume Jacot, Jaime Santo-Domingo, Marine R-C Kraus, Jerome N. Feige and Umberto De Marchi
Nutrients 2020, 12(2), 538; https://doi.org/10.3390/nu12020538 - 19 Feb 2020
Cited by 31 | Viewed by 4305
Abstract
Pancreatic β-cells secrete insulin to lower blood glucose, following a meal. Maintenance of β-cell function is essential to preventing type 2 diabetes. In pancreatic β-cells, mitochondrial matrix calcium is an activating signal for insulin secretion. Recently, the molecular identity of the mitochondrial calcium [...] Read more.
Pancreatic β-cells secrete insulin to lower blood glucose, following a meal. Maintenance of β-cell function is essential to preventing type 2 diabetes. In pancreatic β-cells, mitochondrial matrix calcium is an activating signal for insulin secretion. Recently, the molecular identity of the mitochondrial calcium uniporter (MCU), the transporter that mediates mitochondrial calcium uptake, was revealed. Its role in pancreatic β-cell signal transduction modulation was clarified, opening new perspectives for intervention. Here, we investigated the effects of a mitochondrial Ca2+-targeted nutritional intervention strategy on metabolism/secretion coupling, in a model of pancreatic insulin-secreting cells (INS-1E). Acute treatment of INS-1E cells with the natural plant flavonoid and MCU activator kaempferol, at a low micromolar range, increased mitochondrial calcium rise during glucose stimulation, without affecting the expression level of the MCU and with no cytotoxicity. Enhanced mitochondrial calcium rises potentiated glucose-induced insulin secretion. Conversely, the MCU inhibitor mitoxantrone inhibited mitochondrial Ca2+ uptake and prevented both glucose-induced insulin secretion and kaempferol-potentiated effects. The kaempferol-dependent potentiation of insulin secretion was finally validated in a model of a standardized pancreatic human islet. We conclude that the plant product kaempferol activates metabolism/secretion coupling in insulin-secreting cells by modulating mitochondrial calcium uptake. Full article
(This article belongs to the Special Issue Effects of Dietary Intake on Pancreas)
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18 pages, 634 KiB  
Communication
Effects of Nutrient Intake during Pregnancy and Lactation on the Endocrine Pancreas of the Offspring
by Valentine Suzanne Moullé and Patricia Parnet
Nutrients 2019, 11(11), 2708; https://doi.org/10.3390/nu11112708 - 08 Nov 2019
Cited by 9 | Viewed by 6359
Abstract
The pancreas has an essential role in the regulation of glucose homeostasis by secreting insulin, the only hormone with a blood glucose lowering effect in mammals. Several circulating molecules are able to positively or negatively influence insulin secretion. Among them, nutrients such as [...] Read more.
The pancreas has an essential role in the regulation of glucose homeostasis by secreting insulin, the only hormone with a blood glucose lowering effect in mammals. Several circulating molecules are able to positively or negatively influence insulin secretion. Among them, nutrients such as fatty acids or amino acids can directly act on specific receptors present on pancreatic beta cells. Dietary intake, especially excessive nutrient intake, is known to modify energy balance in adults, resulting in pancreatic dysfunction. However, gestation and lactation are critical periods for fetal development and pup growth and specific dietary nutrients are required for optimal growth. Feeding alterations during these periods will impact offspring development and increase the risk of developing metabolic disorders in adulthood, leading to metabolic programming. This review will focus on the influence of nutrient intake during gestation and lactation periods on pancreas development and function in offspring, highlighting the molecular mechanism of imprinting on this organ. Full article
(This article belongs to the Special Issue Effects of Dietary Intake on Pancreas)
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12 pages, 2082 KiB  
Article
Short-Term High-Starch, Low-Protein Diet Induces Reversible Increase in β-cell Mass Independent of Body Weight Gain in Mice
by Atsushi Masuda, Yusuke Seino, Masatoshi Murase, Shihomi Hidaka, Megumi Shibata, Takeshi Takayanagi, Yoshihisa Sugimura, Yoshitaka Hayashi and Atsushi Suzuki
Nutrients 2019, 11(5), 1045; https://doi.org/10.3390/nu11051045 - 10 May 2019
Cited by 6 | Viewed by 3637
Abstract
Long-term exposure to a high starch, low-protein diet (HSTD) induces body weight gain and hyperinsulinemia concomitantly with an increase in β-cell mass (BCM) and pancreatic islets number in mice; however, the effect of short-term exposure to HSTD on BCM and islet number has [...] Read more.
Long-term exposure to a high starch, low-protein diet (HSTD) induces body weight gain and hyperinsulinemia concomitantly with an increase in β-cell mass (BCM) and pancreatic islets number in mice; however, the effect of short-term exposure to HSTD on BCM and islet number has not been elucidated. In the present study, we investigated changes in body weight, plasma insulin levels, BCM and islet number in mice fed HSTD for 5 weeks followed by normal chow (NC) for 2 weeks. BCM and islet number were increased in mice fed HSTD for 5 weeks compared with those in mice fed NC. On the other hand, mice fed HSTD for 5 weeks followed by NC for 2 weeks (SN) showed decreased BCM and insulin levels, compared to mice fed HSTD for 7 weeks, and no significant differences in these parameters were observed between SN and the control NC at 7 weeks. No significant difference in body weight was observed among HSTD, NC and SN fed groups. These results suggest that a high-starch diet induces an increase in BCM in a manner independent of body weight gain, and that 2 weeks of NC feeding is sufficient for the reversal of the morphological changes induced in islets by HSTD feeding. Full article
(This article belongs to the Special Issue Effects of Dietary Intake on Pancreas)
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13 pages, 2556 KiB  
Article
High Levels of Prebiotic Resistant Starch in Diet Modulate Gene Expression and Metabolomic Profile in Pancreatic Cancer Xenograft Mice
by Concetta Panebianco, Annacandida Villani and Valerio Pazienza
Nutrients 2019, 11(4), 709; https://doi.org/10.3390/nu11040709 - 27 Mar 2019
Cited by 12 | Viewed by 3838
Abstract
Cancer initiation and protection mainly derives from a systemic metabolic environment regulated by dietary patterns. Less is known about the impact of nutritional interventions in people with a diagnosis of cancer. The aim of our study was to investigate the effect of a [...] Read more.
Cancer initiation and protection mainly derives from a systemic metabolic environment regulated by dietary patterns. Less is known about the impact of nutritional interventions in people with a diagnosis of cancer. The aim of our study was to investigate the effect of a diet rich in resistant starch (RS) on cell pathways modulation and metabolomic phenotype in pancreatic cancer xenograft mice. RNA-Seq experiments on tumor tissue showed that 25 genes resulted in dysregulated pancreatic cancer in mice fed with an RS diet, as compared to those fed with control diet. Moreover, in these two different mice groups, six serum metabolites were deregulated as detected by LC–MS analysis. A bioinformatic prediction analysis showed the involvement of the differentially expressed genes on insulin receptor signaling, circadian rhythm signaling, and cancer drug resistance among the three top canonical pathways, whilst cell death and survival, gene expression, and neurological disease were among the three top disease and biological functions. These findings shed light on the genomic and metabolic phenotype, contributing to the knowledge of the mechanisms through which RS may act as a potential supportive approach for enhancing the efficacy of existing cancer treatments. Full article
(This article belongs to the Special Issue Effects of Dietary Intake on Pancreas)
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