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Molecular Basis of Pancreatic Secretion and Metabolism
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Molecular Basis of Pancreatic Secretion and Metabolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 4923

Special Issue Editor

Dr. Dongki Yang

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Guest Editor
Department of Physiology, College of Medicine, Gachon University, Incheon 21999, Republic of Korea
Interests: acute pancreatitis; cystic fibrosis; chronic pancreatitis; pancreatic bicarbonate secretion; salivary gland function and dysfunction

Special Issue Information

Dear Colleagues,

The pancreas is a human organ that has two important functions: exocrine function related to digestive diseases and endocrine function related to diabetes, etc. The exocrine function plays an important role in digestion, and the endocrine function, which secretes various hormones such as insulin, glucagon, and somatostatin into the blood, plays an essential function in various metabolic functions in the body.

The pancreatic juice secreted from the pancreas into the digestive tract contains a high concentration of bicarbonate ions, so it neutralizes the acidity of food that has passed from the stomach to the duodenum, preventing damage to the duodenal mucosa caused by hydrochloric acid or pepsin, preventing the destruction of various digestive enzymes, and increasing their activity. Therefore, the first aim of this Special Issue is to elucidate in detail the mechanism by which the pancreas secretes bicarbonate ions. Among the various hormones secreted by the endocrine function of the pancreas, insulin and glucagon play an important role in the bioavailability of glucose, the main energy source of our body, and somatostatin has a wide range of inhibitory functions in the intestines. Our second goal is to understand the disease mechanisms that result from reductions and elevations in the hormones involved in these metabolism pathways.

Dr. Dongki Yang
Guest Editor

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Keywords

  • exocrine of the pancreas
  • endocrine of the pancreas
  • acute pancreatitis
  • chronic pancreatitis
  • cystic fibrosis
  • pancreatic metabolic hormones
  • pancreatic metabolic disease
  • mechanism of pancreatic bicarbonate secretion
  • the sodium bicarbonate cotransporter (NBC)
  • cystic fibrosis transmembrane conductance regulator (CFTR)
  • regulators of the ion channels and ion transporters involved in secretion

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Published Papers (4 papers)

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Research

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14 pages, 4820 KiB  
Article
Single-Cell RNA Sequencing Outperforms Single-Nucleus RNA Sequencing in Analyzing Pancreatic Cell Diversity and Gene Expression in Goats
by Jie Cheng, Tianxi Zhang, Yan Cheng, Kefyalew Gebeyew, Zhiliang Tan and Zhixiong He
Int. J. Mol. Sci. 2025, 26(8), 3916; https://doi.org/10.3390/ijms26083916 - 21 Apr 2025
Viewed by 338
Abstract
The objective of this study was to determine whether single-cell RNA sequencing (scRNA-seq) or single-nucleus RNA sequencing (snRNA-seq) was more effective for studying the goat pancreas. Pancreas tissues from three healthy 10-day-old female Xiangdong black goats were processed into single-cell and single-nucleus suspensions. [...] Read more.
The objective of this study was to determine whether single-cell RNA sequencing (scRNA-seq) or single-nucleus RNA sequencing (snRNA-seq) was more effective for studying the goat pancreas. Pancreas tissues from three healthy 10-day-old female Xiangdong black goats were processed into single-cell and single-nucleus suspensions. These suspensions were then used to compare cellular composition and gene expression levels following library construction and sequencing. Both scRNA-seq and snRNA-seq were eligible for primary analysis but produced different cell identification profiles in pancreatic tissue. Both methods successfully annotated pancreatic acinar cells, ductal cells, alpha cells, beta cells, and endothelial cells. However, pancreatic stellate cells, immune cells, and delta cells were uniquely annotated by scRNA-seq, while pancreatic stem cells were uniquely identified by snRNA-seq. Furthermore, the genes related to digestive enzymes showed a higher expression in scRNA-seq than in snRNA-seq. In the present study, scRNA-seq detected a great diversity of pancreatic cell types and was more effective in profiling key genes than snRNA-seq, demonstrating that scRNA-seq was better suited for studying the goat pancreas. However, the choice between scRNA-seq and snRNA-seq should consider the sample compatibility, technical differences, and experimental objectives. Full article
(This article belongs to the Special Issue Molecular Basis of Pancreatic Secretion and Metabolism)
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24 pages, 3788 KiB  
Article
A Two-Hour Fetal Glucagon Infusion Stimulates Hepatic Catabolism of Amino Acids in Fetal Sheep
by Amelia R. Tanner, Sarah N. Cilvik, Marjorie A. Nguyen, Evgenia Dobrinskikh, Russell V. Anthony, Stephanie R. Wesolowski and Paul J. Rozance
Int. J. Mol. Sci. 2025, 26(5), 1904; https://doi.org/10.3390/ijms26051904 - 22 Feb 2025
Viewed by 615
Abstract
Postnatally, glucagon acutely lowers plasma amino acid (AA) concentrations by stimulating hepatic AA catabolism, but its fetal actions remain unclear. This study tested whether a 2 h fetal glucagon infusion would stimulate hepatic AA catabolism and inhibit placental AA transfer. Late-gestation pregnant sheep [...] Read more.
Postnatally, glucagon acutely lowers plasma amino acid (AA) concentrations by stimulating hepatic AA catabolism, but its fetal actions remain unclear. This study tested whether a 2 h fetal glucagon infusion would stimulate hepatic AA catabolism and inhibit placental AA transfer. Late-gestation pregnant sheep (0.9 gestation) underwent surgical, vascular catheterization and received fetal glucagon (n = 8) or vehicle infusions (n = 8) in a crossover design with a 48 h washout period. Nutrient uptake and utilization were assessed during each infusion, and fetal liver and placental tissue were collected post-infusion under hyperglucagonemic (n = 4) or vehicle (n = 4) conditions. Glucagon receptor was identified in fetal hepatocyte and trophoblast cells. Glucagon reduced fetal plasma AA concentrations by 20% (p = 0.0103) and increased plasma glucose by 47% (p = 0.0152), leading to a three-fold rise in fetal plasma insulin (p = 0.0459). Hepatic gene expression associated with AA catabolism and gluconeogenesis increased (p < 0.0500) following glucagon infusion, and hepatic metabolomic analysis showed enrichment in AA metabolism pathways. However, placental AA transfer was unaffected by 2 h fetal glucagon infusions. In conclusion, a 2 h glucagon infusion stimulates hepatic glucose production and enhances AA catabolism in the fetal liver, lowering plasma AA concentrations. The primary acute effects of fetal glucagon are hepatic, as placental AA transfer is unchanged. Full article
(This article belongs to the Special Issue Molecular Basis of Pancreatic Secretion and Metabolism)
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17 pages, 3033 KiB  
Article
The Synergistic Impact of Glycolysis, Mitochondrial OxPhos, and PEP Cycling on ATP Production in Beta Cells
by Vladimir Grubelnik, Jan Zmazek and Marko Marhl
Int. J. Mol. Sci. 2025, 26(4), 1454; https://doi.org/10.3390/ijms26041454 - 10 Feb 2025
Viewed by 953
Abstract
Pancreatic beta cells regulate insulin secretion in response to glucose by generating ATP, which modulates ATP-sensitive potassium channels (KATP) channel activity and Ca2+ dynamics. We present a model of ATP production in pancreatic beta cells, focusing on ATP dynamics within [...] Read more.
Pancreatic beta cells regulate insulin secretion in response to glucose by generating ATP, which modulates ATP-sensitive potassium channels (KATP) channel activity and Ca2+ dynamics. We present a model of ATP production in pancreatic beta cells, focusing on ATP dynamics within the bulk cytosol, submembrane region, and microdomains near KATP channels. ATP is generated through glycolysis, mitochondrial oxidative phosphorylation (OxPhos), and glycolytic pyruvate kinase-mediated phosphoenolpyruvate (PEP) production, supported by PEP cycling between mitochondria and the cytosol. The model examines ATP production in relation to Ca2+ oscillations, elucidating their interdependent dynamics. Our findings demonstrate that both mitochondrial OxPhos and PEP-mediated ATP production contribute substantially to cellular ATP levels. Specifically, glycolysis and mitochondrial OxPhos are crucial for the initial (first-phase) increase in bulk and subplasmalemmal ATP, effectively “filling up” the ATP pool in beta cells. In the second phase, coordinated cycling between OxPhos and PEP pathways enables cost-effective fine-tuning of ATP levels, with localized effects in the KATP channel microdomains. This model addresses and clarifies the recent debate regarding the mechanisms by which sufficient ATP concentrations are achieved to close KATP channels in glucose-stimulated beta cells, offering novel insights into the regulation of energy production and KATP channel activity. Full article
(This article belongs to the Special Issue Molecular Basis of Pancreatic Secretion and Metabolism)
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Review

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16 pages, 805 KiB  
Review
Inflammatory Processes: Key Mediators of Oncogenesis and Progression in Pancreatic Ductal Adenocarcinoma (PDAC)
by Liu Yang, Shuangying Qiao, Ge Zhang, Aiping Lu and Fangfei Li
Int. J. Mol. Sci. 2024, 25(20), 10991; https://doi.org/10.3390/ijms252010991 - 12 Oct 2024
Cited by 1 | Viewed by 2374
Abstract
Associations between inflammation and cancer were first discovered approximately 160 years ago by Rudolf Virchow, who observed that tumors were infiltrated with inflammatory cells, and defined inflammation as a pathological condition. Inflammation has now emerged as one of the key mediators in oncogenesis [...] Read more.
Associations between inflammation and cancer were first discovered approximately 160 years ago by Rudolf Virchow, who observed that tumors were infiltrated with inflammatory cells, and defined inflammation as a pathological condition. Inflammation has now emerged as one of the key mediators in oncogenesis and tumor progression, including pancreatic ductal adenocarcinoma (PDAC). However, the role of inflammatory processes in cancers is complicated and controversial, and the detailed regulatory mechanisms are still unclear. This review elucidates the dynamic interplay between inflammation and immune regulation, microenvironment alteration, metabolic reprogramming, and microbiome risk factors in PDAC, committing to exploring a deeper understanding of the role of crucial inflammatory pathways and molecules for providing insights into therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Basis of Pancreatic Secretion and Metabolism)
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