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Biomedicines
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Pancreatic Alpha Cell and Beta Cell Function: The Good Guys...
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Pancreatic Alpha Cell and Beta Cell Function: The Good Guys and the Bad Guys Affecting Regulation and Interaction of Alpha and Beta Cells

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7251

Special Issue Editor

Dr. Giovanni Pacini

E-Mail Website
Guest Editor
Independent Researcher, 35142 Padova, Italy
Interests: glucose metabolism; insulin sensitivity; insulin secretion; beta cell function; insulin clearance; alpha cell function; gestational diabetes; type 2 diabetes; animal models; mathematical modelling

Special Issue Information

Dear Colleagues,

Glucose homeostasis is regulated by several processes. The main ones are summarized in the so-called “ominous octet”, including insulin secretion, hepatic glucose production, glucose uptake, incretin effect, glucagon secretion, glucose reabsorption, lipolysis, and neurotransmitter function. All these processes involve different bodily organs and tissues. However, if we rank such organs and tissues for their relevance in glucose homeostasis, there is no doubt that the winner is the pancreas, as it is in charge of both insulin secretion from the beta cells and glucagon secretion from the alpha cells. In this Special Issue, we will focus on the function of both alpha and beta cells.

In this Special Issue, we are interested in studies that provide further insight in one or more of the indicated issues, since, despite much knowledge being already available, many aspects need further elucidation and deeper insight. Relevant studies may be both at the cellular or tissue level and at the whole-body level. In addition, we also welcome studies based on the development or application of mathematical modelling for the investigation of the illustrated issues. Indeed, mathematical modelling can help in explaining or quantifying some physiological/pathophysiological processes that are hardly measurable in vivo, and on the other hand can trigger new experiments for deeper investigations and insights in the topics of interest. In this Special Issue, we welcome both original articles and other types of articles, such as reviews, meta-analyses, and commentaries.

More schematically, the scope of the Special Issue includes, but is not limited to:

  • Endogenous substances stimulating or inhibiting glucagon secretion.
  • Endogenous substances stimulating or inhibiting insulin secretion.
  • Pharmacological agents with effects on glucagon or insulin secretion.
  • Nutrients with effects on glucagon or insulin secretion.
  • The interplay between alpha cell and beta cell function.
  • Does physical exercise affect insulin secretion or glucagon inhibition?
  • Environmental and other factors affecting alpha cell and beta cell function.
  • Mathematical modelling and artificial intelligence in alpha cell and beta cell function.

Dr. Giovanni Pacini
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • alpha cell function
  • beta cell function
  • glucagon secretion
  • insulin secretion
  • cell apoptosis
  • paracrine regulation
  • incretin hormones
  • glucagon-like-peptide-1
  • GLP-1 receptor agonist
  • dual receptor agonist
  • environmental toxicity
  • mathematical modelling
  • artificial intelligence

Published Papers (3 papers)

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Research

17 pages, 997 KiB  
Article
Glucometabolism in Kidney Transplant Recipients with and without Posttransplant Diabetes: Focus on Beta-Cell Function
by Amelie Kurnikowski, Benedetta Salvatori, Michael Krebs, Klemens Budde, Kathrin Eller, Julio Pascual, Micaela Morettini, Christian Göbl, Manfred Hecking and Andrea Tura
Biomedicines 2024, 12(2), 317; https://doi.org/10.3390/biomedicines12020317 - 30 Jan 2024
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Abstract
Posttransplant diabetes mellitus (PTDM) is a common complication after kidney transplantation. Pathophysiologically, whether beta-cell dysfunction rather than insulin resistance may be the predominant defect in PTDM has been a matter of debate. The aim of the present analysis was to compare glucometabolism in [...] Read more.
Posttransplant diabetes mellitus (PTDM) is a common complication after kidney transplantation. Pathophysiologically, whether beta-cell dysfunction rather than insulin resistance may be the predominant defect in PTDM has been a matter of debate. The aim of the present analysis was to compare glucometabolism in kidney transplant recipients with and without PTDM. To this aim, we included 191 patients from a randomized controlled trial who underwent oral glucose tolerance tests (OGTTs) 6 months after transplantation. We derived several basic indices of beta-cell function and insulin resistance as well as variables from mathematical modeling for a more robust beta-cell function assessment. Mean ± standard deviation of the insulin sensitivity parameter PREDIM was 3.65 ± 1.68 in PTDM versus 5.46 ± 2.57 in NON-PTDM. Model-based glucose sensitivity (indicator of beta-cell function) was 68.44 ± 57.82 pmol∙min−1∙m−2∙mM−1 in PTDM versus 143.73 ± 112.91 pmol∙min−1∙m−2∙mM−1 in NON-PTDM, respectively. Both basic indices and model-based parameters of beta-cell function were more than 50% lower in patients with PTDM, indicating severe beta-cell impairment. Nonetheless, some defects in insulin sensitivity were also present, although less marked. We conclude that in PTDM, the prominent defect appears to be beta-cell dysfunction. From a pathophysiological point of view, patients at high risk for developing PTDM may benefit from intensive treatment of hyperglycemia over the insulin secretion axis. Full article
(This article belongs to the Special Issue Pancreatic Alpha Cell and Beta Cell Function: The Good Guys and the Bad Guys Affecting Regulation and Interaction of Alpha and Beta Cells)
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30 pages, 2089 KiB  
Article
The Glycemic Curve during the Oral Glucose Tolerance Test: Is It Only Indicative of Glycoregulation?
by Daniela Vejrazkova, Marketa Vankova, Petra Lukasova, Martin Hill, Josef Vcelak, Andrea Tura, Denisa Chocholova and Bela Bendlova
Biomedicines 2023, 11(5), 1278; https://doi.org/10.3390/biomedicines11051278 - 25 Apr 2023
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Abstract
The shape of the glycemic curve during the oral glucose tolerance test (OGTT), interpreted in the correct context, can predict impaired glucose homeostasis. Our aim was to reveal information inherent in the 3 h glycemic trajectory that is of physiological relevance concerning the [...] Read more.
The shape of the glycemic curve during the oral glucose tolerance test (OGTT), interpreted in the correct context, can predict impaired glucose homeostasis. Our aim was to reveal information inherent in the 3 h glycemic trajectory that is of physiological relevance concerning the disruption of glycoregulation and complications beyond, such as components of metabolic syndrome (MS). Methods: In 1262 subjects (1035 women, 227 men) with a wide range of glucose tolerance, glycemic curves were categorized into four groups: monophasic, biphasic, triphasic, and multiphasic. The groups were then monitored in terms of anthropometry, biochemistry, and timing of the glycemic peak. Results: Most curves were monophasic (50%), then triphasic (28%), biphasic (17.5%), and multiphasic (4.5%). Men had more biphasic curves than women (33 vs. 14%, respectively), while women had more triphasic curves than men (30 vs. 19%, respectively) (p < 0.01). Monophasic curves were more frequent in people with impaired glucose regulation and MS compared to bi-, tri-, and multiphasic ones. Peak delay was the most common in monophasic curves, in which it was also most strongly associated with the deterioration of glucose tolerance and other components of MS. Conclusion: The shape of the glycemic curve is gender dependent. A monophasic curve is associated with an unfavorable metabolic profile, especially when combined with a delayed peak. Full article
(This article belongs to the Special Issue Pancreatic Alpha Cell and Beta Cell Function: The Good Guys and the Bad Guys Affecting Regulation and Interaction of Alpha and Beta Cells)
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9 pages, 2236 KiB  
Communication
Contribution of GIP and GLP-1 to the Insulin Response to Oral Administration of Glucose in Female Mice
by Bo Ahrén
Biomedicines 2023, 11(2), 591; https://doi.org/10.3390/biomedicines11020591 - 16 Feb 2023
Cited by 1 | Viewed by 1389
Abstract
It has previously been shown that the incretin effect accounts for ≈50% of the insulin response to oral glucose in normal mice. Now, I have proceeded and studied the contribution of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) to the insulin response [...] Read more.
It has previously been shown that the incretin effect accounts for ≈50% of the insulin response to oral glucose in normal mice. Now, I have proceeded and studied the contribution of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) to the insulin response to oral glucose in female mice by using receptor antagonists. A specific GIP receptor antagonist (mGIP(3-30); 50 or 500 nmol/kg), a specific GLP-1 receptor antagonist (exendin(9-39); 3 or 30 nmol/kg), the combination of mGIP (500 nmol/kg) and exendin(9-39) (30 nmol/kg), or saline was given intravenously four minutes after administration of glucose (50 mg) through a gastric tube in anesthetized C57/BL6J mice (n = 95) with samples obtained before glucose administration and after 15, 30 and 60 min. The insulinogenic index, determined as the area under the 60 min curve for insulin (AUCinsulin) divided by the AUCglucose, was used to reflect the insulin response. It was found that the insulinogenic index was reduced by 67 ± 4% by mGIP(3-30) (p < 0.001), by 60 ± 14% by exendin(9-39) (p = 0.007) and by 61 ± 14% by the combination of mGIP(3-30) and exendin(9-39) (p = 0.043), both at their highest doses, compared to animals injected with glucose in the same experimental series. It is concluded that both GIP and GLP-1 are required for a normal incretin effect in female mice, that they contribute similarly to the insulin response, and that it is unlikely that there is another incretin hormone in this species. Full article
(This article belongs to the Special Issue Pancreatic Alpha Cell and Beta Cell Function: The Good Guys and the Bad Guys Affecting Regulation and Interaction of Alpha and Beta Cells)
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