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Nutrients
Special Issues
Glucose Metabolism in Obese and Diabetic Patients
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Glucose Metabolism in Obese and Diabetic Patients

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 5 July 2024 | Viewed by 1947

Special Issue Editor

Dr. Takao Kimura

E-Mail Website
Guest Editor
Department of Clinical Laboratory Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi 371-8511, Gunma, Japan
Interests: obesity; glucose metabolism; insulin resistance; lipid metabolism; exercise; food science

Special Issue Information

Dear Colleagues,

Addressing the rise of diabetes and obesity/overweight is an urgent global challenge. Over 70% of deaths worldwide are caused by noncommunicable diseases (NCDs), and diabetes and obesity/overweight are major risk factors for NCDs. Reducing diabetes and obesity/overweight is an important strategy to prevent and control NCDs globally. Dealing with this issue at the level of individuals and societies requires a multifaceted and multilayered cooperative system in all fields, including medicine, nutrition, exercise physiology, agriculture, economics, education, and government policy. This Special Issue examines tools for preventing and managing diabetes and obesity/overweight from an interdisciplinary perspective. To achieve this goal, elucidation of glucose metabolism in obese and diabetic patients is essential. We look forward to reports on medicines, supplements, screening system, eating habits, exercise, education, lifestyle interventions, wearable devices, applications, and strategies that are effective in preventing and managing diabetes and obesity/overweight.

The purpose of this Special Issue of Nutrients, entitled “Glucose Metabolism in Obese and Diabetic Patients”, is to further contribute to the current nutritional evidence. Experimental research, systematic and meta-analyses, and narrative reviews are welcome.

Dr. Takao Kimura
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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • diabetes mellitus
  • obesity
  • overweight
  • diet
  • exercise
  • food
  • gut microbiota
  • metabolomics
  • microbial metabolites
  • nutrition
  • supplement
  • aging
  • lipid metabolism
  • glucose metabolism
  • insulin sensitivity
  • insulin resistance
  • insulin release
  • incretin
  • gender difference
  • body composition

Published Papers (2 papers)

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Research

20 pages, 5116 KiB  
Article
Calorie Restriction Using High-Fat/Low-Carbohydrate Diet Suppresses Liver Fat Accumulation and Pancreatic Beta-Cell Dedifferentiation in Obese Diabetic Mice
by Xiao Lei, Emi Ishida, Satoshi Yoshino, Shunichi Matsumoto, Kazuhiko Horiguchi and Eijiro Yamada
Nutrients 2024, 16(7), 995; https://doi.org/10.3390/nu16070995 - 28 Mar 2024
Viewed by 710
Abstract
In diabetes, pancreatic β-cells gradually lose their ability to secrete insulin with disease progression. β-cell dysfunction is a contributing factor to diabetes severity. Recently, islet cell heterogeneity, exemplified by β-cell dedifferentiation and identified in diabetic animals, has attracted attention as an underlying molecular [...] Read more.
In diabetes, pancreatic β-cells gradually lose their ability to secrete insulin with disease progression. β-cell dysfunction is a contributing factor to diabetes severity. Recently, islet cell heterogeneity, exemplified by β-cell dedifferentiation and identified in diabetic animals, has attracted attention as an underlying molecular mechanism of β-cell dysfunction. Previously, we reported β-cell dedifferentiation suppression by calorie restriction, not by reducing hyperglycemia using hypoglycemic agents (including sodium-glucose cotransporter inhibitors), in an obese diabetic mice model (db/db). Here, to explore further mechanisms of the effects of food intake on β-cell function, db/db mice were fed either a high-carbohydrate/low-fat diet (db-HC) or a low-carbohydrate/high-fat diet (db-HF) using similar calorie restriction regimens. After one month of intervention, body weight reduced, and glucose intolerance improved to a similar extent in the db-HC and db-HF groups. However, β-cell dedifferentiation did not improve in the db-HC group, and β-cell mass compensatory increase occurred in this group. More prominent fat accumulation occurred in the db-HC group livers. The expression levels of genes related to lipid metabolism, mainly regulated by peroxisome proliferator-activated receptor α and γ, differed significantly between groups. In conclusion, the fat/carbohydrate ratio in food during calorie restriction in obese mice affected both liver lipid metabolism and β-cell dedifferentiation. Full article
(This article belongs to the Special Issue Glucose Metabolism in Obese and Diabetic Patients)
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13 pages, 4298 KiB  
Article
Phogrin Regulates High-Fat Diet-Induced Compensatory Pancreatic β-Cell Growth by Switching Binding Partners
by Chisato Kubota, Ryoko Torii, Masahiro Hosaka, Toshiyuki Takeuchi, Hiroshi Gomi and Seiji Torii
Nutrients 2024, 16(1), 169; https://doi.org/10.3390/nu16010169 - 04 Jan 2024
Viewed by 929
Abstract
The receptor protein tyrosine phosphatase phogrin primarily localizes to hormone secretory granules in neuroendocrine cells. Concurrent with glucose-stimulated insulin secretion, phogrin translocates to pancreatic β-cell plasma membranes, where it interacts with insulin receptors (IRs) to stabilize insulin receptor substrate 2 (IRS2) that, in [...] Read more.
The receptor protein tyrosine phosphatase phogrin primarily localizes to hormone secretory granules in neuroendocrine cells. Concurrent with glucose-stimulated insulin secretion, phogrin translocates to pancreatic β-cell plasma membranes, where it interacts with insulin receptors (IRs) to stabilize insulin receptor substrate 2 (IRS2) that, in turn, contributes to glucose-responsive β-cell growth. Pancreatic β-cell development was not altered in β-cell-specific, phogrin-deficient mice, but the thymidine incorporation rate decreased in phogrin-deficient islets with a moderate reduction in IRS2 protein expression. In this study, we analyzed the β-cell response to high-fat diet stress and found that the compensatory expansion in β-cell mass was significantly suppressed in phogrin-deficient mice. Phogrin–IR interactions occurred only in high-fat diet murine islets and proliferating β-cell lines, whereas they were inhibited by the intercellular binding of surface phogrin under confluent cell culture conditions. Thus, phogrin could regulate glucose-stimulated compensatory β-cell growth by changing its binding partner from another β-cell phogrin to IR in the same β-cells. Full article
(This article belongs to the Special Issue Glucose Metabolism in Obese and Diabetic Patients)
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