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Nutritional and Hormonal Control of Glucose Metabolism
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Nutritional and Hormonal Control of Glucose 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: closed (31 October 2024) | Viewed by 4753

Special Issue Editor

Dr. Joao Paulo Camporez

E-Mail Website
Guest Editor
Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Ribeirao Preto, Brazil
Interests: biochemistry; genetics and molecular biology medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glucose is essential for energy consumption, serving as the primary metabolic fuel for mammals. In order to be utilized as an energy source, glucose needs to be transported across the cell membrane into the cytoplasm, facilitated through protein carrier molecules. The maintenance of normal glucose metabolism, such as producing glucose by the liver during fasting and storing or using glucose postprandially, plays a pivotal role for glucose to be utilizable in most tissue cells. Other nutrients (such as lipids and amino acids) and hormones (such as insulin, glucocorticoids, glucagon, growth hormone, and sex hormones) can modulate glucose metabolism. However, these processes are profoundly altered in pathological conditions, such as insulin resistance, obesity, type 1 and type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and the set of these situations called metabolic syndrome.

This Special Issue explores current advances in the regulation of glucose metabolism on a molecular level. The topics covered by this Special Issue include the impact of nutrients or hormones in molecular targets in central tissues that modulates glucose metabolism (such as skeletal muscle, liver, adipose tissue, pancreas, and central nervous system). Manuscripts dealing with other challenging molecular issues involving glucose metabolism are welcome.

Dr. Joao Paulo Camporez
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • glucose
  • lipids
  • amino acids
  • insulin resistance
  • obesity
  • NAFLD
  • hormones
  • metabolic syndrome
  • diabetes

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Published Papers (2 papers)

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Research

16 pages, 3298 KiB  
Article
Phenylbutyrate and Dichloroacetate Enhance the Liquid-Stored Boar Sperm Quality via PDK1 and PDK3
by Zhihua Guo, Yan Zhang, Anqi Huang, Qingyong Ni and Changjun Zeng
Int. J. Mol. Sci. 2023, 24(23), 17091; https://doi.org/10.3390/ijms242317091 - 4 Dec 2023
Cited by 1 | Viewed by 1782
Abstract
Artificial insemination (AI) with liquid-stored semen is the most prevalent and efficient assisted reproduction technique in the modern pork industry. Pyruvate dehydrogenase complex component X (PDHX) was demonstrated to be associated with sperm metabolism and affected the boar sperm viability, motility, and fertility. [...] Read more.
Artificial insemination (AI) with liquid-stored semen is the most prevalent and efficient assisted reproduction technique in the modern pork industry. Pyruvate dehydrogenase complex component X (PDHX) was demonstrated to be associated with sperm metabolism and affected the boar sperm viability, motility, and fertility. Pyruvate Dehydrogenase Kinases (PDKs) are the key metabolic enzymes that regulate pyruvate dehydrogenase complex (PDHC) activity and also the conversion from glycolysis to oxidative phosphorylation. In the present study, two PDK inhibitors, Dichloroacetate (DCA) and Phenylbutyrate (4-PBA), were added to an extender and investigated to determine their regulatory roles in liquid-stored boar sperm at 17 °C. The results indicated that PDK1 and PDK3 were predominantly located at the head and flagella of the boar sperm. The addition of 2 mM DCA and 0.5 mM 4-PBA significantly enhanced the sperm motility, plasma membrane integrity (PMI), mitochondrial membrane potential (MMP), and ATP content. In addition, DCA and 4-PBA exerted their effects by inhibiting PDK1 and PDK3, respectively. In conclusion, DCA and 4-PBA were found to regulate the boar sperm metabolic activities via PDK1 and PDK3. These both can improve the quality parameters of liquid-stored boar sperm, which will help to improve and optimize liquid-stored boar semen after their addition in the extender. Full article
(This article belongs to the Special Issue Nutritional and Hormonal Control of Glucose Metabolism)
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15 pages, 5408 KiB  
Article
Estradiol Protects Female ApoE KO Mice against Western-Diet-Induced Non-Alcoholic Steatohepatitis
by Layanne C. C. Araujo, Alessandra G. Cruz, Felipe N. Camargo, Felipe G. Sucupira, Gabriela V. Moreira, Sandro L. Matos, Andressa G. Amaral, Gilson Masahiro Murata, Carla R. O. Carvalho and Joao Paulo Camporez
Int. J. Mol. Sci. 2023, 24(12), 9845; https://doi.org/10.3390/ijms24129845 - 7 Jun 2023
Cited by 6 | Viewed by 2294
Abstract
The prevalence of non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), is higher in men than in women of reproductive age, and postmenopausal women are especially susceptible to developing the disease. Aim: we evaluated if female apolipoprotein E (ApoE) [...] Read more.
The prevalence of non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), is higher in men than in women of reproductive age, and postmenopausal women are especially susceptible to developing the disease. Aim: we evaluated if female apolipoprotein E (ApoE) KO mice were protected against Western-diet (WD)-induced NASH. Methods: Female ovariectomized (OVX) ApoE KO mice or sham-operated (SHAM) mice were fed either a WD or a regular chow (RC) for 7 weeks. Additionally, OVX mice fed a WD were treated with either estradiol (OVX + E2) or vehicle (OVX). Results: Whole-body fat, plasma glucose, and plasma insulin were increased and associated with increased glucose intolerance in OVX mice fed a WD (OVX + WD). Plasma and hepatic triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) hepatic enzymes were also increased in the plasma of OVX + WD group, which was associated with hepatic fibrosis and inflammation. Estradiol replacement in OVX mice reduced body weight, body fat, glycemia, and plasma insulin associated with reduced glucose intolerance. Treatment also reduced hepatic triglycerides, ALT, AST, hepatic fibrosis, and inflammation in OVX mice. Conclusions: These data support the hypothesis that estradiol protects OVX ApoE KO mice from NASH and glucose intolerance. Full article
(This article belongs to the Special Issue Nutritional and Hormonal Control of Glucose Metabolism)
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