Special Issue "Nutrient and Hormone Sensing Mechanisms and Signaling Pathways"

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

Deadline for manuscript submissions: 20 April 2022.

Special Issue Editors

Dr. Kim Loh
E-Mail Website
Guest Editor
Diabetes & Metabolic Disease Laboratory, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, VIC 3065, Australia
Interests: Neuropeptide Y (NPY); AMP-activated protein kinase (AMPK); diabetes; beta-cell biology; energy expenditure; glucose metabolism
Dr. Chieh-Hsin Yang
E-Mail
Guest Editor
Diabetes & Metabolic Disease Laboratory, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, VIC 3065, Australia
Interests: Neuropeptide Y (NPY); AMP-activated protein kinase (AMPK); diabetes; beta-cell biology; glucose metabolism

Special Issue Information

Dear Colleagues,

We are extremely pleased to announce that in this Special Issue of Nutrients, we are planning to bring together articles that discuss the mechanisms and signaling pathways that are involved in nutrient and hormone sensing.

The ability of the body to sense and react to changes in nutrient status and hormone levels in the circulation is critical in eliciting metabolic adaptation and survival responses. Mechanisms and pathways involved in nutrient and hormone sensing of metabolic tissues such as the brain, liver, pancreas, and adipose tissue have been extensively studied over the last decade. These mechanisms and pathways are commonly dysregulated in human metabolic diseases such as obesity, diabetes, and cardiovascular disease. Hence, an improved understanding of nutrient and hormone sensing mechanisms will be extremely valuable for the development of more effective therapeutic approaches for metabolic diseases.

This Special Issue, entitled “Nutrient and Hormone Sensing Mechanisms and Signaling Pathways”, aims to improve our understanding of the mechanisms by which the body senses nutrients and hormones under physiological and pathophysiological conditions. We welcome different types of manuscript submissions, including original research and review articles (systematic reviews and meta-analyses). Potential topics may include but are not limited to the associations between nutrients (e.g., lipids, amino acids, and sugars) and/or metabolic hormones (e.g., insulin, ghrelin, adiponectin, and leptin) and health outcomes including obesity, type 2 diabetes, fatty liver disease, and cardiovascular disease.

Dr. Kim Loh
Dr. Chieh-Hsin Yang
Guest Editors

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 papers will be 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 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 2400 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

  • lipids
  • cholesterol
  • sugars
  • amino acids
  • cardiovascular disease
  • fatty liver disease
  • obesity
  • type 2 diabetes
  • obesity
  • inflammation
  • insulin
  • adiponectin
  • leptin
  • ghrelin

Published Papers (1 paper)

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Research

Article
Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
Nutrients 2021, 13(11), 4015; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13114015 - 10 Nov 2021
Viewed by 482
Abstract
Genistein (GEN) has been shown to significantly inhibit hepatic triglyceride accretion triggered by estrogen deficiency. The main purpose of this in vitro study was to investigate the function and molecular mechanism of estrogen receptor β (ERβ) in regulating hepatic lipid metabolism induced by [...] Read more.
Genistein (GEN) has been shown to significantly inhibit hepatic triglyceride accretion triggered by estrogen deficiency. The main purpose of this in vitro study was to investigate the function and molecular mechanism of estrogen receptor β (ERβ) in regulating hepatic lipid metabolism induced by GEN. Different doses of GEN or GEN with an ERβ antagonist were treated with HepG2 cells. Results showed that 25 μM GEN significantly diminished triglyceride levels. Meanwhile, GEN downregulated the levels of genes and proteins involved in lipogenesis, such as sterol-regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FASN), and stearoyl-coenzyme A desaturase 1 (SCD1), and upregulated the gene and protein levels of the regulation factors responsible for fatty acid β-oxidation, such as carnitine palmitoyltransferase 1α (CPT-1α) and peroxisome proliferator-activated receptor α (PPARα). Furthermore, 25 μM GEN reduced the levels of phosphorylation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Moreover, most of these effects from GEN were reverted by pretreatment with the antagonist of ERβ. In conclusion, GEN improved hepatic lipid metabolism by activating ERβ and further modulation of Akt/mTOR signals. The results provide novel aspects of the regulatory mechanism of ERβ on hepatic lipid metabolism and might help to profoundly understand the functions of food-derived phytoestrogens in preventing and treating hepatic steatosis in postmenopausal women. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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