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Nutrients
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Nutrient and Hormone Sensing Mechanisms and Signaling Pathways
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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: closed (30 November 2022) | Viewed by 21641

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 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; 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 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

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

Published Papers (7 papers)

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Research

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20 pages, 4272 KiB  
Article
A Candidate Gliotransmitter, L-β-Aminoisobutyrate, Contributes to Weight Gain and Metabolic Complication Induced by Atypical Antipsychotics
by Kouji Fukuyama, Eishi Motomura and Motohiro Okada
Nutrients 2023, 15(7), 1621; https://doi.org/10.3390/nu15071621 - 27 Mar 2023
Cited by 3 | Viewed by 1227
Abstract
Lurasidone and quetiapine are effective atypical mood-stabilizing antipsychotics, but lurasidone and quetiapine are listed as lower-risk and high-risk for weight gain/metabolic complications, respectively. The pathophysiology of the discrepancy of metabolic adverse reactions between these antipsychotics remains to be clarified. The GABA isomer, β-aminoisobutyric [...] Read more.
Lurasidone and quetiapine are effective atypical mood-stabilizing antipsychotics, but lurasidone and quetiapine are listed as lower-risk and high-risk for weight gain/metabolic complications, respectively. The pathophysiology of the discrepancy of metabolic adverse reactions between these antipsychotics remains to be clarified. The GABA isomer, β-aminoisobutyric acid (BAIBA) enantiomer, was recently re-discovered as myokine via an AMP-activated protein kinase activator (AMPK) enhancer and inhibitory gliotransmitter. Notably, activation of AMPK in peripheral organs improves, but in the hypothalamus, it aggravates metabolic disturbances. Therefore, we determined effects of chronic administration of lurasidone and quetiapine on intracellular and extracellular levels of the BAIBA enantiomer. L-BAIBA is a major BAIBA enantiomer in the hypothalamus and astrocytes, whereas L-BAIBA only accounted for about 5% of total plasma BAIBA enantiomers. Chronic lurasidone administration did not affect body weight but decreased the L-BAIBA level in hypothalamus and cultured astrocytes, whereas chronic quetiapine administration increased body weight and the L-BAIBA level in hypothalamus and astrocytes. Contrary, neither lurasidone nor quetiapine affected total plasma levels of the BAIBA enantiomer since D-BAIBA levels were not affected by these antipsychotics. These results suggest that activation of intracellular L-BAIBA signaling is, at least partially, involved in the pathophysiology of metabolic adverse reaction of quetiapine. Furthermore, this study also demonstrated that lurasidone and quetiapine suppressed and enhanced astroglial L-BAIBA release induced by ripple-burst stimulation (which physiologically contributes to cognitive memory integration during sleep), respectively. Therefore, L-BAIBA probably contributes to the pathophysiology of not only metabolic adverse reactions, but also a part of clinical action of lurasidone or quetiapine. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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24 pages, 9167 KiB  
Article
L-Citrulline Supplementation Restrains Ferritinophagy-Mediated Ferroptosis to Alleviate Iron Overload-Induced Thymus Oxidative Damage and Immune Dysfunction
by Tongtong Ba, Dai Zhao, Yiqin Chen, Cuiping Zeng, Cheng Zhang, Sai Niu and Hanchuan Dai
Nutrients 2022, 14(21), 4549; https://doi.org/10.3390/nu14214549 - 28 Oct 2022
Cited by 8 | Viewed by 2319
Abstract
L-citrulline (L-cit) is a key intermediate in the urea cycle and is known to possess antioxidant and anti-inflammation characteristics. However, the role of L-cit in ameliorating oxidative damage and immune dysfunction against iron overload in the thymus remains unclear. This study explored the [...] Read more.
L-citrulline (L-cit) is a key intermediate in the urea cycle and is known to possess antioxidant and anti-inflammation characteristics. However, the role of L-cit in ameliorating oxidative damage and immune dysfunction against iron overload in the thymus remains unclear. This study explored the underlying mechanism of the antioxidant and anti-inflammation qualities of L-cit on iron overload induced in the thymus. We reported that L-cit administration could robustly alleviate thymus histological damage and reduce iron deposition, as evidenced by the elevation of the CD8+ T lymphocyte number and antioxidative capacity. Moreover, the NF-κB pathway, NCOA4-mediated ferritinophagy, and ferroptosis were attenuated. We further demonstrated that L-cit supplementation significantly elevated the mTEC1 cells’ viability and reversed LDH activity, iron levels, and lipid peroxidation caused by FAC. Importantly, NCOA4 knockdown could reduce the intracellular cytoplasmic ROS, which probably relied on the Nfr2 activation. The results subsequently indicated that NCOA4-mediated ferritinophagy was required for ferroptosis by showing that NCOA4 knockdown reduced ferroptosis and lipid ROS, accompanied with mitochondrial membrane potential elevation. Intriguingly, L-cit treatment significantly inhibited the NF-κB pathway, which might depend on restraining ferritinophagy-mediated ferroptosis. Overall, this study indicated that L-cit might target ferritinophagy-mediated ferroptosis to exert antioxidant and anti-inflammation capacities, which could be a therapeutic strategy against iron overload-induced thymus oxidative damage and immune dysfunction. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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20 pages, 6022 KiB  
Article
Renoprotective Effect of Pediococcus acidilactici GKA4 on Cisplatin-Induced Acute Kidney Injury by Mitigating Inflammation and Oxidative Stress and Regulating the MAPK, AMPK/SIRT1/NF-κB, and PI3K/AKT Pathways
by Wen-Hsin Lin, Wen-Ping Jiang, Chin-Chu Chen, Li-Ya Lee, You-Shan Tsai, Liang-Hsuan Chien, Ya-Ni Chou, Jeng-Shyan Deng and Guan-Jhong Huang
Nutrients 2022, 14(14), 2877; https://doi.org/10.3390/nu14142877 - 13 Jul 2022
Cited by 11 | Viewed by 2369
Abstract
Acute kidney injury (AKI) describes a sudden loss of kidney function and is associated with a high mortality. Pediococcus acidilactici is a potent producer of bacteriocin and inhibits the growth of pathogens during fermentation and food storage; it has been used in the [...] Read more.
Acute kidney injury (AKI) describes a sudden loss of kidney function and is associated with a high mortality. Pediococcus acidilactici is a potent producer of bacteriocin and inhibits the growth of pathogens during fermentation and food storage; it has been used in the food industry for many years. In this study, the potential of P. acidilactici GKA4 (GKA4) to ameliorate AKI was investigated using a cisplatin-induced animal model. First, mice were given oral GKA4 for ten days and intraperitoneally injected with cisplatin on the seventh day to create an AKI mode. GKA4 attenuated renal histopathological alterations, serum biomarkers, the levels of inflammatory mediators, and lipid oxidation in cisplatin-induced nephrotoxicity. Moreover, GKA4 significantly decreased the expression of inflammation-related proteins and mitogen-activated protein kinase (MAPK) in kidney tissues. Eventually, GKA4 also increased the levels of related antioxidant enzymes and pathways. Consistently, sirtuin 1 (SIRT1) upregulated the level of autophagy-related proteins (LC3B, p62, and Beclin1). Further studies are needed to check our results and advance our knowledge of the mechanism whereby PI3K inhibition (wortmannin) reverses the effect of GKA4 on cisplatin-treated AKI. Taken together, GKA4 provides a therapeutic target with promising clinical potential after cisplatin treatment by reducing oxidative stress and inflammation via the MAPK, AMP-activated protein kinase (AMPK)/SIRT1/nuclear factor kappa B (NF-κB), and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) axes. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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14 pages, 1873 KiB  
Article
Role of Leu72Met of GHRL and Gln223Arg of LEPR Variants on Food Intake, Subjective Appetite, and Hunger-Satiety Hormones
by Tania Sanchez-Murguia, Nathaly Torres-Castillo, Lisset Magaña-de la Vega, Saraí Citlalic Rodríguez-Reyes, Wendy Campos-Pérez and Erika Martínez-López
Nutrients 2022, 14(10), 2100; https://doi.org/10.3390/nu14102100 - 18 May 2022
Cited by 1 | Viewed by 2406
Abstract
Appetite regulation has been recognized as a promising target for the prevention of obesity, which has become a worldwide health issue. Polymorphisms in the genes of hormones or receptors including Leu72Met for ghrelin and Gln223Arg for the leptin receptor could play a role [...] Read more.
Appetite regulation has been recognized as a promising target for the prevention of obesity, which has become a worldwide health issue. Polymorphisms in the genes of hormones or receptors including Leu72Met for ghrelin and Gln223Arg for the leptin receptor could play a role in dietary intake, hunger, and satiety process. The aim of this study was to analyze subjective appetite assessments, dietary intake, and appetite hormones in relationship to these polymorphisms. Subjects (n = 132) with normal BMIs were enrolled. Dietary intake was analyzed with 3-day diet records. Subjective appetite was measured by visual analogue scales. Biochemical parameters were measured after 12 h of fasting and 120′ following ingestion of a test meal. Ghrelin and leptin levels were measured by ELISA assay (enzyme-linked immunosorbent assay) and insulin by chemiluminescence assay. The polymorphisms were determined by allelic discrimination using TaqMan® probes. Fasting ghrelin levels differed significantly between men and women. The consumption of fruit and bread/starch with added sugar servings, as indicated by dietary records, and measured ghrelin levels were higher in carriers of Leu72Met/Met72Met compared to Leu72Leu carriers; total sugar intake was higher in Gln223Gln carriers than in Gln223Arg/Arg223Arg carriers. In conclusion, the Leu72Met and Gln223Arg polymorphism in ghrelin and LEPR may contribute to differential responses to a standardized meal as evidenced by higher postprandial levels of ghrelin and may also contribute to a higher dietary sugar intake. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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15 pages, 5826 KiB  
Article
Methionine Restriction Prevents Lipopolysaccharide-Induced Acute Lung Injury via Modulating CSE/H2S Pathway
by Jiaxiang Duan, Lunli Xiang, Zhen Yang, Li Chen, Jianteng Gu, Kaizhi Lu, Daqing Ma, Hailin Zhao, Bin Yi, Hongwen Zhao and Jiaolin Ning
Nutrients 2022, 14(2), 322; https://doi.org/10.3390/nu14020322 - 13 Jan 2022
Cited by 7 | Viewed by 2383
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) result in high mortality, whereas effective treatments are limited. Methionine restriction (MR) has been reported to offer various benefits against multiple pathological processes of organ injuries. However, it remains unknown whether MR has [...] Read more.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) result in high mortality, whereas effective treatments are limited. Methionine restriction (MR) has been reported to offer various benefits against multiple pathological processes of organ injuries. However, it remains unknown whether MR has any potential therapeutic value for ALI/ARDS. The current study was set to investigate the therapeutic potential of MR on lipopolysaccharide (LPS)-induced ALI and its underlying mechanisms. We found that MR attenuated LPS-induced pulmonary edema, hemorrhage, atelectasis, and alveolar epithelial cell injuries in mice. MR upregulated cystathionine-gamma-lyase (CSE) expression and enhanced the production of hydrogen sulfide (H2S). MR also inhibited the activation of Toll-like receptors 4 (TLR4)/NF-κB/NOD-like receptor protein 3 (NLRP3), then reduced IL-1β, IL-6, and TNF-α release and immune cell infiltration. Moreover, the protective effects of MR on LPS-induced ALI were abrogated by inhibiting CSE, whereas exogenous H2S treatment alone mimicked the protective effects of MR in Cse−/− mice after LPS administration. In conclusion, our findings showed that MR attenuated LPS-induced lung injury through CSE and H2S modulation. This work suggests that developing MR towards clinical use for ALI/ARDS patients may be a valuable strategy. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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14 pages, 2539 KiB  
Article
Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
by Hong Qin, Ziyu Song, Horia Shaukat and Wenya Zheng
Nutrients 2021, 13(11), 4015; https://doi.org/10.3390/nu13114015 - 10 Nov 2021
Cited by 9 | Viewed by 2651
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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Review

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9 pages, 538 KiB  
Review
An Overview of Obesity, Cholesterol, and Systemic Inflammation in Preeclampsia
by Morgan C. Alston, Leanne M. Redman and Jennifer L. Sones
Nutrients 2022, 14(10), 2087; https://doi.org/10.3390/nu14102087 - 17 May 2022
Cited by 17 | Viewed by 7276
Abstract
Preeclampsia (PE), an inflammatory state during pregnancy, is a significant cause of maternal and fetal morbidity and mortality. Adverse outcomes associated with PE include hypertension, proteinuria, uterine/placental abnormalities, fetal growth restriction, and pre-term birth. Women with obesity have an increased risk of developing [...] Read more.
Preeclampsia (PE), an inflammatory state during pregnancy, is a significant cause of maternal and fetal morbidity and mortality. Adverse outcomes associated with PE include hypertension, proteinuria, uterine/placental abnormalities, fetal growth restriction, and pre-term birth. Women with obesity have an increased risk of developing PE likely due to impaired placental development from altered metabolic homeostasis. Inflammatory cytokines from maternal adipose tissue and circulating cholesterol have been linked to systemic inflammation, hypertension, and other adverse outcomes associated with PE. This review will summarize the current knowledge on the role of nutrients, obesity, and cholesterol signaling in PE with an emphasis on findings from preclinical models. Full article
(This article belongs to the Special Issue Nutrient and Hormone Sensing Mechanisms and Signaling Pathways)
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