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Advance in Nutrition and Metabolic Homeostasis

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

Deadline for manuscript submissions: closed (11 May 2023) | Viewed by 6218

Special Issue Editors


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Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: oxidative metabolism; nutrition; obesity; metaflammation; mitochondrial function; aging; insulin resistance
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: nutrition; metabolic efficiency; obesity; inflammation; mitochondrial function; oxidative stress; diet-induced disorders; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: nutrition; metabolism

Special Issue Information

Dear Colleagues,

The synergistic relationship between nutrition and metabolism is the key to maintaining a healthy body. To date, energy homeostasis is easily altered by malnutrition, improper lifestyle, and overfeeding. Even the amount and quality of each nutritional component are closely related to the impairment of whole-body metabolic homeostasis. The current obesity epidemic suggests that energy homeostasis is poorly efficient in the modern human dietary environment. Disrupted metabolic flexibility is associated with many pathological conditions, including metabolic syndrome, diabetes, cardiovascular and neurological diseases, and cancer. Metabolic homeostasis is mediated at the level of several key peripheral organs, including the gastrointestinal tract with its microbiome, the most metabolically active organs (liver, skeletal muscle, and adipocytes), and the nervous system, the master homeostatic regulator that detects metabolic input to coordinate tissue-specific responses via peripheral hormone and neuronal signalling. This Special Issue aims to collect original research and review articles describing the impact of the nutrients and their metabolites in the regulation and coordination of the vast number of cellular processes that operate to maintain metabolic homeostasis. Data collection may help redefine preventive and therapeutic strategies in an effort to promote healthy living.

Prof. Dr. Maria Pina Mollica
Dr. Giovanna Trinchese
Dr. Angela Catapano
Guest Editors

Manuscript Submission Information

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Keywords

  • diet
  • metabolism
  • energy homeostasis
  • metabolic flexibility
  • non-communicable diseases
  • metabolic pathways
  • nutrients
  • meta-inflammation
  • microbiome
  • central nervous system

Published Papers (4 papers)

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Research

9 pages, 253 KiB  
Article
Eight-Day Fast and a Single Bout of Exercise: The Effect on Serum Methylarginines and Amino Acids in Men
by Joanna Reczkowicz, Jakub Kortas, Ulana Juhas, Malgorzata Zychowska, Andzelika Borkowska, Karol Pilis, Ewa Ziemann, Zuzanna Sobol and Jedrzej Antosiewicz
Nutrients 2023, 15(13), 2981; https://doi.org/10.3390/nu15132981 - 30 Jun 2023
Viewed by 922
Abstract
Changes in serum concentration of methylarginines and amino acids after exercise are well documented, whereas the effects of exercise applied together with fasting are still debated and not thoroughly studied. Thus, we hypothesised that alterations in methylarginines such as ADMA, SDMA and L-NMMA [...] Read more.
Changes in serum concentration of methylarginines and amino acids after exercise are well documented, whereas the effects of exercise applied together with fasting are still debated and not thoroughly studied. Thus, we hypothesised that alterations in methylarginines such as ADMA, SDMA and L-NMMA might be responsible for decreased exercise performance after 8 days of fasting. Additionally, we propose that conditions in which the human body is exposed to prolonged fasting for more than a week elicit a distinctly different response to exercise than after overnight fasting. A group of 10 healthy men with previous fasting experience participated in the study. The exercise test was performed until exhaustion with a gradually increasing intensity before and after the 8-day fast. Blood samples were collected before and immediately after exercise. ADMA, SDMA, L-NMMA, dimethylamine and amino acids were analysed in serum samples by ID-LC-MS/MS. SDMA, L-NMMA and dimethylamine significantly decreased after 8 days of fasting, whereas ADMA did not change. BCAA, Phe, alanine and some other amino acids increased after fasting. Exercise-induced changes in amino acids were distinct after an 8-day fast compared to overnight fasting. A decrease in physical performance accompanied all of these alterations. In conclusion, our data indicate that neither methyl-arginine changes nor the Trp/BCAA ratio can explain exercise-induced fatigue after fasting. However, the observed decrease in hArg concentration suggests the limited synthesis of creatine, possibly contributing to reduced physical performance. Full article
(This article belongs to the Special Issue Advance in Nutrition and Metabolic Homeostasis)
19 pages, 9478 KiB  
Article
Nutrient-Dependent Mitochondrial Fission Enhances Osteoblast Function
by Ciro Menale, Giovanna Trinchese, Immacolata Aiello, Giulia Scalia, Monica Dentice, Maria Pina Mollica, Nal Ae Yoon and Sabrina Diano
Nutrients 2023, 15(9), 2222; https://doi.org/10.3390/nu15092222 - 08 May 2023
Viewed by 1666
Abstract
Background: The bone synthesizing function of osteoblasts (OBs) is a highly demanding energy process that requires nutrients. However, how nutrient availability affects OBs behavior and bone mineralization remain to be fully understood. Methods: MC3T3-E1 cell line and primary OBs (OBs) cultures were treated [...] Read more.
Background: The bone synthesizing function of osteoblasts (OBs) is a highly demanding energy process that requires nutrients. However, how nutrient availability affects OBs behavior and bone mineralization remain to be fully understood. Methods: MC3T3-E1 cell line and primary OBs (OBs) cultures were treated with physiological levels of glucose (G; 5.5 mM) alone or with the addition of palmitic acid (G+PA) at different concentrations. Mitochondria morphology and activity were evaluated by fluorescence microscopy, qPCR, and oxygen consumption rate (OCR) measurement, and OBs function was assessed by mineralization assay. Results: The addition of non-lipotoxic levels of 25 μM PA to G increased mineralization in OBs. G+25 μM PA exposure reduced mitochondria size in OBs, which was associated with increased activation of dynamin-related protein 1, a mitochondrial fission protein, enhanced mitochondria OCR and ATP production, and increased expression of oxidative phosphorylation genes. Treatment with Mdivi-1, a putative inhibitor of mitochondrial fission, reduced osteogenesis and mitochondrial respiration in OBs. Conclusions: Our results revealed that OBs function was enhanced in the presence of glucose and PA at 25 μM. This was associated with increased OBs mitochondrial respiration and dynamics. These results suggest a role for nutrient availability in bone physiology and pathophysiology. Full article
(This article belongs to the Special Issue Advance in Nutrition and Metabolic Homeostasis)
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14 pages, 1666 KiB  
Article
An Acute Bout of Endurance Exercise Does Not Prevent the Inhibitory Effect of Caffeine on Glucose Tolerance the following Morning
by Karoline T. Fenne, Matthieu Clauss, Daniela Schäfer Olstad, Egil I. Johansen and Jørgen Jensen
Nutrients 2023, 15(8), 1941; https://doi.org/10.3390/nu15081941 - 18 Apr 2023
Viewed by 1735
Abstract
Caffeine reduces glucose tolerance, whereas exercise training improves glucose homeostasis. The aim of the present study was to investigate the effect of caffeine on glucose tolerance the morning after an acute bout of aerobic exercise. Methods: The study had a 2 × 2 [...] Read more.
Caffeine reduces glucose tolerance, whereas exercise training improves glucose homeostasis. The aim of the present study was to investigate the effect of caffeine on glucose tolerance the morning after an acute bout of aerobic exercise. Methods: The study had a 2 × 2 factorial design. Oral glucose tolerance tests (OGTT) were performed after overnight fasting with/without caffeine and with/without exercise the evening before. Eight healthy young active males were included (Age 25.5 ± 1.5 years; 83.9 ± 9.0 kg; VO2max: 54.3 ± 7.0 mL·kg−1·min−1). The exercise session consisted of 30 min cycling at 71% of VO2max followed by four 5 min intervals at 84% with 3 min of cycling at 40% of VO2max between intervals. The exercise was performed at 17:00 h. Energy expenditure at each session was ~976 kcal. Lactate increased to ~8 mM during the exercise sessions. Participants arrived at the laboratory the following morning at 7.00 AM after an overnight fast. Resting blood samples were taken before blood pressure and heart rate variability (HRV) were measured. Caffeine (3 mg/kg bodyweight) or placebo (similar taste/flavor) was ingested, and blood samples, blood pressure and HRV were measured after 30 min. Next, the OGTTs were initiated (75 g glucose dissolved in 3 dL water) and blood was sampled. Blood pressure and HRV were measured during the OGTT. Caffeine increased the area under curve (AUC) for glucose independently of whether exercise was done the evening before (p = 0.03; Two-way ANOVA; Interaction: p = 0.835). Caffeine did not significantly increase AUC for C-peptides compared to placebo (p = 0.096), and C-peptide response was not influenced by exercise. The acute bout of exercise did not significantly improve glucose tolerance the following morning. Diastolic blood pressure during the OGTT was slightly higher after intake of caffeine, independent of whether exercise was performed the evening before or not. Neither caffeine nor exercise the evening before significantly influenced HRV. In conclusion, caffeine reduced glucose tolerance independently of whether endurance exercise was performed the evening before. The low dose of caffeine did not influence heart rate variability but increased diastolic blood pressure slightly. Full article
(This article belongs to the Special Issue Advance in Nutrition and Metabolic Homeostasis)
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24 pages, 13802 KiB  
Article
Leaf Extract of Perilla frutescens (L.) Britt Promotes Adipocyte Browning via the p38 MAPK Pathway and PI3K-AKT Pathway
by Fancheng Chen, Silin Wu, Dejian Li, Jian Dong and Xiaowei Huang
Nutrients 2023, 15(6), 1487; https://doi.org/10.3390/nu15061487 - 20 Mar 2023
Cited by 1 | Viewed by 1381
Abstract
The leaf of Perilla frutescens (L.) Britt (PF) has been reported to negatively affect adipocyte formation, inhibit body-fat formation, and lower body weight. However, its effect on adipocyte browning remains unknown. Thus, the mechanism of PF in promoting adipocyte browning was investigated. The [...] Read more.
The leaf of Perilla frutescens (L.) Britt (PF) has been reported to negatively affect adipocyte formation, inhibit body-fat formation, and lower body weight. However, its effect on adipocyte browning remains unknown. Thus, the mechanism of PF in promoting adipocyte browning was investigated. The ingredients of PF were acquired from the online database and filtered with oral bioavailability and drug-likeness criteria. The browning-related target genes were obtained from the Gene Card database. A Venn diagram was employed to obtain the overlapped genes that may play a part in PF promoting adipocyte browning, and an enrichment was analysis conducted based on these overlapped genes. A total of 17 active ingredients of PF were filtered, which may regulate intracellular receptor-signaling pathways, the activation of protein kinase activity, and other pathways through 56 targets. In vitro validation showed that PF promotes mitochondrial biogenesis and upregulates brite adipocyte-related gene expression. The browning effect of PF can be mediated by the p38 MAPK pathway as well as PI3K-AKT pathway. The study revealed that PF could promote adipocyte browning through multitargets and multipathways. An in vitro study validated that the browning effect of PF can be mediated by both the P38 MAPK pathway and the PI3K-AKT pathway. Full article
(This article belongs to the Special Issue Advance in Nutrition and Metabolic Homeostasis)
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