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Nutritional Biochemistry

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 19693

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Special Issue Editor

Prof. Dr. Shih-Min Hsia

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Guest Editor

School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan
Interests: agricultural science; functional food; reproductive endocrine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nutritional biochemistry involves a wide range of fields, including biology, chemistry, cell function and metabolism, preclinical nutrition, macronutrients and energy, and nutrigenomics. Previous research has explored the operation of nutritional biochemistry through different methods, confirming the mechanism and related pathways regulated by nutritional biochemistry at the cellular level, simulating the intake required by the human body through animal experiments, applying it to humans in clinical nutrition trials, and finally establishing the optimal balance with diet and nutritional requirements. A large number of studies on nutritional biochemistry have focused not only on uncovering the relationship between diet and disease but also on revealing the importance of nutritional intake in the development of cancer.

The scope of nutritional biochemical research is wide, and there are still many molecular mechanisms that need to be elucidated. To provide more advantageous evidence, this Special Issue is expected to recruit research on the improvement of diseases or cancer with nutritional nutraceuticals or active compounds and to seek to develop strategies to reduce the side effects of clinical drugs.

Prof. Dr. Shih-Min Hsia
Guest Editor

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Keywords

biology
chemistry
cell function and metabolism
preclinical nutrition
macronutrients and energy
nutrigenomics

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Published Papers (7 papers)

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Editorial

Jump to: Research, Other

3 pages, 166 KiB

Open AccessEditorial

Nutritional Biochemistry

by Shih Min Hsia

Int. J. Mol. Sci. 2023, 24(11), 9661; https://doi.org/10.3390/ijms24119661 - 2 Jun 2023

Viewed by 1757

Abstract

Nutritional biochemistry involves a wide range of fields, and many studies on nutritional biochemistry have focused not only on uncovering the relationship between diet and disease but also on revealing the importance of nutritional intake in the development of cancer [...] Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

Research

Jump to: Editorial, Other

19 pages, 4953 KiB

Open AccessArticle

Piperine Improves Lipid Dysregulation by Modulating Circadian Genes Bmal1 and Clock in HepG2 Cells

by Weiyun Zhang, Chi-Tang Ho and Muwen Lu

Int. J. Mol. Sci. 2022, 23(10), 5611; https://doi.org/10.3390/ijms23105611 - 17 May 2022

Cited by 19 | Viewed by 2962

Abstract

Metabolic disorders are closely associated with the dysregulation of circadian rhythms. Many bioactive components with lipid metabolism-regulating effects have been reported to function through circadian clock-related mechanisms. As the main pungent principle of black pepper, piperine (PIP) has been demonstrated to possess anti-obesity bioactivity by affecting hepatic lipid metabolism-related factors. However, whether the circadian clock genes Bmal1 and Clock are involved in the protective effect of PIP against lipid metabolism disorders remains unknown. In this work, oleic acid (OA) induced lipid accumulation in HepG2 cells. The effect of PIP on redox status, mitochondrial functions, and circadian rhythms of core clock genes were evaluated. Results revealed that PIP alleviated circadian desynchrony, ROS overproduction, and mitochondrial dysfunction. A mechanism study showed that PIP could activate the SREBP-1c/PPARγ and AMPK/AKT-mTOR signaling pathways in a Bmal1/Clock-dependent manner in HepG2 cells. These results indicated that Bmal1 and Clock played important roles in the regulating effect of PIP on hepatic lipid homeostasis. Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

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18 pages, 2176 KiB

Open AccessArticle

Functional Characterization of the Solute Carrier LAT-1 (SLC7A5/SLC3A2) in Human Brain Capillary Endothelial Cells with Rapid UPLC-MS/MS Quantification of Intracellular Isotopically Labelled L-Leucine

by Cindy Bay, Gzona Bajraktari-Sylejmani, Walter E. Haefeli, Jürgen Burhenne, Johanna Weiss and Max Sauter

Int. J. Mol. Sci. 2022, 23(7), 3637; https://doi.org/10.3390/ijms23073637 - 26 Mar 2022

Cited by 8 | Viewed by 2759 | Correction

Abstract

The solute carrier L-type amino acid transporter 1 (LAT-1/SLC7A5) is a viable target for drug delivery to the central nervous system (CNS) and tumors due to its high abundance at the blood–brain barrier and in tumor tissue. LAT-1 is only localized on the cell surface as a heterodimer with CD98, which is not required for transporter function. To support future CNS drug-delivery development based on LAT-1 targeting, we established an ultra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) assay for stable isotopically labeled leucine ([¹³C₆, ¹⁵N]-L-leucine), with a dynamic range of 0.1–1000 ng/mL that can be applied for the functional testing of LAT-1 activity when combined with specific inhibitors and, consequently, the LAT-1 inhibition capacity of new compounds. The assay was established in a 96-well format, facilitating high-throughput experiments, and, hence, can support the screening for novel inhibitors. Applicable recommendations of the US Food and Drug Administration and European Medicines Agency for bioanalytical method validation were followed to validate the assay. The assay was applied to investigate the IC₅₀ of two well-known LAT-1 inhibitors on hCMEC/D3 cells: the highly specific LAT-1 inhibitor JPH203, which was also used to demonstrate LAT-1 specific uptake, and the general system L inhibitor BCH. In addition, the [¹³C₆, ¹⁵N]-L-leucine uptake was determined on two human brain capillary endothelial cell lines (NKIM-6 and hCMEC/D3), which were characterized for their expressional differences of LAT-1 at the protein and mRNA level and the surface amount of CD98. The IC₅₀ values of the inhibitors were in concordance with previously reported values. Furthermore, the [¹³C₆, ¹⁵N]-L-leucine uptake was significantly higher in hCMEC/D3 cells compared to NKIM-6 cells, which correlated with higher expression of LAT-1 and a higher surface amount of CD98. Therefore, the UPLC-MS/MS quantification of ([¹³C₆, ¹⁵N]-L-leucine is a feasible strategy for the functional characterization of LAT-1 activity in cells or tissue. Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

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12 pages, 2137 KiB

Open AccessArticle

Lycium barbarum Polysaccharides and Capsaicin Inhibit Oxidative Stress, Inflammatory Responses, and Pain Signaling in Rats with Dextran Sulfate Sodium-Induced Colitis

by Yu-Shan Chen, Yu Zhi Lian, Wen-Chao Chen, Chun-Chao Chang, Alexey A. Tinkov, Anatoly V. Skalny and Jane C.-J. Chao

Int. J. Mol. Sci. 2022, 23(5), 2423; https://doi.org/10.3390/ijms23052423 - 22 Feb 2022

Cited by 19 | Viewed by 3061

Abstract

Ulcerative colitis (UC) is an inflammatory disease with chronic relapsing symptoms. This study investigated the effects of Lycium barbarum polysaccharides (LBP) and capsaicin (CAP) in dextran sulfate sodium (DSS)-induced UC rats. Rats were divided into normal, DSS-induced UC, and UC treated with 100 mg LBP/kg bw, 12 mg CAP/kg bw, or 50 mg LBP/kg bw and 6 mg CAP/kg bw. Rats were fed LBP or CAP orally by gavage for 4 weeks, and UC model was established by feeding 5% DSS in drinking water for 6 days during week 3. Oral CAP and mixture significantly reduced disease activity index. Oral LBP significantly decreased serum malondialdehyde, interleukin (IL)-6, colonic tumor necrosis factor (TNF)-α levels, and protein expression of transient receptor potential cation channel V1 (TRPV1) and transient receptor potential ankyrin 1 (TRPA1), but increased serum catalase activity. Oral CAP significantly suppressed serum IL-6, colonic TRPV1 and TRPA1 protein expression, but elevated IL-10 levels, serum superoxide dismutase and catalase activities. The mixture of LBP and CAP significantly reduced serum IL-6, colonic TNF-α and TRPA1 protein. In conclusion, administration of LBP and/or CAP attenuate DSS-induced UC symptoms through inhibiting oxidative stress, proinflammatory cytokines, and protein expression of TRPV1 and TRPA1. Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

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12 pages, 3500 KiB

Open AccessArticle

Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries

by Yu-Chen Hou, Man-Hui Pai, Jin-Ming Wu, Po-Jen Yang, Po-Chu Lee, Kuen-Yuan Chen, Sung-Ling Yeh and Ming-Tsan Lin

Int. J. Mol. Sci. 2021, 22(23), 13003; https://doi.org/10.3390/ijms222313003 - 30 Nov 2021

Cited by 10 | Viewed by 2737

Abstract

This study investigated the effects of l-glutamine (Gln) and/or l-leucine (Leu) administration on sepsis-induced skeletal muscle injuries. C57BL/6J mice were subjected to cecal ligation and puncture to induce polymicrobial sepsis and then given an intraperitoneal injection of Gln, Leu, or Gln plus Leu beginning at 1 h after the operation with re-injections every 24 h. All mice were sacrificed on either day 1 or day 4 after the operation. Blood and muscles were collected for analysis of inflammation and oxidative damage-related biomolecules. Results indicated that both Gln and Leu supplementation alleviated sepsis-induced skeletal muscle damage by reducing monocyte infiltration, calpain activity, and mRNA expression levels of inflammatory cytokines and hypoxia-inducible factor-1α. Furthermore, septic mice treated with Gln had higher percentages of blood anti-inflammatory monocytes and muscle M2 macrophages, whereas Leu treatment enhanced the muscle expressions of mitochondrion-related genes. However, there were no synergistic effects when Gln and Leu were simultaneously administered. These findings suggest that both Gln and Leu had prominent abilities to attenuate inflammation and degradation of skeletal muscles in the early and/or late phases of sepsis. Moreover, Gln promoted the switch of leukocytes toward an anti-inflammatory phenotype, while Leu treatment maintained muscle bioenergetic function. Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

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20 pages, 11637 KiB

Open AccessArticle

Hydroxygenkwanin Increases the Sensitivity of Liver Cancer Cells to Chemotherapy by Inhibiting DNA Damage Response in Mouse Xenograft Models

by Chin-Chuan Chen, Chi-Yuan Chen, Shu-Fang Cheng, Tzong-Ming Shieh, Yann-Lii Leu, Wen-Yu Chuang, Kuang-Ting Liu, Shir-Hwa Ueng, Yin-Hwa Shih, Li-Fang Chou and Tong-Hong Wang

Int. J. Mol. Sci. 2021, 22(18), 9766; https://doi.org/10.3390/ijms22189766 - 9 Sep 2021

Cited by 5 | Viewed by 3045

Abstract

Molecules involved in DNA damage response (DDR) are often overexpressed in cancer cells, resulting in poor responses to chemotherapy and radiotherapy. Although treatment efficacy can be improved with the concomitant use of DNA repair inhibitors, the accompanying side effects can compromise the quality of life of patients. Therefore, in this study, we identified a natural compound that could inhibit DDR, using the single-strand annealing yeast-cell analysis system, and explored its mechanisms of action and potential as a chemotherapy adjuvant in hepatocellular carcinoma (HCC) cell lines using comet assay, flow cytometry, Western blotting, immunofluorescence staining, and functional analyses. We developed a mouse model to verify the in vitro findings. We found that hydroxygenkwanin (HGK) inhibited the expression of RAD51 and progression of homologous recombination, thereby suppressing the ability of the HCC cell lines to repair DNA damage and enhancing their sensitivity to doxorubicin. HGK inhibited the phosphorylation of DNA damage checkpoint proteins, leading to apoptosis in the HCC cell lines. In the mouse xenograft model, HGK enhanced the sensitivity of liver cancer cells to doxorubicin without any physiological toxicity. Thus, HGK can inhibit DDR in liver cancer cells and mouse models, making it suitable for use as a chemotherapy adjuvant. Full article

(This article belongs to the Special Issue Nutritional Biochemistry)

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