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The Role of Natural Products in Obesity and Other Metabolic...
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The Role of Natural Products in Obesity and Other Metabolic Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Phytochemicals and Human Health".

Deadline for manuscript submissions: closed (14 December 2023) | Viewed by 10851

Special Issue Editor

Dr. Yan Li

E-Mail Website1 Website2
Guest Editor
State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China
Interests: nutrition; food science; cereal; metabolism; metabolic homeostasis; obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity occurs when energy expenditure is chronically lower than energy consumption (from food), and this considerably increases the risk of developing several life-threatening metabolic diseases, such as type 2 diabetes, nonalcoholic fatty liver diseases and cardiovascular diseases. Recently, natural products have shown tremendous potential in combatting obesity and related metabolic diseases via different mechanisms, including appetite, lipid homeostasis, adipocytes, inflammation, and intestinal bacteria. This Special Issue will address new basic and clinical research data on functional ingredients; antiobesity effects and mechanisms; and therapeutic strategies for metabolic diseases with the use of natural products. This Special Issue invites all researchers working with natural products and obesity or other metabolic diseases to submit original in vitro, animal and human research manuscripts, cohort studies, systematic literature reviews and meta-analyses.

Dr. Yan Li
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. 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

  • natural products
  • obesity
  • metabolism
  • metabolic diseases
  • functional food
  • functional ingredients
  • dietary supplements
  • diabetes
  • cardiovascular diseases

Published Papers (5 papers)

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Research

20 pages, 18887 KiB  
Article
Lactobacillus paracasei JY062 Alleviates Glucolipid Metabolism Disorders via the Adipoinsular Axis and Gut Microbiota
by Yue Su, Jing Ren, Jingwen Zhang, Jiapeng Zheng, Qi Zhang, Yueling Tian, Yu Zhang, Yujun Jiang and Wei Zhang
Nutrients 2024, 16(2), 267; https://doi.org/10.3390/nu16020267 - 16 Jan 2024
Cited by 1 | Viewed by 1232
Abstract
Glycolipid metabolic disorders (GLMD) refer to a series of metabolic disorders caused by abnormal processes of glucose and lipid synthesis, decomposition, and absorption in the body, leading to glucose and lipid excess, insulin resistance, and obesity. Probiotic intervention is a new strategy to [...] Read more.
Glycolipid metabolic disorders (GLMD) refer to a series of metabolic disorders caused by abnormal processes of glucose and lipid synthesis, decomposition, and absorption in the body, leading to glucose and lipid excess, insulin resistance, and obesity. Probiotic intervention is a new strategy to alleviate metabolic syndrome. Lactobacillus paracasei JY062 (L. paracasei JY062) was separated from the Tibet-fermented dairy products. The results demonstrated a strong ability to relieve blood glucose disorders, blood lipid disorders, and tissue damage. The LPH group had the best effect, significantly decreasing the total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), leptin, insulin, and free fatty acid (FFA) concentrations and increasing the high-density lipoprotein cholesterol, adiponectin, and GLP-1 level compared to HFD-group mice. L. paracasei JY062 could activate the APN-AMPK pathway, increased AdipoQ, AMPK GLUT-4, and PGC-1α mRNA expression and decreased SREBP-1c, ACC, and FAS mRNA expression. L. paracasei JY062 intervention decreased the relative abundance of harmful bacteria, increased the relative abundance of beneficial bacteria, and restored the imbalance of gut microbiota homeostasis caused by a high-glucose-fat diet. L. paracasei JY062 alleviated glucolipid metabolism disorders via the adipoinsular axis and gut microbiota. This study provided a theoretical basis for probiotics to ameliorate glucolipid metabolism disorders by regulating the adipoinsular axis. Full article
(This article belongs to the Special Issue The Role of Natural Products in Obesity and Other Metabolic Diseases)
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17 pages, 4552 KiB  
Article
Citrus p-Synephrine Improves Energy Homeostasis by Regulating Amino Acid Metabolism in HFD-Induced Mice
by Junying Bai, Xiang Tan, Sheng Tang, Xin Liu, Linzi Shao, Chen Wang and Linhua Huang
Nutrients 2024, 16(2), 248; https://doi.org/10.3390/nu16020248 - 12 Jan 2024
Viewed by 1200
Abstract
p-Synephrine is a common alkaloid widely distributed in citrus fruits. However, the effects of p-synephrine on the metabolic profiles of individuals with energy abnormalities are still unclear. In the study, we investigated the effect of p-synephrine on energy homeostasis and [...] Read more.
p-Synephrine is a common alkaloid widely distributed in citrus fruits. However, the effects of p-synephrine on the metabolic profiles of individuals with energy abnormalities are still unclear. In the study, we investigated the effect of p-synephrine on energy homeostasis and metabolic profiles using a high fat diet (HFD)-induced mouse model. We found that p-synephrine inhibited the gain in body weight, liver weight and white adipose tissues weight induced by HFD. p-Synephrine supplementation also reduced levels of serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) but not to a statistically significant degree. Histological analysis showed that HFD induced excessive lipid accumulation and glycogen loss in the liver and adipocyte enlargement in perirenal fat tissue, while p-synephrine supplementation reversed the changes induced by HFD. Moreover, HFD feeding significantly increased mRNA expression levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and reduced the mRNA expression level of interleukin-10 (IL-10) compared to the control group, while p-synephrine supplementation significantly reversed these HFD-induced changes. Liver and serum metabolomic analysis showed that p-synephrine supplementation significantly altered small molecule metabolites in liver and serum in HFD mice and that the changes were closely associated with improvement of energy homeostasis. Notably, amino acid metabolism pathways, both in liver and serum samples, were significantly enriched. Our study suggests that p-synephrine improves energy homeostasis probably by regulating amino acid metabolism in HFD mice, which provides a novel insight into the action mechanism of p-synephrine modulating energy homeostasis. Full article
(This article belongs to the Special Issue The Role of Natural Products in Obesity and Other Metabolic Diseases)
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14 pages, 1572 KiB  
Article
Effects of Free Linoleic Acid and Oleic Acid in Sesame Meal Extract as Pancreatic Lipase Inhibitors on Postprandial Triglyceridemia: A Randomized, Double-Blind, Placebo-Controlled, Crossover Study in Healthy Volunteers
by Xuan Li, Hiroaki Yamada, Sayo Morita, Yusuke Yamashita, Youngil Kim, Takashi Kometani, Nikesh Narang, Toma Furuta and Mujo Kim
Nutrients 2023, 15(7), 1748; https://doi.org/10.3390/nu15071748 - 3 Apr 2023
Cited by 3 | Viewed by 3034
Abstract
A great number of chemically diverse pancreatic lipase (PL) inhibitors have been identified to tackle obesity; however, very few of them have entered clinical studies. The ethanolic extract of sesame meal is a potent PL inhibitor, and its activity hinges exclusively on two [...] Read more.
A great number of chemically diverse pancreatic lipase (PL) inhibitors have been identified to tackle obesity; however, very few of them have entered clinical studies. The ethanolic extract of sesame meal is a potent PL inhibitor, and its activity hinges exclusively on two free fatty acids: linoleic acid and oleic acid, which were proven to reduce postprandial triglyceride excursion in rats. Herein, to investigate the clinical efficacy of the sesame meal extract, in a crossover trial, 30 healthy volunteers were randomized to receive the sesame meal extract containing experimental food or placebo along with a high-fat meal. Treatment with the sesame meal extract significantly lowered the incremental postprandial serum triglyceride concentration and reduced the incremental area under the curve (iAUC) by 16.8% (p-value = 0.03) compared to placebo. Significant decreases in postprandial remnant-like lipoprotein particle cholesterol and low-density lipoprotein particles were also observed, whereas high-density lipoprotein cholesterol was increased. These results suggest that treatment with the sesame meal extract significantly reduced the postprandial excursion of triglycerides and improved the lipidemic profile after high dietary fat intake in healthy individuals, indicating the substantial potential of free linoleic acid and oleic acid and natural products rich in these compounds for the management of obesity and related conditions. Full article
(This article belongs to the Special Issue The Role of Natural Products in Obesity and Other Metabolic Diseases)
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12 pages, 1654 KiB  
Article
Low-Carbohydrate Diet Modulates Glucose–Lipid Utilization in Skeletal Muscle of Diabetic Mice
by Yan Li, Zi Yang, Yu Wang, Mingcong Fan, Chenzhipeng Nie, Lamei Xue, Li Wang and Haifeng Qian
Nutrients 2023, 15(6), 1513; https://doi.org/10.3390/nu15061513 - 21 Mar 2023
Cited by 3 | Viewed by 2046
Abstract
Type 2 diabetes is associated with many complications, including skeletal muscle atrophy. Ketogenic diets and low-carbohydrate diets (LCD) have recently been introduced as dietary interventions in patients with diabetes, but their effects on glucose and lipid metabolism in skeletal muscle have not been [...] Read more.
Type 2 diabetes is associated with many complications, including skeletal muscle atrophy. Ketogenic diets and low-carbohydrate diets (LCD) have recently been introduced as dietary interventions in patients with diabetes, but their effects on glucose and lipid metabolism in skeletal muscle have not been studied. In the current study, we compared the effects of LCD and ketogenic diet on glucose and lipid metabolism in skeletal muscle of diabetic mice. C57BL/6J mice with type 2 diabetes, constructed by a high-fat diet combined with streptozotocin, were fed a standard diet, a high-fat diet, an LCD, or a ketogenic diet for 14 weeks, respectively. Here, we found that the LCD, rather than the ketogenic diet, retained skeletal muscle weight and suppressed the expression of atrophy-related genes in diabetic mice. In addition, the LCD had more glycolytic/type IIb myofiber content and inhibited forkhead box O1 and pyruvate dehydrogenase kinase 4 expression, leading to improved glucose utilization. However, the ketogenic diet maintained more oxidative/type I myofibers. Moreover, compared with the ketogenic diet, the LCD decreased intramuscular triglycerides content and muscle lipolysis, suggesting improvement in lipid metabolism. Taken together, these data suggested that the LCD improved glucose utilization, and inhibited lipolysis and atrophy in skeletal muscle of diabetic mice, while the ketogenic diet showed metabolic disorders in skeletal muscle. Full article
(This article belongs to the Special Issue The Role of Natural Products in Obesity and Other Metabolic Diseases)
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14 pages, 3335 KiB  
Article
Iodide Excess Inhibits Thyroid Hormone Synthesis Pathway Involving XBP1-Mediated Regulation
by Jing Yu, Siyi Shen, Ying Yan, Lingxiao Liu, Rongkui Luo, Shengnan Liu, Yuting Wu, Yuying Li, Jingjing Jiang and Hao Ying
Nutrients 2023, 15(4), 887; https://doi.org/10.3390/nu15040887 - 9 Feb 2023
Cited by 1 | Viewed by 2261
Abstract
Iodine is an essential micronutrient for producing thyroid hormone (TH); however, iodide excess can lead to adverse thyroidal effects. Unfortunately, the lack of a proper in vitro model system hampered the studies of the effect of iodide excess on thyroid physiology and pathology. [...] Read more.
Iodine is an essential micronutrient for producing thyroid hormone (TH); however, iodide excess can lead to adverse thyroidal effects. Unfortunately, the lack of a proper in vitro model system hampered the studies of the effect of iodide excess on thyroid physiology and pathology. Here, we demonstrated that excessive iodide intake downregulated the genes related to TH synthesis in the thyroids of mice. Since sodium iodide has no effect on these genes in cultured cell lines, we developed a three-dimensional (3D) culture system to enable the murine thyrocytes to form organoids in vitro with thyroid follicle-like structures and function and found that the in vivo effect of iodide excess could be mimicked in these thyroid organoids. Our data indicate that iodide excess mainly activated the XBP1-mediated unfolded protein response in both murine thyroid and thyroid organoids, while activation of XBP1 was able to mimic the sodium iodide effect on genes for the synthesis of TH in murine thyroid organoids. Lastly, our results suggest that XBP1 might transcriptionally repress the genes involved in the synthesis of TH. Based on these findings, we propose that iodide excess inhibits the transcription of genes related to TH synthesis through a mechanism involving XBP1-mediated action. Full article
(This article belongs to the Special Issue The Role of Natural Products in Obesity and Other Metabolic Diseases)
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