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Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications

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

Deadline for manuscript submissions: closed (25 April 2022) | Viewed by 17221

Special Issue Editor

Prof. Dr. Lu Cai

E-Mail Website
Guest Editor
1. Pediatric Research Institute, The Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA
2. Wendy Novak Diabetes Care Center, Departments of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA
Interests: understanding the cellular and molecular mechanisms of diabetes-induced cardiovascular diseases; nutrients relevant to of oxidative stress, including any nutrients that can activate Nrf2, and its downstream antioxidants in the pathogenesis of diabetic cardiomyopathy, and radiation damage; roles of trace elements such as zinc and iron and related metallothionein in the development of diabetic complications; clinically used medicinces that are repurposed utilazation for un-regulating Nrf2 or metallothionein; environmental contaminations of heavy metals such as cadmium and its health effect
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Both obesity and diabetes are global health threatens, however the mortality of these patients are attributed their complications or specifically called metabolic syndrome and diabetic cardiovarscular complications. Therefore the reviews or original studies on their pathogeneic mechanisms, and interventionally application of nutrients, natural products that sufficiently stimulates body’s defense system such as anti-oxidative stress and inflammation as well as improvement of insulin signaling (resistance) are welcome. In addition, in order to accelerate the clinical translation, currently FDA-approved or clinically-commonly used medicines that are repurposed for appying to stimulating Nrf2-mediated antioxidative and anti-inflammation, and Akt-mediated insulin signaling pathway are more welcome.

Prof. Dr. Lu Cai
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

  • Understanding the cellular and molecular mechanisms of diabetes-, obesity- or metabolic abnormalitiy-induced chronic diseases
  • Nutrients relevant to of oxidative stress, including any nutrients that can activate Nrf2, Akt, metallothion
  • Nrf2 downstream antioxidants in preventing the pathogenesis of diabetic complications
  • Roles of trace elements such as zinc and iron and related metallothionein in the development of diabetic complications.
  • Clinically used medicinces that are repurposed utilazation for un-regulating Nrf2 or metallothionein
  • Environmental contaminations of heavy metals such as cadmium and its health effect

Published Papers (7 papers)

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Editorial

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3 pages, 200 KiB  
Editorial
Impact of Nutrition or FDA-Approved Medicine Repurposing on Metabolic Syndrome and Diabetic Complications
by Lu Cai
Nutrients 2023, 15(11), 2515; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15112515 - 29 May 2023
Viewed by 1018
Abstract
Both obesity and diabetes are global health threats due to their high risk of developing different complications [...] Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)

Research

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18 pages, 13552 KiB  
Article
Effects of Inflammatory Factor Expression Regulated by 12/15 Lipoxygenase on Obesity-Related Nephropathy
by Nian Liu, Yang Liu, Dan Dong, Jinyu Yu and Hang Yuan
Nutrients 2022, 14(13), 2743; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14132743 - 30 Jun 2022
Cited by 1 | Viewed by 1745
Abstract
Background: It has been demonstrated that 12/15-lipoxygenase (LO) contributes to insulin resistance by promoting beta cells’ exposure to inflammation. We investigate the mechanism by which 12/15-LO regulates the expression of inflammatory factors in obesity-related glomerular disease (ORG). Methods: Glomerular mesangial cells were treated [...] Read more.
Background: It has been demonstrated that 12/15-lipoxygenase (LO) contributes to insulin resistance by promoting beta cells’ exposure to inflammation. We investigate the mechanism by which 12/15-LO regulates the expression of inflammatory factors in obesity-related glomerular disease (ORG). Methods: Glomerular mesangial cells were treated with metabolite of 12/15-LO, and the expression of inflammatory factors was measured. Cell histones methylation in 12/15-LO related metabolic memory process were evaluated by chromatin immunoprecipitation (ChIP) assays. Wild-type (WT) and 12/15-LO knockout mice were fed a high-fat diet (HFD) to induce ORG. Results: 12(S)-HETE increased TNF-α, MCP-1, and IL-6 mRNA expression. Inhibition of 12/15-LO reduced the expression of inflammatory factors stimulated by PA or TNF-α. ChIP assays showed that 12(S)-HETE increased H3K4me modification in the TNF-α, IL-6, and MCP-1 gene promoters, and decreased H3K9me3 modification in the MCP-1 and IL-6 gene promoter. Urinary albumin excretion was greater in HFD-fed than in standard fat diet-fed mice, but both urinary protein and microalbumin amounts were lower in HFD-fed 12/15-LO knockout than in WT mice. The levels of TNF-α, IL-6, and MCP-1 in serum and renal cortex were higher in WT than in 12/15-LO knockout mice. Conclusions: 12/15-LO may regulate the expression of inflammatory factors in ORG by methylation of histones in the promoter regions of genes encoding inflammatory factors, sustaining the inflammatory phenotype of ORG. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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19 pages, 7055 KiB  
Article
11β-HSD1 Inhibitor Alleviates Non-Alcoholic Fatty Liver Disease by Activating the AMPK/SIRT1 Signaling Pathway
by Ying Chen, Jiali Li, Meng Zhang, Wei Yang, Wenqi Qin, Qinzhou Zheng, Yanhui Chu, Yan Wu, Dan Wu and Xiaohuan Yuan
Nutrients 2022, 14(11), 2358; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14112358 - 06 Jun 2022
Cited by 11 | Viewed by 2696
Abstract
We investigated the effect of an 11β-HSD1 inhibitor (H8) on hepatic steatosis and its mechanism of action. Although H8, a curcumin derivative, has been shown to alleviate insulin resistance, its effect on non-alcoholic fatty liver disease (NAFLD) remains unknown. Rats were fed a [...] Read more.
We investigated the effect of an 11β-HSD1 inhibitor (H8) on hepatic steatosis and its mechanism of action. Although H8, a curcumin derivative, has been shown to alleviate insulin resistance, its effect on non-alcoholic fatty liver disease (NAFLD) remains unknown. Rats were fed a high-fat diet (HFD) for 8 weeks, intraperitoneally injected with streptozotocin (STZ) to induce NAFLD, and, then, treated with H8 (3 or 6 mg/kg/day) or curcumin (6 mg/kg/day) for 4 weeks, to evaluate the effects of H8 on NAFLD. H8 significantly alleviated HFD+STZ-induced lipid accumulation, fibrosis, and inflammation as well as improved liver function. Moreover, 11β-HSD1 overexpression was established by transfecting animals and HepG2 cells with lentivirus, carrying the 11β-HSD1 gene, to confirm that H8 improved NAFLD, by reducing 11β-HSD1. An AMP-activated protein kinase (AMPK) inhibitor (Compound C, 10 μM for 2 h) was used to confirm that H8 increased AMPK, by inhibiting 11β-HSD1, thereby restoring lipid metabolic homeostasis. A silencing-related enzyme 1 (SIRT1) inhibitor (EX572, 10 μM for 4 h) and a SIRT1 activator (SRT1720, 1 μM for 4 h) were used to confirm that H8 exerted anti-inflammatory effects, by elevating SIRT1 expression. Our findings demonstrate that H8 alleviates hepatic steatosis, by inhibiting 11β-HSD1, which activates the AMPK/SIRT1 signaling pathway. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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Graphical abstract

15 pages, 2479 KiB  
Article
Diosmetin Targeted at Peroxisome Proliferator-Activated Receptor Gamma Alleviates Advanced Glycation End Products Induced Neuronal Injury
by Mei Chou Lai, Wayne Young Liu, Shorong-Shii Liou and I-Min Liu
Nutrients 2022, 14(11), 2248; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14112248 - 27 May 2022
Cited by 5 | Viewed by 1993
Abstract
The present study aimed to evaluate the role of diosmetin in alleviating advanced glycation end products (AGEs)-induced Alzheimer’s disease (AD)-like pathology and to clarify the action mechanisms. Before stimulation with AGEs (200 μg/mL), SH-SY5Y cells were treated with diosmetin (10 μmol/L), increasing cell [...] Read more.
The present study aimed to evaluate the role of diosmetin in alleviating advanced glycation end products (AGEs)-induced Alzheimer’s disease (AD)-like pathology and to clarify the action mechanisms. Before stimulation with AGEs (200 μg/mL), SH-SY5Y cells were treated with diosmetin (10 μmol/L), increasing cell viability. The induction of AGEs on the reactive oxygen species overproduction and downregulation of antioxidant enzyme activities, including superoxide dismutase, glutathione peroxidase, and catalase, were ameliorated by diosmetin. Amyloid precursor protein upregulation, accompanied by increased production of amyloid-β, caused by AGEs, was reversed by diosmetin. In the presence of diosmetin, not only β-site amyloid precursor protein cleaving enzyme1 expression was lowered, but the protein levels of insulin-degrading enzyme and neprilysin were elevated. Diosmetin protects SH-SY5Y cells from endoplasmic reticulum (ER) stress response to AGEs by suppressing ER stress-induced glucose regulated protein 78, thereby downregulating protein kinase R-like endoplasmic reticulum kinase, eukaryotic initiation factor 2 α, activating transcription factor 4, and C/EBP homologous protein. Diosmetin-pretreated cells had a lower degree of apoptotic DNA fragmentation; this effect may be associated with B-cell lymphoma (Bcl) 2 protein upregulation, Bcl-2-associated X protein downregulation, and decreased activities of caspase-12/-9/-3. The reversion of diosmetin on the AGEs-induced harmful effects was similar to that produced by pioglitazone. The peroxisome proliferator-activated receptor (PPAR)γ antagonist T0070907 (5 μmol/L) abolished the beneficial effects of diosmetin on AGEs-treated SH-SY5Y cells, indicating the involvement of PPARγ. We conclude that diosmetin protects neuroblastoma cells against AGEs-induced ER injury via multiple mechanisms and may be a potential option for AD. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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15 pages, 31501 KiB  
Article
Krill Oil Inhibits NLRP3 Inflammasome Activation in the Prevention of the Pathological Injuries of Diabetic Cardiomyopathy
by Xuechun Sun, Xiaodan Sun, Huali Meng, Junduo Wu, Xin Guo, Lei Du and Hao Wu
Nutrients 2022, 14(2), 368; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14020368 - 15 Jan 2022
Cited by 14 | Viewed by 3457
Abstract
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of [...] Read more.
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of DCM. In the present study, we investigate the effect of krill oil (KO) on the prevention of DCM using a mouse model of DM induced by streptozotocin and a high-fat diet. The diabetic mice developed pathological features, including cardiac fibrosis, apoptosis and inflammatory cell infiltration, the effects of which were remarkably prevented by KO. Mechanistically, KO reversed the DM-induced cardiac expression of profibrotic and proinflammatory genes and attenuated DM-enhanced cardiac oxidative stress. Notably, KO exhibited a potent inhibitory effect on NLR family pyrin domain containing 3 (NLRP3) inflammasome that plays an important role in DCM. Further investigation showed that KO significantly upregulated the expression of Sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which are negative regulators of NLRP3. The present study reports for the first time the preventive effect of KO on the pathological injuries of DCM, providing SIRT3, PGC-1α and NLRP3 as molecular targets of KO. This work suggests that KO supplementation may be a viable approach in clinical prevention of DCM. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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13 pages, 3572 KiB  
Article
Associations between Serum Betaine, Methyl-Metabolizing Genetic Polymorphisms and Risk of Incident Type 2 Diabetes: A Prospective Cohort Study in Community-Dwelling Chinese Adults
by Xiaoting Lu, Rongzhu Huang, Shuyi Li, Aiping Fang, Yuming Chen, Si Chen, Fan Wang, Xinlei Lin, Zhaoyan Liu and Huilian Zhu
Nutrients 2022, 14(2), 362; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14020362 - 15 Jan 2022
Cited by 7 | Viewed by 1773
Abstract
Previous studies have explored associations between betaine and diabetes, but few have considered the effects of genes on them. We aimed to examine associations between serum betaine, methyl-metabolizing genetic polymorphisms and the risk of type 2 diabetes in Chinese adults. This prospective study [...] Read more.
Previous studies have explored associations between betaine and diabetes, but few have considered the effects of genes on them. We aimed to examine associations between serum betaine, methyl-metabolizing genetic polymorphisms and the risk of type 2 diabetes in Chinese adults. This prospective study comprised 1565 subjects aged 40–75 without type 2 diabetes at baseline. Serum betaine was measured by high-performance liquid chromatography tandem mass spectrometry. Genotyping of methyl-metabolizing genes was detected by Illumina ASA-750K arrays. Cox proportional hazards model was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During a median of 8.9 years of follow-up, 213 participants developed type 2 diabetes. Compared with participants in the lowest quartile of serum betaine, those in the highest quartile had lower risk of type 2 diabetes, adjusted HRs (95%CIs) was 0.46 (0.31, 0.69). For methylenetetrahydrofolate reductase (MTHFR) G1793A (rs2274976) and MTHFR A1298C (rs1801131), participants carrying 1793GA + AA and 1298AC + CC had lower risk of type 2 diabetes. Interactions of serum betaine and genotype of MTHFR G1793A and MTHFR A1298C could be found influencing type 2 diabetes risk. Our findings indicate that higher serum betaine, mutations of MTHFR G1793A and A1298C, as well as the joint effects of them, are associated with lower risk of type 2 diabetes. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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Review

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8 pages, 400 KiB  
Review
Vitamin B12 Deficiency in Patients with Diabetes on Metformin: Arab Countries
by Jwaher Haji Alhaji
Nutrients 2022, 14(10), 2046; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14102046 - 13 May 2022
Cited by 9 | Viewed by 3921
Abstract
Background: Diabetes is a global pandemic, especially in Arab countries. Aim: The goal of this study was to review the published studies that were conducted to determine the relationship between metformin treatment for type 2 diabetes mellitus (T2DM) and vitamin B12 deficiency and [...] Read more.
Background: Diabetes is a global pandemic, especially in Arab countries. Aim: The goal of this study was to review the published studies that were conducted to determine the relationship between metformin treatment for type 2 diabetes mellitus (T2DM) and vitamin B12 deficiency and to identify possible complications in this relationship. Methods: I searched for all relevant studies published in English before 2020 on the PubMed and Web of Knowledge databases using the following terms: “metformin”, “vitamin B12”, “neuropathy”, “diabetes mellitus”, and Middle Eastern countries. Results: Eleven studies were included in this review which indicated an association between taking metformin and B12 deficiency in patients with T2DM in Arab countries. This B12 deficiency was found to be negatively associated with the dose and duration of metformin therapy. The physician’s knowledge of current ADA recommendations regarding supplementation with and screening of the B12 level for T2DM patients on metformin was also found to have an effect. Conclusion: Metformin therapy is associated with B12 deficiency among people with T2DM in Arabic countries. Thus, diabetes must be managed in compliance with current guidelines and recommendations, and B12 levels must be routinely monitored, particularly in those who have been long-term takers of metformin, to ensure the suitable management of diabetes and its complications. Full article
(This article belongs to the Special Issue Impact of Nutrition or FDA-Approved Medicine Repurposing Utilization on Metabolic Syndrome and Diabetic Complications)
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