The Role of Nutrients and Food Components in Liver and Gastrointestinal Health and Disease

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

Deadline for manuscript submissions: 15 June 2024 | Viewed by 1468

Special Issue Editor


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Guest Editor
Department of Dietetics and Nutrition, Florida International University, Miami, FL 33199, USA
Interests: zinc; autophagy; trace elements; alcoholic liver disease; nutrigenomics; aging

Special Issue Information

Dear Colleagues,

The liver–gut axis is a bidirectional communication system between the liver and the gut. Both organs communicate with each other via the biliary tract, the portal vein, and the systemic circulation. A well-balanced and functional liver–gut axis is associated with overall health.

Alterations in gut barrier permeability, the composition of the gut microbiome, and circulating levels of enterohepatic bile acids, induced by certain types of diet, have been implicated in the etiopathogenesis of liver diseases. On the other hand, the role of specific nutrients and food components in microbiome composition and the liver–gut axis has begun to be elucidated. Certain nutrients and food components are believed to prevent or alleviate liver disease by targeting the gut microbiome.

In this Special Issue, we aim to collect articles providing new and relevant information regarding the role of specific nutrients and food components in the microbiome and the gut–liver axis. This includes, but is not limited to, studies on (1) the effect of nutrient inadequacy/supplementation, (2) the efficacy of phytochemical supplementation, (3) the effect of certain types of diets, and (4) the role of single nucleotide polymorphisms (SNPs) in the interplay between diet and the liver–gut axis. We welcome original articles as well as narrative and systematic reviews.

Dr. Juan P. Liuzzi
Guest Editor

Manuscript Submission Information

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Keywords

  • liver
  • gut
  • intestine
  • microbiome
  • microbiota
  • vitamins
  • minerals
  • phytochemicals
  • deficiency
  • supplementation
  • gut barrier permeability
  • non-alcoholic fatty liver

Published Papers (1 paper)

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Research

19 pages, 3907 KiB  
Article
Metformin Inefficiency to Lower Lipids in Vitamin B12 Deficient HepG2 Cells Is Alleviated via Adiponectin-AMPK Axis
by Joseph Boachie, Victor Zammit, Ponnusamy Saravanan and Antonysunil Adaikalakoteswari
Nutrients 2023, 15(24), 5046; https://doi.org/10.3390/nu15245046 - 08 Dec 2023
Viewed by 1339
Abstract
Background: Prolonged metformin treatment decreases vitamin B12 (B12) levels, whereas low B12 is associated with dyslipidaemia. Some studies have reported that metformin has no effect on intrahepatic triglyceride (TG) levels. Although AMP-activated protein kinase (AMPK) activation via adiponectin lowers hepatic TG content, its [...] Read more.
Background: Prolonged metformin treatment decreases vitamin B12 (B12) levels, whereas low B12 is associated with dyslipidaemia. Some studies have reported that metformin has no effect on intrahepatic triglyceride (TG) levels. Although AMP-activated protein kinase (AMPK) activation via adiponectin lowers hepatic TG content, its role in B12 deficiency and metformin has not been explored. We investigated whether low B12 impairs the beneficial effect of metformin on hepatic lipid metabolism via the AMPK-adiponectin axis. Methods: HepG2 was cultured using custom-made B12-deficient Eagle’s Minimal Essential Medium (EMEM) in different B12-medium concentrations, followed by a 24-h metformin/adiponectin treatment. Gene and protein expressions and total intracellular TG were measured, and radiochemical analysis of TG synthesis and seahorse mitochondria stress assay were undertaken. Results: With low B12, total intracellular TG and synthesized radiolabelled TG were increased. Regulators of lipogenesis, cholesterol and genes regulating fatty acids (FAs; TG; and cholesterol biosynthesis were increased. FA oxidation (FAO) and mitochondrial function were decreased, with decreased pAMPKα and pACC levels. Following metformin treatment in hepatocytes with low B12, the gene and protein expression of the above targets were not alleviated. However, in the presence of adiponectin, intrahepatic lipid levels with low B12 decreased via upregulated pAMPKα and pACC levels. Again, combined adiponectin and metformin treatment ameliorated the low B12 effect and resulted in increased pAMPKα and pACC, with a subsequent reduction in lipogenesis, increased FAO and mitochondrion function. Conclusions: Adiponectin co-administration with metformin induced a higher intrahepatic lipid-lowering effect. Overall, we emphasize the potential therapeutic implications for hepatic AMPK activation via adiponectin for a clinical condition associated with B12 deficiency and metformin treatment. Full article
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