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Amino Acid and Sugar Metabolism in Disease

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

Deadline for manuscript submissions: 20 August 2026 | Viewed by 838

Editor


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Guest Editor
1. Animal and Veterinary Research Center (CECAV), Associate Laboratory for Animal and Veterinary Sciences (AL4AnimalS), University of Trás-os-Montes and Alto Douro (UTAD), 5000-801 Vila Real, Portugal
2. Centre for the Research and Technology of Agro-Environmental and Biological Sciences (CITAB), University of Trás-os-Montes and Alto Douro (UTAD), 5000-801 Vila Real, Portugal
Interests: metabolic diseases; metabolic disturbances; carbohydrate metabolism; aminoacid metabolism

Special Issue Information

Dear Colleagues,

The International Journal of Molecular Sciences is pleased to announce a Special Issue focusing on the metabolism of amino acids, sugars, and sweeteners in disease. This Special Issue will explore how alterations in these fundamental metabolic pathways may contribute to human pathology, ranging from inherited disorders to acquired metabolic dysfunctions.

Inborn errors of metabolism, caused by genetically encoded enzyme deficiencies, remain a critical research area due to the inconvenient metabolic paths and, in certain cases,  the accumulation of toxic metabolites and their profound effects on neurological, cardiovascular, and hepatic systems. Likewise, disturbances in carbohydrate, amino acid and natural and synthetic sugar substitute metabolism underpin widespread health problems, including diabetes mellitus and metabolic syndrome. The increasing consumption of natural and artificial sweeteners introduces further complexity, as their biotransformation may modify metabolic routes, alter microbiota composition, and generate unexpected systemic effects. The situation becomes even more intricate when food additives are ingested in mixtures, potentially reshaping enzymatic activity, redox balance, and metabolic resilience.

We invite researchers to contribute original articles and reviews addressing the molecular and biochemical mechanisms linking amino acid, sugar, and sweetener metabolism to health and disease. Topics of interest include (but are not limited to):

  • Novel genetically determined metabolic disorders and associated toxic metabolites;
  • Mechanistic studies of altered pathways in amino acid and carbohydrate metabolism;
  • The metabolic impact of natural and artificial sweeteners;
  • Interactions between nutrients, additives, and the gut microbiome.

This Special Issue aims to provide a comprehensive platform for advancing knowledge and fostering innovative strategies in diagnosis, therapy, and nutrition.

Dr. V. Tkach
Guest Editor

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Keywords

  • metabolic diseases
  • metabolic disturbances
  • carbohydrate metabolism
  • aminoacid metabolism
  • artificial sweeteners
  • metabolic path alterations

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Published Papers (1 paper)

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Research

25 pages, 36457 KB  
Article
Comparison of Anti-Acute Phase Effect of CIGB-258 and Its Wild-Type Peptide (E18-3) in a Hyperinflammatory and Acute Bleeding Model of Zebrafish: A Surface Plasmon Resonance Study to Compare Binding Affinity with High-Density Lipoproteins
by Kyung-Hyun Cho, Yunki Lee, Sang Hyuk Lee, Ashutosh Bahuguna, Seung Hee Baek, María del Carmen Domínguez-Horta and Gillian Martínez-Donato
Int. J. Mol. Sci. 2026, 27(10), 4516; https://doi.org/10.3390/ijms27104516 - 18 May 2026
Cited by 1 | Viewed by 507
Abstract
The study compares the effects of the HSP60-derived mutated peptide (CIGB-258) and its wild-type peptide (E18-3) on preventing carboxymethyllysine (CML)- and ethanol (Et-OH)-induced hemorrhagic events and acute toxicity in zebrafish. The results suggest a 67% survivability and swimming recovery in CIGB-258-treated zebrafish compared [...] Read more.
The study compares the effects of the HSP60-derived mutated peptide (CIGB-258) and its wild-type peptide (E18-3) on preventing carboxymethyllysine (CML)- and ethanol (Et-OH)-induced hemorrhagic events and acute toxicity in zebrafish. The results suggest a 67% survivability and swimming recovery in CIGB-258-treated zebrafish compared to only 20% in the CML+Et-OH-treated group. No effect of E18-3 was noticed on CML+Et-OH-impaired zebrafish survivability and swimming ability. Similarly, no effect of E18-3 was noticed on the CML+Et-OH-disturbed blood oxidative and antioxidant variables. In contrast, CIGB-258 showed a notable 35% lower rate of oxidized contents, and 2.0-fold and 1.2-fold higher paraoxonase (PON) and ferric ion reduction activity (FRA), respectively, than in the E18-3 group. Also, the CML+Et-OH-induced dyslipidemia was substantially prevented by the CIGB-258, whereas no protective effect of E18-3 was noticed. Similarly, the CML+Et-OH-triggered hepatic inflammation, steatosis, kidney damage, severe gastrointestinal bleeding, and intestinal fibrosis were successfully mitigated by co-treatment with CIGB-258. Surface plasmon resonance analysis revealed a substantial binding affinity of CIGB-258 for HDL2 and HDL3, characterized by association rate constants (Ka) of 14.78 and 6.20 μM−1s−1, dissociation rate constants (Kd) of 0.35 s−1 and 0.22 s−1, and equilibrium dissociation constants (KD) of 0.024 and 0.035 μM, respectively. In conclusion, CIGB-258 exerted a substantial impact on CML+Et-OH-triggered adverse events, with high affinity for HDL, whereas E18-3 exposure remained unaffected and failed to produce any beneficial effects. Full article
(This article belongs to the Special Issue Amino Acid and Sugar Metabolism in Disease)
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