Oxidized Pork Induces Hepatic Steatosis by Impairing Thyroid Hormone Function in Mice

Ge, Yueting; Yang, Yuhui; Jiang, Yuge; Feng, Chuanxing; Li, Bowen; Sun, Jin; Tang, Xue; Shi, Yonghui; Li, Guowei

doi:10.1002/mnfr.202100602

Cited by 16 publications

(17 citation statements)

References 59 publications

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“…Previous studies found that changes in the inflammatory profile and oxidation status (REDOX) induce increased D3 activity in acute illness situations [36][37][38]. Here we observed that in a model of chronic disease, the accumulation of hepatic fat, via high-fat diet, induces inflammatory changes and a consequent increase in the production of reactive oxygen species (ROS) [39][40][41][42][43][44]. These data reinforce the direct association between the inflammatory profile and the REDOX state with diminished T3 levels, via an increase in D3 activity and a reduction in D1.…”

Section: Discussionmentioning

confidence: 74%

Understanding the Progression of Metabolic Dysfunction Asso-Ciated Fatty Liver Disease (MAFLD): Early Effect on Mitochon-Dria and Krebs Cycle Due to Type 3 Deiodinase Dysfunction

Marschner¹,

Roginski²,

Ribeiro³

et al. 2022

Preprint

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Metabolic dysfunction associated fatty liver disease (MAFLD) has gained worldwide attention as a public health problem. Nonetheless, lack of enough mechanistic knowledge restrains effective treatments. It is known that T3 regulate hepatic lipid metabolism, and mitochondrial function. Liver dysfunction of T3 contributes to MAFLD, but its role is not fully understood. Objective: To evaluate the role of T3 dysfunction in the progression of MAFLD in an animal model. Method-ology: Male/adult Sprague Dawley rats (n=20) were allocated to a control group (standard di-et–2.93kcal/g) and diet group (CDHF–4.3kcal/g). Euthanasia took place in the 28th week. D3 ac-tivity and expression, UCP2 and D1 expression, REDOX status, mitochondrial, Krebs cycle and endoplasmic reticulum homeostasis in liver tissue were measured. Results: We observed an in-crease in D3 activity/expression (P<0.001) related to increased TBARS and carbonyls and GSH reduction in the MAFLD group (P<0.05). There was a T3-dependent decrease in UCP2 expression (P=0.01), mitochondrial capacity, respiratory activity with increased endoplasmic reticulum stress in the MAFLD group (P < 0.001). Surprisingly, in and environment with lower T3 levels we observed an augmented alpha-ketoglutarate dehydrogenase (KGDH) and glutamate dehydro-genase (GDH) enzymes activity (P<0.05). Conclusion: Induced D3, triggered by changes in the REDOX state, decreases T3 availability, and hepatic mitochondrial capacity. The Krebs cycle en-zymes were altered as well as reticulum stress. Taken together, these results shed new light on the role of T3 metabolism in MAFLD and new treatment opportunities.

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Section: Discussionmentioning

confidence: 74%

Understanding the Progression of Metabolic Dysfunction Asso-Ciated Fatty Liver Disease (MAFLD): Early Effect on Mitochon-Dria and Krebs Cycle Due to Type 3 Deiodinase Dysfunction

Marschner¹,

Roginski²,

Ribeiro³

et al. 2022

Preprint

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“…The cell studies used the administration of FFAs [ 29 ] or palmitic and oleic acid [ 30 ]. The animal models show heterogeneity regarding the induction of the model, but the vast majority used ae high fat diet (HFD) [ 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 ]; one study used a pork-derived diet [ 41 ], while other models did not induce MAFLD but induced situations of hypo and hyperthyroidism [ 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ], subsequently evaluating its effects on the liver. Most of the selected articles included some type of hormone supplementation.…”

Section: Resultsmentioning

confidence: 99%

Influence of Altered Thyroid Hormone Mechanisms in the Progression of Metabolic Dysfunction Associated with Fatty Liver Disease (MAFLD): A Systematic Review

et al. 2022

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We performed a systematic review of the mechanisms of thyroid hormones (THs) associated with metabolic dysfunction associated with fatty liver disease (MAFLD). This systematic review was registered under PROSPERO (CRD42022323766). We searched the MEDLINE (via PubMed) and Embase databases from their inception to March 2022. We included studies that assessed thyroid function by measuring the serum level of THs and those involved in MAFLD. We excluded reviews, case reports, editorials, letters, duplicate studies and designed controls. Forty-three studies included MAFLD, eleven analyzed THs, and thirty-two evaluated the mechanisms of THs in MAFLD. Thyroid hormones are essential for healthy growth, development and tissue maintenance. In the liver, THs directly influence the regulation of lipid and carbohydrate metabolism, restoring the homeostatic state of the body. The selected studies showed an association of reduced levels of THs with the development and progression of MAFLD. In parallel, reduced levels of T3 have a negative impact on the activation of co-regulators in the liver, reducing the transcription of genes important in hepatic metabolism. Overall, this is the first review that systematically synthesizes studies focused on the mechanism of THs in the development and progression of MAFLD. The data generated in this systematic review strengthen knowledge of the impact of TH changes on the liver and direct new studies focusing on therapies that use these mechanisms.

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“…The long-term consumption of dityrosine-rich food is associated with a variety of diseases, such as liver and kidney fibrosis, obesity, diabetes, cardiovascular disease, Alzheimer's disease, and aging (B. Ding, Tang et al, 2017;Ge et al, 2021Ge et al, , 2022Gutiérrez et al, 2015; Z. L. Li et al, 2017;Z. L. Li et al, 2016;Lu et al, 2020;Mo et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

“…At that time, dityrosine research was mainly focused on food and biological samples. Recent research indicates that dityrosine can act as an oxidative-stress marker in the human body, inducing oxidative stress and metabolic syndrome (Ge et al, 2022;Lu et al, 2020;Yang, Zhang et al, 2017). This discovery has revived dityrosine research, with emphasis on its biochemistry and pathobiology.…”

Section: Introductionmentioning

confidence: 99%

“…Dityrosine exists widely in the food system, especially in meat, dairy, and egg products (B. Li, Mo et al., 2019; Duan et al., 2018; Ge et al., 2020; Hellwig, 2020). The long‐term consumption of dityrosine‐rich food is associated with a variety of diseases, such as liver and kidney fibrosis, obesity, diabetes, cardiovascular disease, Alzheimer's disease, and aging (B. Li, Ge et al., 2019; Ding, Tang et al., 2017; Ge et al., 2021, 2022; Gutiérrez et al., 2015; Z. L. Li et al., 2017; Z. L. Li et al., 2016; Lu et al., 2020; Mo et al., 2022).…”

Section: Introductionmentioning

confidence: 99%

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Dityrosine in food: A review of its occurrence, health effects, detection methods, and mitigation strategies

Yang

Ding

et al. 2022

Comp Rev Food Sci Food Safe

Self Cite

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Protein and amino acid oxidation in food products produce many new compounds, of which the reactive and toxic compound dityrosine, derived from oxidized tyrosine, is the most widely studied. The high reactivity of dityrosine enables this compound to induce oxidative stress and disrupt thyroid hormone function, contributing to the pathological processes of several diseases, such as obesity, diabetes, cognitive dysfunction, aging, and age‐related diseases. From the perspective of food safety and human health, protein‐oxidation products in food are the main concern of consumers, health management departments, and the food industry. This review highlights the latest research on the formation pathways, toxicity, detection methods, occurrence in food, and mitigation strategies for dityrosine. Furthermore, the control of dityrosine in family cooking and food‐processing industry has been discussed. Food‐derived dityrosine primarily originates from high‐protein foods, such as meat and dairy products. Considering its toxicity, combining rapid high sensitivity dityrosine detection techniques with feasible control methods could be an effective strategy to ensure food safety and maintain human health. However, the current dityrosine detection and mitigation strategies exhibit some inherent characteristics and limitations. Therefore, developing technologies for rapid and effective dityrosine detection and control at the industrial level is necessary.

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Oxidized Pork Induces Hepatic Steatosis by Impairing Thyroid Hormone Function in Mice

Cited by 16 publications

References 59 publications

Understanding the Progression of Metabolic Dysfunction Asso-Ciated Fatty Liver Disease (MAFLD): Early Effect on Mitochon-Dria and Krebs Cycle Due to Type 3 Deiodinase Dysfunction

Understanding the Progression of Metabolic Dysfunction Asso-Ciated Fatty Liver Disease (MAFLD): Early Effect on Mitochon-Dria and Krebs Cycle Due to Type 3 Deiodinase Dysfunction

Influence of Altered Thyroid Hormone Mechanisms in the Progression of Metabolic Dysfunction Associated with Fatty Liver Disease (MAFLD): A Systematic Review

Dityrosine in food: A review of its occurrence, health effects, detection methods, and mitigation strategies

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