Dietary zinc restriction promotes degeneration of the endocrine pancreas in mice

Sisnande, Tháyna; Lima, Cleverton Kleiton Freitas de; Silva, Dayana Cabral da; Beninatto, Thayana Moulin; Alves, Natália Leão; Amaral, Mariana J. do; Miranda-Alves, Leandro; Lima, L.M.T.R.

doi:10.1016/j.bbadis.2020.165675

Cited by 14 publications

(22 citation statements)

References 60 publications

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“…and increased circulating glucagon levels in type 2 diabetic model mice (leptin receptor-deficient db/db mice), suggesting that lower zinc status aggravates glucose metabolism 57) . A study using a type 1 diabetic model mice also showed that dietary zinc restriction promoted degradation of the endocrine pancreas, resulting in augmented hyperglycemia 58) . Given these animal studies, zinc deficiency is likely to be associated with the development of both type 1 and type 2 diabetes.…”

Section: -3 Role Of Zinc In Insulin Signalingmentioning

confidence: 99%

The Role of Zinc Homeostasis in the Prevention of Diabetes Mellitus and Cardiovascular Diseases

Tamura

2021

JAT

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Zinc is an essential micronutrient for human health and is involved in various biological functions, such as growth, metabolism, and immune function. In recent years, research on intracellular zinc dynamics has progressed, and it has become clear that zinc transporters strictly control intracellular zinc localization, zinc regulates the functions of various proteins and signal transduction pathways as a second messenger similar to calcium ions, and intracellular zinc dyshomeostasis is associated with impaired insulin synthesis, secretion, sensitivity, lipid metabolism, and vascular function. Numerous animal and human studies have shown that zinc deficiency may be associated with the risk factors for diabetes and cardiovascular diseases (CVDs) and zinc administration might be beneficial for the prevention and treatment of these diseases. Therefore, an understanding of zinc biology may help the establishment of novel strategies for the prevention and treatment of diabetes and CVDs. This review will summarize the current knowledge on the role of zinc homeostasis in the pathogenesis of diabetes and atherosclerosis and will discuss the potential of zinc in the prevention of these diseases.in the skin and liver, and the remaining 2%-3% is in all the other tissues, including blood and blood vessels. Zinc deficiency is well known to be involved in various disorders in the whole-body, such as growth failure, immune disorders, and dysgeusia 5) . Furthermore, zinc deficiency also increases the risk for diabetes and CVDs 6, 7) . Recent findings have shown that intracellular zinc homeostasis regulated by zinc transporters is involved in the regulation of insulin synthesis, secretion, sensitivity, and vascular function 6,8) . This review will discuss the role of impaired intracellular zinc homeostasis in the pathogenesis of diabetes and atherosclerosis and whether zinc supplementation is beneficial for the prevention of these diseases. Intracellular Zinc HomeostasisZinc is a divalent cation and can bind to ~10% of all proteins found in the human body and functionsCopyright©2021 Japan Atherosclerosis Society This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.

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Section: -3 Role Of Zinc In Insulin Signalingmentioning

confidence: 99%

The Role of Zinc Homeostasis in the Prevention of Diabetes Mellitus and Cardiovascular Diseases

Tamura

2021

JAT

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“…[132][133][134] More importantly, Zn dietary restriction induces endocrine pancreatic degeneration with the detection of toxic oligomer-like immunoreponsive material in mice pancreatic islets. 135 Metallothionein, 136 ZIP, and Zn transporters (ZnT), 137 among other gatekeepers controlling Zn homeostasis, would act as triage-determining molecular switches. These same biomacromolecules would be one out of the most susceptible genetic mutation points in triggering amyloidosis pathways, and both gain or loss of function mutations could exert a deterministic role.…”

Section: Type 2 Diabetesmentioning

confidence: 99%

“…The more common lab model is murine (mouse and rat), known for the alleged lack of responsiveness for amyloid formation regardless of the nature of the amyloid polypeptide, although recently demonstrated the oligomer/amyloid phenomena in vitro/ in vivo. 134,135,357,358 Thus, dietary intervention (restriction > repletion) should prove of limited interpretation under the current analytical perspective. Typically, transgenic mice models are used, expressing high amounts of the human-related peptide (amylin, Aβ, α-syn, etc.)…”

Section: The In Vivo Allometric Argumentmentioning

confidence: 99%

Nutrient‐sensing amyloid metastasis

Lima

Sisnande

2022

BioFactors

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Amyloids are organized suprastructural polypeptide arrangements. The prevalence of amyloid‐related processes of pathophysiological relevance has been linked to aging‐related degenerative diseases. Besides the role of genetic polymorphisms on the relative risk of amyloid diseases, the contributions of nongenetic ontogenic cluster of factors remain elusive. In recent decades, mounting evidences have been suggesting the role of essential micronutrients, in particular transition metals, in the regulation of amyloidogenic processes, both directly (such as binding to amyloid proteins) or indirectly (such as regulating regulatory partners, processing enzymes, and membrane transporters). The features of transition metals as regulatory cofactors of amyloid proteins and the consequences of metal dyshomeostasis in triggering amyloidogenic processes, as well as the evidences showing amelioration of symptoms by dietary supplementation, suggest an exaptative role of metals in regulating amyloid pathways. The self‐ and cross‐talk replicative nature of these amyloid processes along with their systemic distribution support the concept of their metastatic nature. The role of amyloidosis as nutrient sensors would act as intra‐ and transgenerational epigenetic metabolic programming factors determining health span and life span, viability, which could participate as an evolutive selective pressure.

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“…The animals (n=6-8 animals/group), immediately after weaning, were divided into two groups that received regular or zinc deficient diets, and maintained with the assigned diets throughout the experiment. Control group was exclusively fed with the AIN-93 modified chow (with casein replaced by hen egg white solids; Salto's LTDA), formulated with either regular mineral mix (AIN-93G-MX) or zinc-deficient mineral mix formulated without added zinc salts (AIN-93G-MX-ZnDef) as previously reported (Sisnande et al, 2020).…”

Section: Experimental Groupsmentioning

confidence: 99%

“…Furthermore, zinc acts also as a cofactor of tyrosine kinases, enzymes responsible to activate IGF-1 receptor (Wilson et al, 2012). A recent study of our group revealed that zinc restriction produces selective degeneration of the endocrine pancreas in mice (SISNANDE et al, 2020). In the central nervous system (CNS), zinc is an essential micronutrient for the development of memory and learning processes, as well as mediating synaptic plasticity (Hagmeyer et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Dietary zinc restriction induces nociceptive pain with reduced inflammation in mice

Lima

Sisnande

Silva

et al. 2020

Preprint

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Zinc (Zn) is an essential micronutrient involved in a large diversity of cellular metabolism, included in the physiology of nervous system and pain modulation. There is little evidence for the role of Zn nutritional alternations to the onset and progression of neuropathic and inflammatory pain. We investigate the effects of a zinc restricted diet on the development of pain. Weaned mice were submitted to different diets: AIN-93 (38mg/kg of Zn) and Zn-deficient (AIN-93 with 11mg/kg of Zn), during four weeks. Mechanical allodynia was measured weekly using Von Frey hairs. Plantar assays for cold and heat allodynia, formalin-induced nociception and carrageenan-induced mechanical allodynia were performed at the 4th week. Plasma, DRG and livers samples were obtained for biochemical and metabolomics analysis. Zn deficient diet completely changed mice sensitivity pattern, inducing an intense allodynia evoked by mechanical, cold and heat stimulus since weaning and during four weeks. Showed also an increased sensitivity of neurogenic phase of formalin test but the inflammatory pain behavior was drastically reduced. Zn restriction increased the ATF-3 and SOD-1 levels at DRG and reduced that of GFAP, leading an increase of neuronal activation and oxidative stress, and reduced neuroimmune activity. Plasma TNF was also reduced and metabolomics analyses suggest a downregulation of lipid metabolism of arachidonic acid, reinforcing the impact of Zn restriction to the inflammatory response. Reduction of Zn intake interferes in pain circuits, reducing inflammatory pain, however enhancing nociceptive pain. Accordingly, Zn imbalance could be predisposing factor for NP development. Therefore, dietary zinc supplementation and its monitoring present clinical relevance.

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Dietary zinc restriction promotes degeneration of the endocrine pancreas in mice

Cited by 14 publications

References 60 publications

The Role of Zinc Homeostasis in the Prevention of Diabetes Mellitus and Cardiovascular Diseases

The Role of Zinc Homeostasis in the Prevention of Diabetes Mellitus and Cardiovascular Diseases

Nutrient‐sensing amyloid metastasis

Dietary zinc restriction induces nociceptive pain with reduced inflammation in mice

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