Role of Zinc in Zinc-α2-Glycoprotein Metabolism in Obesity: a Review of Literature

Silva, Juliana; Morais, Jennifer Beatriz Silva; Beserra, Jéssica Batista; Santos, Loanne Rocha dos; Melo, Stéfany Rodrigues de Sousa; Sousa, Gustavo Santos de; Neto, Emídio Marques de Matos; Henriques, Gilberto Simeone; Marreiro, Dilina do Nascimento

doi:10.1007/s12011-019-01702-w

Cited by 43 publications

(38 citation statements)

References 53 publications

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“…As indicated by Severo et al in a review of 58 papers on the role of Zn in ZAG metabolism in obesity, obese patients present low serum concentrations of Zn and ZAG, as well as decreased expression of the genes encoding this protein. Severo concludes that Zn acts as an important regulator of the homeostasis of ZAG and that alterations in the distribution of Zn in obese patients may affect the physiological functions of ZAG [ 52 ] (LOE V). ZAG plays an important role in lipid and glucose metabolism and seems to constitute a linkage between Zn and obesity complications.…”

Section: Resultsmentioning

confidence: 99%

The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels

Banach

Nitschke

Krajewska

et al. 2020

IJMS

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Background: Obesity and excess body weight are significant epidemiological issues, not only because they are costly to treat, but also because they are among the leading causes of death worldwide. In 2016, an estimated 40% of the global population was overweight, reflecting the importance of the issue. Obesity is linked to metabolism malfunction and concomitantly with altered mineral levels in the body. In this paper, we review alterations in somatic levels of iron, calcium, magnesium, copper, iodine, chromium, selenium, and zinc in relation to excess body mass. Methodology: An electronic literature search was performed using PubMed. Our search covered original English research articles published over the past five years, culminating in 63 papers included for study. Results: The reviewed papers presented correlation between obesity and hypomagnesemia and hypozincemia. They also indicated that patients with excess body mass present increased body copper levels. Studies have similarly indicated that obesity appears to be associated with lower selenium levels in both blood and urine, which may be correlated with the decline and weakening of defenses against oxidative stress. It has been found that decreased level of chromium is connected with metabolic syndrome. Chromium supplementation influences body mass, but the effect of the supplementation depends on the chemical form of the chromium. It is hypothesized that obesity poses a risk of iodine deficiency and iodine absorption may be disrupted by increased fat intake in obese women. A range of studies have suggested that obesity is correlated with iron deficiency. On the other hand, some reports have indicated that excess body mass may coexist with iron excess. The relation between obesity and body iron level requires further investigation. Calcium signaling seems to be disturbed in obesity, due to the increased production of reactive oxygen species and low level of fast troponin isoform responsible for mediating calcium sensitivity of muscle relaxation. Correlation between excess body mass and calcium levels needs further research. Conclusions: Excess body mass is associated with alterations in mineral levels in the body, in particular hypomagnesemia and decreased selenium (Se) and zinc (Zn) levels. Chromium (Cr) deficiency is associated with metabolic syndrome. Obese patients are at risk of iodine deficiency. Excess body mass is associated with elevated levels of copper (Cu). Data on the association between obesity and iron (Fe) levels are contradictory. Obesity coexists with disturbed calcium (Ca) signaling pathways. The association between obesity and body Ca levels has not been investigated in detail.

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Section: Resultsmentioning

confidence: 99%

The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels

Banach

Nitschke

Krajewska

et al. 2020

IJMS

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“…Along with being modulated by levels of adiposity, ZAG has also been directly implicated in the metabolic action of adipose tissue (18). For example, ZAG has been associated with reduced insulin sensitivity in visceral adipose tissue, suggesting a feedback loop whereby increased visceral adiposity reduces ZAG expression, which in turn may increase adverse metabolic functioning of visceral adipose tissue (31).…”

Section: Discussionmentioning

confidence: 99%

“…The expanding evidence demonstrating the role of ZAG in lipid and glucose homeostasis has led to ZAG becoming a protein of increasing interest for anti-obesity and obesity-related disease therapy (18). In particular, lower levels of ZAG have been reported to be associated with the development and severity of T2DM, however the literature is contradictory, and no summary evidence has been published to date to quantify the magnitude of the association.…”

Section: Introductionmentioning

confidence: 99%

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

Pearsey

Henson

Sargeant

et al. 2020

Rev Endocr Metab Disord

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To systematically review the current literature investigating associations between zinc-alpha2-glycoprotein (ZAG) and dysglycaemia (including type 2 diabetes (T2DM), poly-cystic-ovary syndrome (PCOS), pre-diabetes or insulin resistance). This included relationships between ZAG and continuous measures of insulin and glucose. Additionally, we performed a meta-analysis to estimate the extent that ZAG differs between individuals with or without dysglycaemia; whilst examining the potential influence of adiposity. A systematic search was performed on four databases for studies on circulating ZAG concentrations in adult human populations, comparing healthy controls to individuals with dysglycaemia. Key characteristics, including the mean ZAG concentrations (mg∙L−1), and any correlational statistics between ZAG and continuous measures of glucose, glycated haemoglobin (HbA1c) or insulin were extracted. Meta-analyses were performed to compare metabolically healthy controls to cases, and on studies that compared controls and cases considered overweight or obese (body mass index (BMI) ≥25 kg.m2). 1575 papers were identified and 14 studies (16 cohorts) were considered eligible for inclusion. Circulating ZAG was lower in individuals with dysglycaemia compared to metabolically healthy controls (−4.14 [−8.17, −0.11] mg.L−1; I2 = 98.5%; p < 0.001). When using data from only studies with overweight or obese groups with or without dysglycaemia (three studies (four cohorts); pooled n = 332), the difference in circulating ZAG was no longer significant (−0.30 [−3.67, 3.07] mg. L−1; I2 = 28.0%; p = 0.225). These data suggest that ZAG may be implicated in dysglycaemia, although there was significant heterogeneity across different studies and the mediating effect of adiposity cannot be excluded. Therefore, more research is needed before robust conclusions can be drawn.

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“…Zinc-α-2-glycoprotein is involved the development of AO and T2DM. Previous studies have shown that zinc-α-2glycoprotein was a better predictor for IR than HOMA-IR index (156)(157)(158). Zinc-α-2-glycoprotein acts via interaction with p-ERK and TGF-β1, promoting proliferation of endothelial precursors, suppression of low-grade inflammation, regulation of metabolism of ketone bodies, and increased expression of visfatin in target cells (159,160).…”

Section: Zinc-α-2-glycoproteinmentioning

confidence: 98%

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

Berezin

Lichtenauer

2020

Front. Cardiovasc. Med.

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Adipose tissue dysfunction is a predictor for cardiovascular (CV) events and heart failure (HF) in patient population with obesity, metabolic syndrome, and known type 2 diabetes mellitus. Previous preclinical and clinical studies have yielded controversial findings regarding the role of accumulation of adipose tissue various types in CV risk and HF-related clinical outcomes in obese patients. There is evidence for direct impact of infiltration of epicardial adipocytes into the underlying myocardium to induce adverse cardiac remodeling and mediate HF development and atrial fibrillation. Additionally, perivascular adipocytes accumulation is responsible for release of proinflammatory adipocytokines (adiponectin, leptin, resistin), stimulation of oxidative stress, macrophage phenotype switching, and worsening vascular reparation, which all lead to microvascular inflammation, endothelial dysfunction, atherosclerosis acceleration, and finally to increase in CV mortality. However, systemic effects of white and brown adipose tissue can be different, and adipogenesis including browning of adipose tissue and deficiency of anti-inflammatory adipocytokines (visfatin, omentin, zinc-α2-glycoprotein, glypican-4) was frequently associated with adipose triglyceride lipase augmentation, altered glucose homeostasis, resistance to insulin of skeletal muscles, increased cardiomyocyte apoptosis, lowered survival, and weak function of progenitor endothelial cells, which could significantly influence on HF development, as well as end-organ fibrosis and multiple comorbidities. The exact underlying mechanisms for these effects are not fully understood, while they are essential to help develop improved treatment strategies. The aim of the review is to summarize the evidence showing that adipocyte dysfunction may induce the onset of HF and support advance of HF through different biological mechanisms involving inflammation, pericardial, and perivascular adipose tissue accumulation, adverse and electrical cardiac remodeling, and skeletal muscle dysfunction. The unbalancing effects of natriuretic peptides, neprilysin, and components of renin-angiotensin system, as exacerbating cause of altered adipocytokine signaling Berezin et al. Adipocyte Dysfunction in Heart Failure on myocardium and vasculature, in obesity patients at high risk of HF are disputed. The profile of proinflammatory and anti-inflammatory adipocytokines as promising biomarker for HF risk stratification is discussed in the review.

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Role of Zinc in Zinc-α2-Glycoprotein Metabolism in Obesity: a Review of Literature

Cited by 43 publications

References 53 publications

The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels

The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

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