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.

Immune-mediated cholangiopathies are characterised by the destruction of small and large bile ducts causing bile acid stasis, which leads to subsequent inflammation, fibrosis, and eventual cirrhosis of the liver tissue. A breakdown of peripheral hepatic immune tolerance is a key feature of these diseases. Regulatory T cells (Tregs) are a major anti-inflammatory immune cell subset, and their quantities and functional capacity are impaired in autoimmune liver diseases. Tregs can undergo phenotypic reprogramming towards pro-inflammatory Th1 and Th17 profiles. The inflamed hepatic microenvironment influences and can impede normal Treg suppressive functions. Mast cell (MC) infiltration increases during liver inflammation, and active MCs have been shown to be an important source of pro-inflammatory mediators, thus driving pathogenesis. By influencing the microenvironment, MCs can indirectly manipulate Treg functions and inhibit their suppressive and proliferative activity. In addition, direct cell-to-cell interactions have been identified between MCs and Tregs. It is critical to consider the effects of MCs on the inflammatory milieu of the liver and their influence on Treg functions. This review will focus on the roles and crosstalk of Tregs and MCs during autoimmune cholangiopathy pathogenesis progression.

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