Low selenium status is associated with increased risk of thyroid disease. Increased selenium intake may reduce the risk in areas of low selenium intake that exist not only in China but also in many other parts of the world.
Objective
The trace element selenium (Se) is needed for regular biosynthesis of selenoproteins, which contribute to antioxidative defense systems and affect redox-regulated signaling. Elevated Se intake and selenoprotein expression levels have been associated with impaired hydrogen peroxide-dependent signaling by insulin, leading to hyperglycemia and insulin resistance. The relation of low Se intake with glucose status and carbohydrate metabolism is poorly known.
Research design and methods
A cross sectional analysis among healthy subjects residing in two Chinese counties with different habitual Se intakes was conducted. Fasted glucose levels were related to Se concentrations of 5686 adults by linear regression analysis with Se, body mass index, age, thyroid status, insulin and sex as independent variables.
Results
Serum Se correlated strongly and positively with glucose in the Se-deficient population. There was no strong relationship of Se and glucose in the non-deficient population. Overt hypoglycemia (serum glucose < 2.8 mM) was observed in 19.2% of this random sample of subjects in the Se-deficient and in 1.4% of the moderately supplied population, respectively.
Conclusions
An adequate Se supply constitutes an important factor for glucose homeostasis in human subjects. The interaction between Se status and glucose control is not limited to hyperglycemia, but apparently extends to hypoglycemia risk in Se deficiency. This newly identified relationship may be of relevance for the course of severe disease including major trauma, sepsis and COVID-19, where Se deficiency has been associated with mortality risk.
Graves' disease (GD) is a common organ-specific autoimmune disease with the prevalence between 0.5 and 2% in women. Several lines of evidence indicate that the shed A-subunit rather than the full-length thyrotropin receptor (TSHR) is the autoantigen that triggers autoimmunity and leads to hyperthyroidism. We have for the first time induced GD in female rhesus monkeys, which exhibit greater similarity to patients with GD than previous rodent models. After final immunization, the monkeys injected with adenovirus expressing the A-subunit of TSHR (A-sub-Ad) showed some characteristics of GD. When compared with controls, all the test monkeys had significantly higher TSHR antibody levels, half of them had increased total thyroxine (T 4 ) and free T 4 , and 50% developed goiter. To better understand the underlying mechanisms, quantitative studies on subpopulations of CD4CT helper cells were carried out. The data indicated that this GD model involved a mixed Th1 and Th2 response. Declined Treg proportions and increased Th17:Treg ratio are also observed. Our rhesus monkey model successfully mimicked GD in humans in many aspects. It would be a useful tool for furthering our understanding of the pathogenesis of GD and would potentially shorten the distance toward the prevention and treatment of this disease in human.
The microbiome is in a symbiotic relationship with the host. Among the microbial consortia in the human body, that in the oral cavity is complex. Instead of repeatedly confirming biomarkers of oral and systemic diseases, recent studies have focused on a unified clinical diagnostic standard in microbiology that reduces the heterogeneity caused by individual discrepancies. Research has also been conducted on other topics of greater clinical importance, including bacterial pathogenesis, and the effects of drugs and treatments. In this review, we divide existing research into technology‐driven and hypothesis‐driven, according to whether there is a clear research hypothesis. This classification allows the demonstration of shifts in the direction of oral microbiology research. Based on the shifts, we suggested that establishing clear hypotheses may be the solution to major research challenges.
In Chinese adults, higher habitual protein consumption may be associated with higher adiposity and worse glycaemic control, independent of total energy intake.
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