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A new study recently presented at the annual meeting of the European Association for the Study of Diabetes in Stockholm, Sweden, revealed a high correlation
between a group of common viruses and type 1 diabetes (T1D).
According to the Australian study, people with T1D have an 8-fold
higher risk of contracting enterovirus than people without the disease.
T1D is the most common type of childhood diabetes and has been increasing globally in prevalence in recent decades
.
The immune system of a diabetic person attacks and destroys the insulin-producing β cells in the pancreas, preventing the body from producing enough hormones to properly regulate blood sugar levels
.
Over time, high blood sugar levels may reduce life expectancy and damage the kidneys, feet, eyes, heart, and eyes
.
In addition, diabetic ketoacidosis, a condition that often occurs at the time of T1D diagnosis, involves the accumulation of dangerous substances called ketones in the blood, which can be fatal if left untreated
.
Although the specific cause of the immune system's response remains controversial, it is widely believed that genetic susceptibility and one or more environmental triggers, such as viral infections
, are involved.
Some of the strongest evidence of viral infections points to enteroviruses
.
This very common class of viruses includes those that cause polio and hand-foot-and-mouth disease (HFMD), as well as others that cause milder cold-like symptoms
.
Vaccines to reduce the incidence of T1D by preventing enterovirus infection are already in clinical trials1, and confirming the role of enteroviruses will support this and other efforts
for primary prevention of T1D.
To explore the link in more depth, Sonia Isaacs and colleagues from the Department of Paediatrics and Child Health at the School of Clinical Medicine of the University of New South Wales, Australia, conducted a systematic review and meta-analysis
of existing research on the topic.
This meta-analysis is the largest in the field and included data
from 12,077 participants (aged 0-87 years) from 60 controlled observational studies in the PubMed and Embase databases.
5981 participants had T1D or islet autoimmunity (usually developing T1D).
The remaining 6,096 participants had neither
.
Enteroviral RNA, or proteins, are markers of current or recent infection and are detected
in blood, stool, or tissue samples using a range of advanced, highly sensitive molecular techniques.
Patients with islet autoimmunity are twice as likely to test positive for enterovirus as those without islet autoimmunity
.
People with T1D are 8 times
more likely to have enteroviral infections than people without T1D.
Most importantly, people with T1D were more than
16 times more likely to detect enteroviral infections within a month of T1D diagnosis than people without T1D.
The researchers concluded that there is a clear link
between enterovirus infection and islet autoimmunity and T1D.
Ms.
Isaacs added: "These findings provide further support to ongoing vaccine development efforts to prevent islet autoimmunity, thereby reducing the incidence
of T1D.
"
There are several theories
about how enteroviruses increase the risk of developing T1D.
For example, it is thought that their interaction with specific genes may be important
.
"Our study found that people with T1D who are at both genetic risk and have a first-degree relative with T1D are 29 times
more likely to develop enterovirus infection," Ms Isaacs explained.
"The number, timing and duration of enteroviral infections, and even the location, may also be important
," she continued.
The "leaky gut" hypothesis suggests that viruses originating in the gut can travel along with activated immune cells to the pancreas, where low levels of persistent infection and resulting inflammation can lead to an autoimmune response
.
Viral infections are also thought to play a role in conjunction with other factors, such as diet, imbalance of the gut microbiome, and may even occur in the womb (during pregnancy) or chemical contact
in early childhood.
There's still a lot to learn
.
”