Liver problems – source of diabetes2 types

Update: February 2019

The publication Nature Communications has published the latest data.
research in the field of endocrinology. It turns out that it is
liver takes a key position in the development of diabetes mellitus 2
type The scientists representing UNIGE (Geneva
University, Switzerland), and now strive to explore new approaches to
therapy of this pathology.

According to statistics, diabetes suffers every eleventh
a resident of our planet. Approximately 420 million people have this
diagnosis. More popular among metabolic obesity: so
overweight diagnosed in over 650 million
patients. Obesity is one of the main factors in the development of
endocrinological pathology. The exception was not diabetes:
the connection between these two states has long been known to doctors and
ordinary residents.

Researchers interested in the details of the development process
diabetic pathology. How are all the processes carried out on
level of cells and molecules, as well as how involved in this
excess fat? To find out the truth, scientists have paid attention to
protein PTPR-γ, which is increased with different obesity
severity.

Increased adipocyte count (fat cells)
activates the immune system, leading to inflammatory
body reactions. Liver is also involved in general inflammation. The
the process activates the so-called “transcription factor NF-kβ”,
present in hyperglycemia. This factor provides a synthesis
PTPR-γ. Consequently, the content of the latter in the liver tissue
increases with inflammatory response. It has been confirmed
research on the human sample.

But to even more fully understand the problem, scientists have resorted
to experiments on laboratory animals. Genetically modified
the mice were divided into three test subjects by university staff
groups. In the first group, the expression of PTPR-γ was reduced; in the second,
was at a normal level, in the third – was increased. Scientists
tried to track how these modifications affect the formation
insulin resistance.

As a result, it turned out that:

  1. In the absence of the PTPR-γ protein, obesity developed due to
    excess amount of feed for mice, while diabetes mellitus
    was not observed. Even if scientists injected lipopolysaccharide,
    hyperglycemia and immunity to the action of insulin was not.
  2. With normal levels of PTPR-γ protein in liver cells
    laboratory rodents were at risk of developing
    diabetes. This is confirmation of a sufficiently large role.
    liver in this disease.
  3. With increased formation of PTPR-γ (approximately twice), which
    imitated the state of obesity, accumulated sufficient
    количество сведений для диагностирования сахарного diabetes.

Prior to this, all the functional features of PTPR-γ did not describe either
one researcher. The results can give rise to
попыткам поиска новых методов лечения сахарного диабета 2 types,
because this protein is on the surface of the cell membranes,
which makes him more vulnerable when exposed to medication. Besides,
if you bind two PTPR-γ protein molecules, it stops working,
which also gives an undeniable plus in the future. It only remains
find the substance of natural or artificial origin,
which is able to bind these molecules qualitatively.

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