International Journal of Medical Sciences And Clinical Research
102
https://theusajournals.com/index.php/ijmscr
VOLUME
Vol.05 Issue02 2025
PAGE NO.
102-104
10.37547/ijmscr/Volume05Issue02-19
The effect of glyderinine on glucose transport into
muscle tissue depending on the level of insulin in the
blood
Malikova Gulchexra Yuldashevna
Tashkent Pharmaceutical Institute. Associate Professor of the Department of Toxicological Chemistry. Candidate of Biological Sciences.
Tashkent, 45 Oybek St.
Jurayeva Aziza Abdunazarovna
Tashkent Pharmaceutical Institute of Education and Research. Associate Professor of the Department of Bioorganic Chemistry,
Candidate of Biological Sciences. Tashkent, 45 Oybek St.
Received:
24 December 2024;
Accepted:
26 January 2025;
Published:
28 February 2025
Abstract:
The paper studied glucose in glycerin (18-dehydroglycerretic acid) by comparing the level of transport
to diaphragm muscle tissue with the insulin effect under in vitro conditions. In this case, a 53% decrease in glucose
content in the incubation medium in muscle tissue was to a certain extent the reason for its accumulation as
glycogen (24%). Since the observed changes were similar to the qualitative changes determined by the action of
insulin, the amount of insulin and S-peptide was measured using radioimmun analysis in the rat mine, where
glycerin was sent in this experiment. The results of these studies showed that in animal experiments conducted
in the glyderin laboratory, it was shown that insulin and C-peptide act in both directions. No significant glycemic
reactions to adrenaline were observed in animals taking antidepressants. Therefore, the observed metabolic
changes may be related to the stimulation of insulin secretion.
Keywords:
Diabetes, hexokinase, glycogen, phosphorylase, insulin, C-peptide, radioimmune, incubation.
Introduction:
Normalizing metabolic processes in
diabetes mellitus with the prevention of its various
complications is the object of close attention of
physicians, pharmacologists, biotechnologists and
biochemists. Pharmacotherapy in diabetes mellitus
provides for aspects of increased insulin secretion
depending on the type of diabetes, replacement of
insulin in case of its deficiency and normalization of
existing metabolic disorders. Synthetic derivatives of
sulfonylureas and biguanides and their subsequent
analogues remain the main oral treatment for patients
with non-insulin-dependent diabetes. Unfortunately,
due to the side effects of addiction and, in some cases,
direct toxicity, they have limited use. Therefore,
attempts to develop new antidiabetic drugs that are
convenient for patients and have relatively minimal
side effects are still relevant today.
In all tissues, under physiological conditions, glucose
transport determines its intracellular metabolism,
estimated by the oxidation of glucose to carbon
dioxide. Obviously, transport is the primary limiting
reaction in the utilization of glucose by cells, since in
the absence of insulin, the flow of transferred glucose
is always less than the rate of glucose phosphorylation
(1). The intensity of the main metabolic pathways of
glucose depends on the structural and functional
characteristics of individual tissues.
For example, in human erythrocytes and in animal
livers, the highest rate of glucose transport is observed,
exceeding, by about an order of magnitude, the
corresponding values in other tissues. In muscle and
some other tissues, an increase in the rate of glycolysis
is accompanied by stimulation of glucose extraction
and activation of hexokinase (2).
METHODS
International Journal of Medical Sciences And Clinical Research
103
https://theusajournals.com/index.php/ijmscr
International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
Taking into account the above, and based on the
observed changes in glucose, glycogen, phosphorylase
and hexokinase activity under the action of glyderinine,
in this work we studied the effect of the drug on
glucose transport into muscle tissue, while comparing
the results with the effect of insulin in similar
experimental conditions.
For this purpose, in in vitro experiments, the diaphragm
was incubated in a glucose medium and glucose
consumption was determined by its loss from the
incubation medium and the glycogen content in the
diaphragm (3).
Determination of insulin in blood serum was performed
using radioimmunological kits. The insulin content in
the blood serum of rats according to this method is 30.6
= 7.2 mkED / ml in 1 ml of plasma.
RESULTS AND DISCUSSION
We found (see Table 1) that the drug under study
contributes to the intake of glucose by the diaphragm
by 53% and the accumulation of glycogen in it by 24%.
As can be seen from the data in the table, the effects of
glyderinine on glucose transport and its incorporation
into glycogen are similar to those of insulin, i.e.
glyderinine, like insulin, stimulates glucose transport
through cytoplasmic membranes.
Table 1.
The effect of glyderinine on glucose intake and glycogen content in the diaphragm
(the experiments are the average of 6 definitions)
Indicators
Glucose in
microns / g
Glycogen in mg%
1
before incubation
(control)
2,81 ± 0,55
54,5 + 5,02
2
after incubation
4,28 ± 0,59*
67,8 + 6,13
3
insulin in iu/ml
4.40 ± 0.54*
68,5 +4,6*
The differences are significant - p<0.05 from the
control.
These facts can be used to interpret the mechanism of
the metabolic effect of the drug. It seems to us that,
based on in vitro experiments without insulin or in vivo
at steady-state concentrations of insulin in the blood,
the established increase in glucose transport and
glycogen synthesis in skeletal muscles, combined with
the effect of insulin on phosphorylase and hexokinase
activity, is to a certain extent due to tissue reaction or
the insulin-like effect of the drug, or they are mediated
through increased insulin secretion in beta cells of the
islets of Langerhans of the pancreas.
Clarifying this may help in understanding the
stimulation of membrane glucose transport under the
influence of glyderinine. Therefore, in a series of
studies, we determined the levels of insulin and C-
peptide in the blood by radioimmune analysis in rats
treated with glyderinine in these dosages normally and
against the background of administration of the
counterinsular hormone epinephrine 0.7-0.8 mg/kg
div weight 20 minutes before slaughter (see Table 2).
Table 2.
The effect of glyderinine on the blood levels of insulin and C-peptide in rats is normal
and against the background of adrenaline administration
Indicators of
Glyderinine
Glyderinine + adrenaline
The amount of
the administered
drug is
Insulin in
micrograms/
ml
C- peptide in
pg/ml С-
Insulin in
micrograms/ml
C- peptide in pg/ml
Control (without
introduction)
11,85 + 1,92
0,44 + 0,14
9,38 + 1,23
0,233 + 0,134
once
17,06 + 1,38*
0,90 + 0,29*
16,88 + 2,29
0,650 + 0,109*
International Journal of Medical Sciences And Clinical Research
104
https://theusajournals.com/index.php/ijmscr
International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
three times
19,40 + 1,14*
1,13 + 0,37*
17,76 + 1,81
0,783 + 0,107*
Sevenfold
20,88 + 2 ,86*
1,23 + 0,45*
21,15 + 1.82
1,133 + 0,349*
Currently, the simultaneous determination of C-
peptide serves as a yardstick.
* Confidence - p<0.05-0.01.
Currently, the simultaneous determination of C-
peptide serves as a measure of the level of insulin
secretion and liver extraction. This attitude has
developed in view of the significant and highly variable
extraction of insulin by the liver. Since it is known that
C-
peptide and insulin are secreted by β
-cells at an
equimolar concentration and that C-peptide is not
extracted by the liver in significant quantities, the
determination of C-peptide in peripheral blood has
become widely used to assess the endogenous
secretory activity of β
-cells.
In our experience, the administration of glyderinine
contributed to a significant increase in the level of
insulin in the blood, the rise of which depended on the
amount of the drug administered. A similar trend took
place with respect to the quantitative change of the C-
peptide, only with a difference exceeding the control
values by more than two times (see Table 2). A marked
increase in the level of C-peptide compared with insulin
is convincing evidence of stimulation of insulin
secretion under the influence of glyderinine. The
discrepancy between the quantitative level of insulin
and C-peptide is obviously related to the breakdown of
insulin in the liver by the enzyme insulinase. Therefore,
the ratio of C-peptide to insulin, if taken conventionally
equal to 1 normally, increased to 2.7 with repeated
administration under the influence of the drug (see
Table 2). In the light of the results obtained, it can be
assumed that insulin is a possible mediator in the
implementation of the metabolic effect of glyderinine
at the intracellular level. It is well known from the
literature that epinephrine is an antagonist of insulin in
the regulation of glucose transport and glycogen
synthesis. When adrenaline was administered to
animals in amounts that created physiological stress,
hyperglycemia was accompanied by a decrease in
glucose utilization and insulin secretion (3). In our
experiments, after the introduction of adrenaline,
there was indeed a decrease in the level of insulin in
the blood, but it was statistically unreliable. Therefore,
the decreases in insulin and C-peptide detected only
with the introduction of epinephrine can be considered
as a downward trend. While epinephrine administered
while receiving glyderinine could not cause any
detectable change. On the contrary, both the amounts
of insulin and C-peptide in this series of experiments, as
well as the previous series with only one glyderinin,
increased 2-3 times compared with the control.
Comparing the indicators shown in the tables, it is easy
to see that the adrenaline effect on insulin secretion
does not manifest itself when administered
concomitantly with glyderinine.
CONCLUSION
Consequently, the glycemic changes we found caused
by the studied drug are due to the stimulation of
endogenous insulin secretion.
Since the animals received glyderinine previously in
vivo, the experimental data can be interpreted as a
result of the insulin-like effect of the drug.
REFERENCES
Czech m.p Аmer. I. mеd.
- 1981, V. 70.-
№
1.- P.142-150
Siipson I., Gushman S.W., Annu. Rеv. Вiochem.
-1986,
V.55.-P.1059-1089.
Абдуллаев А.Х. Теs.qoun./ 4
-
Всесоюз. совещание
патафизиол.
-
М., 1989.
-
Т 3.
- C.1014
