Abstract:
Diabetes mellitus is a chronic metabolic disorder which is associated with hyperglycemia. It is caused by a
derangement in the secretion or function of the endocrinal portion of the pancreas. There is a close anatomical and
functional relationship between its exocrine and endocrine portions. The current study was designed to evaluate the changes
in amylase levels in diabetic patients and study the correlation of amylase activity with chronic hyperglycemia and duration
of diabetes mellitus. The results of study were revealed that amylase activity was low in diabetic patients compared with
control and there was negative correlation between amylase activity and hyperglycemia and duration .
Keywords: Amylase Activity, Diabetes Mellitus, Endocrine1. Introduction
Diabetes mellitus is a metabolic disorder characterized
by the presence of abnormally high blood glucose levels
(hyperglycemia). It is caused by defective in insulin
secretion, defective action or both [1]. Individuals with
uncontrolled diabetes mellitus are unable to transport
glucose into fat and muscle cells and are thus said to
demonstrate glucose intolerance [2]. The classic symptoms
of diabetes are excessive urination (polyuria), thirst
(polydipsia) and (polyphagia), and weight loss [3].
Diabetes is now ranked among one of the most common
non-communicable diseases in the world. It falls within
4th–5th leading cause of death in most developed countries
[4].
The pancreas is a mixed exocrine-endocrine gland, with
the exocrine portion of the gland making up the greatest
volume (84%). Ductal cells and blood vessels make up
around 4% of the volume, while the endocrine part makes
up 2% of the volume. The other part (10%) is occupied by
an extracellular matrix. The acinar tissue in the pancreas is
in the close vicinity of the islets. Because of this close
morphological relationship, functional interactions are
likely to occur between the exocrine and endocrine
pancreas in any disease, which affect this organ [5].
Anatomically, the blood from the islets bathes the acinar
cells by way of an islet-exocrine portal system [6]. There is
also morphological evidence that indicates that the
pancreatic exocrine function may be influenced by the
pancreatic endocrine hormones. Insulin has a trophic effect
on the exocrine pancreas, especially on the peri-insular
acini. A progressive damage to the pancreatic acinar cells is
seen in insulin deficiency. The pancreatic exocrine tissue in
a diabetic patient becomes fibrosed and it shows a reduced
response to the hormonal stimulation [7,8].
Clinical investigation observations indicate close relation
between pancreatic exo- and endocrine parts. Insulin
dysfunction and glucagon activation is due to pancreatic
impairment The decreased production of exocrine secretion
also influence on insulin deficiency (Interestingly, the
relation between insulin and glucagon concentrations in
extracellular fluid and their antagonistic actions also seem
to play a key role in pancreatic exocrine function disorders.
Insulin secretion is enhancing the exocrine activity like
alpha amylase functions but glucagon inhibits it [9].
Diabetes mellitus and exocrine pancreatic dysfunction in
perk-/- mice reveals a role for translational control in
secretary cell survival [10].
In type 2 Diabetes mellitus, the continuous interstitial
matrix connection between the endocrine and the exocrine
pancreas is lost in animal models and humans, which
results in a dysfunctional insulino-acinar-ductal-incretin