20
portion of blood glucose enters liver and skeletal muscle cells and here monosaccharaides are converted into polysaccharide glycogen. Therefore, insulin stimulates
glycogen production (glycogenesis) and also stimulates its decomposition to glucose
and ultimately its release into the bloodstream. Insulin deficiency leads to diabetes
mellitus, especially type I (juvenile diabetes). In type II diabetes, the pancreas yields
enough insulin, but the target areas of body do not respond to it [1].
Insulin is the hormone that produces actions directly or indirectly on most parts
of the body, except for the brain. Significant function of insulin is to stimulate many
tissues, especially the liver, fat, and muscles to absorb glucose. Uptake of glucose
by cells reduces glucose in blood and enhances the availability of glucose for cellular responses where glucose is involved. Therefore, glucose uptake can exacerbate
glucose oxidation, and glycogen and fat synthesis. Insulin does not alter the brain’s
absorption of glucose and does not have any effect on active transport of glucose in
the gastrointestinal epithelial cells and renal tubules. As mentioned above, insulin
triggers glycogenesis. Furthermore, it also escalates the enzymatic activity that catalyzes the rate-limiting step in glycogenesis. It also augments the level of triglycerides by inhibiting the breakdown of triglycerides and by stimulating the production
of triglycerides by synthesis of fatty acids and glycerophosphates. Insulin can also
enhance the net synthesis of proteins, thereby stimulating the active membrane
transport of amino acids, especially into muscles. It also affects other hepatic
enzymes, but the exact mechanism by which insulin induces these modifications is
not well comprehended [3].
Glucagon
These alpha cells of islets of Langerhans secrete glucagon. Glucagon has the following functions:
• It increases the glucose synthesis from the liver by pyruvate, lactate, glycerol,
and amino acids by gluconeogenesis, hence glucose level in the plasma is also
increased.
• It rises the decomposition of triglycerides in adipose tissues, and ultimately there
is increased level of glycerol and fatty acids in the plasma.
• Like beta cells, glucagon secreting alpha cells react to glucose level fluctuations
in the hepatic blood without the involvement of other nerves or hormones.
Glucagon acts in an antagonistic manner to insulin:
1. Glucagon raises plasma glucose in contrary to insulin which increases its uptake
and hence lowers glucose level in the plasma.
2. Glucagon raises the concentrations of fatty acid, while insulin transforms fatty
acids and glycerol to triglycerides, hence inhibits the triglycerides’
decomposition.
The pancreatic alpha and beta cells constitute a push-pull system for controlling
plasma glucose level [4]. A brief summary of different endocrine hormones, their
function, and the diseases related to these hormones is mentioned in Table 1.2 [1,
28, 32–35].
A. Ahsan et al.
portion of blood glucose enters liver and skeletal muscle cells and here monosaccharaides are converted into polysaccharide glycogen. Therefore, insulin stimulates
glycogen production (glycogenesis) and also stimulates its decomposition to glucose
and ultimately its release into the bloodstream. Insulin deficiency leads to diabetes
mellitus, especially type I (juvenile diabetes). In type II diabetes, the pancreas yields
enough insulin, but the target areas of body do not respond to it [1].
Insulin is the hormone that produces actions directly or indirectly on most parts
of the body, except for the brain. Significant function of insulin is to stimulate many
tissues, especially the liver, fat, and muscles to absorb glucose. Uptake of glucose
by cells reduces glucose in blood and enhances the availability of glucose for cellular responses where glucose is involved. Therefore, glucose uptake can exacerbate
glucose oxidation, and glycogen and fat synthesis. Insulin does not alter the brain’s
absorption of glucose and does not have any effect on active transport of glucose in
the gastrointestinal epithelial cells and renal tubules. As mentioned above, insulin
triggers glycogenesis. Furthermore, it also escalates the enzymatic activity that catalyzes the rate-limiting step in glycogenesis. It also augments the level of triglycerides by inhibiting the breakdown of triglycerides and by stimulating the production
of triglycerides by synthesis of fatty acids and glycerophosphates. Insulin can also
enhance the net synthesis of proteins, thereby stimulating the active membrane
transport of amino acids, especially into muscles. It also affects other hepatic
enzymes, but the exact mechanism by which insulin induces these modifications is
not well comprehended [3].
Glucagon
These alpha cells of islets of Langerhans secrete glucagon. Glucagon has the following functions:
• It increases the glucose synthesis from the liver by pyruvate, lactate, glycerol,
and amino acids by gluconeogenesis, hence glucose level in the plasma is also
increased.
• It rises the decomposition of triglycerides in adipose tissues, and ultimately there
is increased level of glycerol and fatty acids in the plasma.
• Like beta cells, glucagon secreting alpha cells react to glucose level fluctuations
in the hepatic blood without the involvement of other nerves or hormones.
Glucagon acts in an antagonistic manner to insulin:
1. Glucagon raises plasma glucose in contrary to insulin which increases its uptake
and hence lowers glucose level in the plasma.
2. Glucagon raises the concentrations of fatty acid, while insulin transforms fatty
acids and glycerol to triglycerides, hence inhibits the triglycerides’
decomposition.
The pancreatic alpha and beta cells constitute a push-pull system for controlling
plasma glucose level [4]. A brief summary of different endocrine hormones, their
function, and the diseases related to these hormones is mentioned in Table 1.2 [1,
28, 32–35].
A. Ahsan et al.