The Function of Insulin
The main
function of insulin is glucose homeostasis. Insulin works to lower the amount
of glucose in the blood. Insulin regulates the amount of glucose in the blood
by causing cells in the liver, skeletal muscles and adipose tissue to take up
glucose from the blood. In
most nonhepatic tissues, insulin increases glucose uptake by increasing the
number of plasma membrane glucose transporters: GLUTs. Glucose uptake in the
liver is the result of an increase in the activity of the enzymes glucokinase,
phosphofructokinase-1 (PFK-1), and pyruvate kinase (PK), the key regulatory
enzymes of glycolysis (King, 2012). The glucose that is taken from the blood is
stored as glycogen in the liver and muscles and as triglycerides in the adipose
tissue.
A small amount of
insulin is continuously secreted from the pancreas. However, as blood glucose levels increase,
this increase is detected by the glucose receptors located on the pancreatic
beta cells which results in an increase in the amount of insulin being secreted
from the pancreas. As blood glucose
levels return to normal then so does the secretion of insulin. Insulin is
typically secreted immediately after eating a meal when carbohydrate levels are
high. If glucose levels are low, the hormone glucagon is secreted which has
opposing effects of insulin.
Figure 1: The control of glucose levels via the secretions of insulin and
glucagon from the pancreas.
While glucose homeostasis is the main function of insulin, it also has plays
a role in several other processes including:
·
Stimulating lipogenesis
·
Diminishing lipolysis
·
Increasing amino acid transport into
cells
·
Modulating transcription
·
Altering the cell content of
numerous mRNAs
·
Stimulating growth
·
DNA synthesis
·
Cell replication
Insulin’s main role is to work to prevent
hyperglycemia. Hyperglycemia is the
medical term for high blood sugar.
Hyperglycemia affects people who have diabetes which can develop from a
resistance to insulin or by the total lack of insulin secretion by the beta
cells of the pancreas.
Type 2 Diabetes, also
known as non-insulin dependent diabetes, is caused by the resistance of cells
to the effects of insulin. Insulin can attach normally to receptors on liver
and muscle cells but certain mechanisms prevent insulin from moving glucose into
these cells where it can be used. Enough insulin is usually produced to
overcome this resistance but eventually the pancreas will not be able produce
enough to overcome the resistance. The resulting very high levels of blood
glucose then beings to damage the beta cells of the pancreas and insulin
secretion is halted completely (PHAC, 2010). While research is still ongoing, insulin
resistance is thought to be due to the inheritance of a number of mutations in
a variety of genes. Mutational analysis of the insulin signalling cascade has
identified a glycine-arginine (Gly-Arg) substitution at codon 972 of the
insulin receptor substrate-1 (IRS-1) gene associated with insulin resistance in
obese individuals (Pedersen, 1990).
Insulin injections are used to treat individuals
with type 1 diabetes to aid in lowering blood glucose levels. Since individuals
with type 2 diabetes have a resistance to insulin, treatment involves a change
in diet that is low in glucose/carbohydrates.
*References can be accessed through links on pictures and citations.*
*References can be accessed through links on pictures and citations.*
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.