Insulin
Insulin has an effect on your metabolism. Insulin is important for metabolism when fasting
and feeding.
Fasting: insulin levels are low (beta-cells secrete less insulin)
- Lipids are mobilized from adipose tissue.
- Amino acids are mobilized from body protein stores within muscle and other tissues.
Lipids and amino acids provide fuel for oxidation and serve as precursors for hepatic
ketogenesis and gluconeogenesis.
Feeding: insulin levels increase (beta-cells secrete more insulin)
- Inhibits mobilization of lipids and amino acids. (Inhibits release)
- Stimulate carbohydrate, lipid, and amino acid uptake by specific insulin-sensitive
target tissues. (Stimulate uptake)
Insulin maintains the concentration of glucose in the
plasma within narrow limits. Between 4-6 mmol/L.
- Below this is hypoglycemia.
- Above this is hyperglycemia.
Beta-cell synthesize and secrete insulin:
Insulin is only made by beta-cells of the islets of Langerhans.
- When the islets are exposed to glucose insulin secretion is stimulated.
- Transcription of the mRNA will encode for preproinsulin, which has
3 domains A, B, and C.
- This is cleaved in the rough endoplasmic reticulum to proinsulin
(still A, B, and C).
- In the Golgi it will be cleaved into insulin (A and B) and C peptide.
C peptide is secreted with insulin in a 1:1 ratio meaning that it can be used
as a useful marker for insulin secretion (type I diabetes also have a low C
peptide concentration).
Insulin is degraded by insulinase mainly in the liver.
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,Insulin effect:
There are two distinct phases of insulin secretion.
- The acute-phase (first phase) is a response that lasts only about 2 to 5 minutes, this is
insulin that has already been packaged in secretory vesicles in the cytosol.
- The late-phase (second phase) also preformed insulin with the contribution of newly
formed insulin. Lasts as long as the blood glucose level remains elevated.
Steps of insulin secretion:
1. Glucose enters the beta cell through the
GLUT2 glucose transporter by
facilitated diffusion.
2. The entering glucose will undergo
glycolysis with the help of glucokinase.
This raises the ATP by phosphorylating
ADP. (NADH/NAD+ ratio also
increases).
3. Because of this increase will cause the
K+ channels to close.
4. The beta-cells will depolarize (become
more less negative)
5. Depolarization activates the Ca2+
channels.
6. This causes an increase influx of Ca2+
and will trigger an even more increase of
Ca2+.
7. This will ultimately lead to insulin
release.
Neural and humoral factors on insulin secretion:
Sympathetic neurons of the pancreas release norepinephrine
which stimulates α-adrenergic more than β-adrenergic (α inhibits
insulin and β stimulates insulin). And though the celiac nerves it
inhibits insulin. Sympathetic inhibits.
Parasympathetic neurons stimulate through the vagus nerve
(which releases acetylcholine) causing an increase in insulin.
Parasympathetic stimulates.
When glucose is given through infusion, insulin levels increase
much less than when it is given oral. This is because of incretins,
incretins stimulate a greater response of insulin. The most important incretins are
cholecystokinin (CCK), glucagon-like intestinal peptide 1 (GLP-1), and gastric
inhibitory polypeptide (GIP). GLP-1 is made in the L-cells of the epithelial of the
intestines. GIP is made in the α-cells of the pancreas.
This can only stimulate insulin secretion when it is given oral because in the blood there is
DPP-4 present, and DPP-4 degrades incretins.
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, Effect on carbohydrate metabolism (glucose):
Muscle tissue cannot take up glucose without the presents of insulin. Meaning that it depends
much of the day on fatty acids for its energy. Under two conditions the muscles do use large
amounts of insulin. One of these is during moderate or heavy exercise, this does not need
much insulin because the contraction of muscle increases translocation of the GLUT4,
causing glucose to enter the cell.
The second condition for usage of large amounts of glucose by muscle is during the few
hours after a meal. Extra insulin causes rapid transport of glucose into the muscle cells.
Instead of being used for energy most of the glucose is stored in the form of muscle glycogen.
Insulin has four major effects on muscle:
1. Insulin stimulates the translocation of GLUT4 so glucose can come in the cell.
2. Insulin enhances the conversion of glucose to glycogen by activating hexokinase and
glycogen synthase.
3. Insulin increases the breakdown of glucose and oxidation.
4. Insulin also stimulates the synthesis of protein in skeletal muscle and slows the
degradation of existing proteins.
One of the most important effects of insulin is to cause most of the glucose absorbed after a
meal to be rapidly stored in the liver in the form of glycogen.
Effect on proteins (amino acids):
- Insulin stimulates transport of many of the amino acids into the cells.
- Insulin increases translation of mRNA.
- Insulin inhibits catabolism of proteins.
- In the liver insulin depresses the rate of gluconeogenesis by decreasing activity of
enzymes that promote gluconeogenesis.
Effect on fat (lipids):
Insulin has several effects that lead to fat storage.
- Insulin increases glucose utilization by most of the body’s tissues, which
automatically decreases fat utilization. But is also increase fatty acid synthesis, occurs
mostly in the liver and will be transported.
- Insulin inhibits lipase. Lipase is an enzyme that cause hydrolysis of triglycerides.
Meaning that fatty acids are not released into the bloodstream.
With the absence of insulin fat will be increase as usage for energy. The excess of fatty acids
in the plasma associated with insulin deficiency also promotes liver conversion of some of
the fatty acids into phospholipids and cholesterol, two of the major products of fat
metabolism.
The excess of usage of fats during insulin deficiency causes ketosis and acidosis. Insulin
deficiency causes large amounts of acetoacetic acid to be formed in the liver cells. Some of
the acetoacetic acid is converted into β-hydroxybutyric acid and acetone. These two
substances along with the acetoacetic acid are called ketone bodies and their presence in
large amounts in the body fluid is called ketosis.
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