ENDOCRINE DRUGS
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Administration + PK
Interactions
Insulin Lispro Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
Insulin Aspart Rapid acting and storage.
Given 15 minutes before a
Insulin Glulisine Peak: 30-90 minutes after injection meal or immediately after
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
and storage.
Regular Insulin Short acting
Given 15 minutes before a
Peak: 50-120 minutes after injection meal or 20 minutes after
Type I diabetes mellitus Hypoglycaemia starting a meal
Insulin Insulin receptor agonist
Type II diabetes mellitus Lipodystrophy
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
Neutral Protamine of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
Intermediate
Hagedorn Insulin and storage. IV infusion in DKA
acting
(AKA Isophane Insulin)
Peak: ~5 hours after administration 3 Injections/day with meals
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression
Insulin Glargine of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Subcutaneous injection
Long acting and storage.
Insulin Detemir Given before sleep
Peak: No peak
Gliclazide Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium
channels on the beta cell membrane. This results in increased beta cell depolarisation as Hypoglycaemia
Glimepiride K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels
Short acting GI disturbance
allowing Ca2+ to rush into the cell causing the release of insulin from vesicles. Oral
sulfonylurea Type II diabetes mellitus
Glipizide
Weight gain
Tolbutamide In patients that are not
overweight SUR1 agonist Hypersensitivity
Or when metformin is Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium Increased sensitivity to ADH
contraindicated channels on the beta cell membrane. This results in increased beta cell depolarisation as leading to water retention and
Long acting K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels possible hyponatraemia
Glibenclamide Oral
sulfonylurea allowing Ca2+ to rush into the cell causing the release of insulin from vesicles.
Has a slow dissociation from the SUR1 receptor so is considered long-acting and therefore
less preferable to short acting due to hypoglycaemic risk.
GI disturbance
Type II diabetes mellitus Reduces cellular ATP by acting on LKB1. This activates AMPK which in turn stimulates Metallic taste in mouth
glycogen storage in skeletal muscle, decreases hepatic glucose production, both of which
Metformin Biguanide LKB1 Oral
First line for overweight decrease blood glucose levels. It also increases tissue insulin sensitivity. Decreased vitamin B12
Hypoglycemics
patients absorption
Lactic acidosis
Type II diabetes mellitus
Hypersensitivity
Nateglinide Meglitinide Given in combination with Oral
metformin when metformin Hypoglycaemia
alone is insufficient
Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium
SUR1 agonist channels on the beta cell membrane. This results in increased beta cell depolarisation as
Type II diabetes mellitus K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels
allowing Ca2+ to rush into the cell causing the release of insulin from vesicles. Hypersensitivity
Given alone and in
Repaglinide Meglitinide Oral
combination with metformin Hypoglycaemia
when metformin alone is
insufficient GI disturbance
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Administration + PK
Interactions
Insulin Lispro Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
Insulin Aspart Rapid acting and storage.
Given 15 minutes before a
Insulin Glulisine Peak: 30-90 minutes after injection meal or immediately after
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
and storage.
Regular Insulin Short acting
Given 15 minutes before a
Peak: 50-120 minutes after injection meal or 20 minutes after
Type I diabetes mellitus Hypoglycaemia starting a meal
Insulin Insulin receptor agonist
Type II diabetes mellitus Lipodystrophy
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression Subcutaneous injection
Neutral Protamine of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Insulin pump
Intermediate
Hagedorn Insulin and storage. IV infusion in DKA
acting
(AKA Isophane Insulin)
Peak: ~5 hours after administration 3 Injections/day with meals
Binds to insulin receptors, activating tyrosine kinase which leads to an increased expression
Insulin Glargine of GLUT4 channels on the cell membrane allowing glucose to enter the cell for energy use Subcutaneous injection
Long acting and storage.
Insulin Detemir Given before sleep
Peak: No peak
Gliclazide Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium
channels on the beta cell membrane. This results in increased beta cell depolarisation as Hypoglycaemia
Glimepiride K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels
Short acting GI disturbance
allowing Ca2+ to rush into the cell causing the release of insulin from vesicles. Oral
sulfonylurea Type II diabetes mellitus
Glipizide
Weight gain
Tolbutamide In patients that are not
overweight SUR1 agonist Hypersensitivity
Or when metformin is Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium Increased sensitivity to ADH
contraindicated channels on the beta cell membrane. This results in increased beta cell depolarisation as leading to water retention and
Long acting K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels possible hyponatraemia
Glibenclamide Oral
sulfonylurea allowing Ca2+ to rush into the cell causing the release of insulin from vesicles.
Has a slow dissociation from the SUR1 receptor so is considered long-acting and therefore
less preferable to short acting due to hypoglycaemic risk.
GI disturbance
Type II diabetes mellitus Reduces cellular ATP by acting on LKB1. This activates AMPK which in turn stimulates Metallic taste in mouth
glycogen storage in skeletal muscle, decreases hepatic glucose production, both of which
Metformin Biguanide LKB1 Oral
First line for overweight decrease blood glucose levels. It also increases tissue insulin sensitivity. Decreased vitamin B12
Hypoglycemics
patients absorption
Lactic acidosis
Type II diabetes mellitus
Hypersensitivity
Nateglinide Meglitinide Given in combination with Oral
metformin when metformin Hypoglycaemia
alone is insufficient
Binds to and agonises the SUR1 receptor on beta cells which closes ATP-gated potassium
SUR1 agonist channels on the beta cell membrane. This results in increased beta cell depolarisation as
Type II diabetes mellitus K+ can no longer leave the cell leading to the activation of voltage-gated Ca2+ channels
allowing Ca2+ to rush into the cell causing the release of insulin from vesicles. Hypersensitivity
Given alone and in
Repaglinide Meglitinide Oral
combination with metformin Hypoglycaemia
when metformin alone is
insufficient GI disturbance
