CoverModule 1.0. Homeostasis, Membranes, Electrophysiology and ANS1.1. Homeostasis1.1.1. Homeostasis Defined1.1.2. Homeostatic Control Systems1.1.3. Feedback Response Loop1.2. Cell Transport; Water & Solutes1.2.1. Fluid Compartments1.2.2. Osmosis1.2.3. Diffusion of Solutes1.2.4. Active Transport1.2.5. Bulk Transport1.3. Electrophysiology1.3.1. Ions and Cell Membranes1.3.2. Membrane Potentials1.3.3. Graded Potential1.3.4. Action Potentials1.3.5. Refractory Periods1.3.6. Propagation of an Action Potential1.4. The Synapse1.5. The Autonomic Nervous System1.5.1. Organization of the Nervous System1.5.2. Structural Organization of the ANS1.5.3. The SNS and the PNS1.5.4. The Enteric Nervous System1.5.5. Physiology of the ANS1.5.6. Neurotransmitters of the ANS1.5.7. Receptors of the ANS1.5.8. Actions of the Autonomic Nervous System1.5.9. Table of Actions for the SNS and PNS and Some Common DrugsModule 2.0. Skeletal Muscle and Special Senses2.1. Structural Organization of Skeletal Muscle2.2.1. Neuromuscular Junction, Excitation-Contraction Coupling2.2.2. Muscle Contractures and Cramps2.3. Whole Muscle Contraction, Fiber Type, Fatigue and Muscle Pharmacology2.3.1. Motor Units2.3.2. Factors that Influence the Force of Contraction2.3.2. Factors that Influence the Force of Muscle Contraction2.3.3. Energy Source for Muscle Contraction2.3.4. Skeletal Muscle Fiber Types2.3.5. Fatigue2.3.6. Muscle Pharmacology2.4. Smooth Muscle2.4.1. Smooth Muscle Contraction2.5. Control of Body Movement2.5.1. Voluntary Control of Muscle2.5.2. Reflexes2.6. Taste and Smell2.6.1. Taste2.6.2. The Sense of Smell2.7. Vision2.7.1. Structure of the Eye2.7.2. Focusing Light on the Retina2.7.3. Converting Light to Action Potentials2.7.4. The Retina2.7.5. Phototransduction2.7.6. Receptive Fields2.8. Hearing and Equilibrium2.8.1. The Nature of Sound2.8.2. The Hearing Apparatus2.8.3. Sound Vibrations to Action Potentials2.8.4. The Sense of Balance and EquilibriumModule 3.0. Cardiovascular System3.1. Structure of the Heart3.1.1. Chambers and Circulation3.2. Cardiac Cell Action Potentials3.2.1. Action Potentials in Cardiac Muscle Cells3.2.2. Action Potentials in Cardiac Autorhythmic cells3.2.3. Cellular Mechanisms of Inotropy and Chronotropy3.3. Electrophysiology of Heart Muscle3.3.1. Heart Conduction System3.3.2. Electrocardiogram (ECG)3.3.3. Abnormal ECG - Current of Injury3.4. The Cardiac Cycle3.4.1. Cardiac cycle3.4.2. Cardiac Measurements and Pressure Volume Loops3.5. Blood vessels and Blood Pressure3.5.1. Arteries and Veins3.5.2. Capillaries3.5.3. Blood Pressure Regulation and Shock3.5.4. Capillary Exchange3.5.5. Myogenic and Paracrine Regulation of Vasoconstriction and Vasodilation3.6. Blood3.6.1. Composition of Blood3.6.2. Hematopoeisis3.6.3. Breaking Down Red Blood Cells3.6.4. HemostasisModule 4.0. Urinary and Respiratory Systems4.1. Function and Structure of the Kidney4.1.1. Urinary System Function4.1.2. Functional Anatomy of the Urinary System4.1.3. The Nephron: Functional Unit of the Kidney4.1.4. The Renal Corpuscle: Bowman's Capsule4.2. Physiology of Urine Production4.2.1. Filtration4.2.2. Renal Clearance4.2.3. Tubular Reabsorption4.2.4. Urine Concentration and Dilution4.2.5. Hormonal Regulation of Urine Production4.3. Acid/Base Balance4.3.1. Buffers4.3.2. Acid/Base Disturbances4.4. The Respiratory System4.4.1. Respiratory System Structure and Function4.4.2. Respiratory Membrane4.4.3. Respiratory pressures and Inspriation/Expiration4.4.4. Alveoli and Surfactant4.4.5. Pneumothorax4.4.6. Pressure-Volume Loops and the Work of Breathing4.5. Gas Exchange and Transport4.5.1. Gas Laws4.5.2. Partial Pressure Gradients in the Lung4.5.3. Alveolar Gas Equation4.5.4. Oxygen and Carbon Dioxide Transport in the Blood4.5.5. Alveolar Ventilation4.5.6. Ventilation/Perfusion Ratio4.6. Chronic Bronchitis and Emphysema4.6.1. Respiratory Control by the Medulla Oblongata4.6.2. Chemicals that Regulate VentilationModule 5.0. Digestive, Endocrine and Reproductive Systems5.1. Functional Anatomy of the Digestive System5.1.1. Layers of the Digestive Tract5.1.2. Enteric Nervous System5.1.3. Organs of the Digestive System5.2. Digestion5.2.1. Carbohydrates5.2.2. Proteins5.2.3. Lipids5.2.4. Lipoproteins5.3. Regulation of Digestive Secretions5.4. Endocrine System5.4.1. Overview of the Endocrine System5.4.2. Hormone Receptors5.4.3. Hormones of the Body5.4.4. Other Hormones: Melatonin and Pheromones5.5. The Hypothalamus and Pituitary Gland5.5.1. Structure and Function of the Hypothalamus and Pituitary Gland5.5.2. The Posterior Pituitary5.5.3. The Anterior Pituitary5.5.4. Growth Hormone5.5.5. Prolactin5.5.6. Thyroid Hormones5.5.7. Adrenal Hormones5.6. Pancreas5.6.1. Insulin and Glucagon5.6.2. Diabetes Mellitus5.7. Reproductive System Anatomy5.7.1. Female Reproductive Anatomy5.7.2. Male Reproductive Anatomy5.7.3. Sexual Development at Puberty5.7.4. Male Reproductive Endocrine Axis5.7.5. Spermatogenesis5.7.6. Female Reproductive System: Oogenesis5.7.7. Ovulation and Fertilization5.7.8. The Ovarian Cycle5.7.9. The Uterine Cycle5.7.10. PregnancyAppendix A. GenderAppendix B. The Placebo EffectB.2.1. The Placebo EffectB.2.2. Examples of the Placebo EffectB.2.3. How do Placebos Work?B.2.4. Are Placebos Ethical?B.2.5. How do we validate actual effectiveness of placebosB.2.6. Tips for evaluating scientific evidenceB.2.7. What about Faith Healingstest chapter

Insulin and Glucagon

Skeletal Muscle 

Since glucose is a polar molecule, it cannot easily cross the plasma membrane and requires special transport proteins called GLUT transporters to enter the cell. There are several different GLUT transporters. We differentiate the different ones by giving them numbers, GLUT-1, GLUT-2, GLUT-3, etc. To date, only one of the GLUT transporters has been shown to require insulin for its action. That transporter is GLUT-4 and that is the one found in skeletal muscle. Therefore, in the absence of insulin skeletal muscle cells cannot import glucose into the cell. The truth is that without insulin the skeletal muscle cells do not even have the transporters in their plasma membrane. They are found in the membranes of vesicles inside the cell. When insulin binds to its receptor a signal is sent to the vesicles initiating the process of exocytosis. In this process the membrane of the vesicles containing GLUT-4 transporters fuses with the plasma membrane, incorporating the vesicular membrane into the plasma membrane. The GLUT-4 transporters that were in the vesicular membrane are now part of the plasma membrane and allow glucose to enter the muscle cell. See image below.

Insertion of GLUT-4 transporters into the plasma membrane of a muscle cell. (A) GLUT transporters shown in the membrane of a secretory vesicle. (B) Vesicle move to the plasma membrane. (C) Vescicular membrane has fused with the plasma membrane, inserting the transporters. 
Image created by BYU-Idaho 2012

Once the glucose gets into the cell, insulin promotes the conversion of glucose into glycogen (glycogenesis). Recall that glycogen is a large storage polymer made of glucose subunits.  In addition, insulin promotes the utilization of glucose for energy by stimulating glycolysis and the oxidation of glucose.

Amino acids in the blood also stimulate insulin secretion. This is because insulin promotes the uptake of amino acids into skeletal muscle cells where they are used to synthesize new proteins.

Due to these actions we say that insulin promotes anabolic reactions. These reactions result in the storage of energy sources in the form of glycogen and proteins. We will see similar actions in both adipose tissue and the liver.

Adipose Tissue (Fat Cells) 

The action of insulin in adipose tissues is similar to the action in skeletal muscle. Fat cells utilize GLUT-4 transporters to import glucose, therefore, insulin increases glucose uptake by these cells.  Adipose cells store some energy in the form of glycogen, but most of the glucose that enters the cell is used to make fatty acids that can then be converted to fat (triglycerides) and stored for future energy needs. Insulin also promotes free fatty acid uptake from the blood which enhances triglyceride formation. Additionally, insulin decreases the activity of the enzyme called hormone-sensitive triglyceride lipase. This enzyme converts triglycerides back to free fatty acids.


Liver cells are a bit different from muscle and fat cells. The glucose transporters in liver cells are GLUT-2 transporters that are always present in the membranes and do not require insulin. Nevertheless, insulin has a big impact on liver function. When glucose is plentiful, insulin promotes energy storage and activates the enzymes that convert glucose to glycogen. In addition, insulin inhibits the breakdown of glycogen. The liver plays an important role in regulating blood glucose levels, forming glycogen when glucose is plentiful and then converting glycogen back to glucose (glycogenolysis) when glucose levels in the blood decrease. Its like food storage, we store food in the good times and then use it in the bad. In the case of our bodies the good times are right after we eat and the bad times are several hours later. This mechanism maintains fairly constant and continuous supplies of glucose for our cells.

Another function of insulin in the liver is to inhibit gluconeogenesis, which is, the conversion of amino acids to glucose.

Thus, the overall action of insulin is to promote the uptake of glucose by the cells, the result of which lowers the levels of glucose in the blood. Also, it stimulates the storage of energy in the cells when nutrients are plentiful. Those storage molecules can later be broken down and released back into the blood to maintain a constant supply of energy to the cells. If it weren’t for this system we would have to eat continually in order to maintain sufficient levels of glucose in our blood. The actions of insulin on the cells of the body are summarized in the table below.

Target Tissue Actions
Skeletal Muscle Increased number of GLUT-4 transporters in plasma membrane (increased glucose uptake) Increased glycogen synthesis (glycogenesis) Increase glycolysis and carbohydrate oxidation Increased amino acid uptake and protein synthesis
Adipose Tissue Increased number of GLUT-4 transporters in plasma membrane (increased glucose uptake) Increased conversion of glucose to fatty acids Increased free fatty acid uptake from the blood Increased triglyceride (fat) formation
Liver Increased glycogen synthesis (glycogenesis) Inhibition of glycogen breakdown (glycogenolysis) Inhibition of gluconeogenesis
Insulin attaches to insulin receptors on skeletal muscle and bone and stimulates the movement of GLUT-4 channels to the membrane to let glucose in. (BG= Blood Glucose)
Image created by BYU-Idaho student Jenna Fransen, Spring 2017
As blood glucose increases, this increases metabolism which increases ATP which attaches to and closes K+ channels which depolarize the cell and cause the release of insulin. 
Image created by J. Shaw at BYU-Idaho Spring 2015

Regulation of Insulin

  1. Plasma glucose: The primary stimulus of insulin secretion is elevated plasma glucose levels. If the plasma glucose concentrations increase above 100mg/dL glucose uptake through the GLUT2 transporter in the beta cells is increased. Note: GLUT2 transporters are not dependent upon insulin like the GLUT4 transporters. Once in the beta cell the glucose is metabolized resulting in an increase in ATP production. Increased ATP interacts with ATP-sensitive K+ channels which causes them to close, resulting in depolarization of the cell membrane. The depolarization results in the opening of voltage-gated Ca2+ channels allowing Ca2+  to enter the cell. The increase in intracellular Ca2+  stimulates exocytosis of the insulin containing vesicles. When glucose levels drop below 100 mg/dL ATP levels drop, the K+ channels open and insulin secretion stops. This is a classic example of negative feedback control.
  1. Plasma amino acids: amino acids in the blood have a similar, albeit slower effect than glucose on the release of insulin by the beta cells.
  1. Gastrointestinal hormones: Prior to any increase in blood glucose or amino acids, insulin release will be increased 50% because of hormones released from cells in the intestines. The primary hormones involved are glucagon-like peptide-1 and gastric inhibitory peptide (these hormones are known collectively as incretins). Both hormones are released from cells of the small intestines in response to nutrient ingestion. This is a type of feed forward mechanism to help prevent a sudden surge in plasma glucose concentrations.
  1. Autonomic nervous system: Parasympathetic activity increases insulin release while sympathetic activity decreases insulin release. It may seem odd that sympathetic activity decreases insulin release since that would limit glucose uptake in the very tissues that need additional energy during physical exertion, namely skeletal muscle. However, as mentioned above, exercise results in incorporation of GLUT4 (independent of insulin) transporters in the active muscles allowing glucose to enter those muscles.


Glucagon, which is secreted by the alpha cells of the islets, generally opposes the actions of insulin in the liver. Glucagon stimulates the breakdown of glycogen to glucose and stimulates gluconeogenesis, both of which serve to increase the release of glucose into the blood and raise plasma glucose levels. The secretion of glucagon is stimulated by low blood sugar levels as well as increased levels of plasma amino acids. Recall that increased levels of amino acids also stimulate insulin secretion. This may seem as somewhat of a paradox. However, the simultaneous release of glucagon and insulin helps to prevent hypoglycemia (low blood glucose levels), especially with low carbohydrate diets. Thus, the ratio of glucagon to insulin plays a very important role in glucose metabolism.

Regulation of Blood Glucose Levels
Author: Open Stax. License: [CC BY 3.0 (], via Wikimedia Commons  Link:

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