Endocrine Anatomy and Physiology

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 07/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2326 times

Endocrine Anatomy and Physiology

Mary E. Lough

Maintaining dynamic equilibrium among the various cells, tissues, organs, and systems of the human body is a highly complex and specialized process. Two systems regulate these critical relationships: the nervous system and the endocrine system. The nervous system communicates by nerve impulses that control skeletal muscle, smooth muscle tissue, and cardiac muscle tissue. The endocrine system controls and communicates by distributing potent hormones throughout the body. Figure 31-1 lists the endocrine glands and their hormones, target tissues, and actions. When stimulated, the endocrine glands secrete hormones into surrounding body fluids. In the circulation, these hormones travel to specific target tissues, where they exert a pronounced effect. Receptors found on or within these specialized target tissue cells are equipped with molecules that recognize the hormone and bind it to the cell, producing a specific response.

Pancreas

Anatomy

The pancreas is a long, triangular organ. It is clinically described as consisting of a head, neck, body, and tail. The head of the organ lies in the C-shaped curvature of the duodenum, and the tail extends behind and below the stomach toward the spleen. The pancreas is approximately 15 cm (6 inches) long and 4 cm (1.5 inches) wide.

Physiology

The physiology of glucose metabolism has traditionally focused exclusively on the pancreas. With increases in knowledge, glucose metabolism physiology has expanded to include cellular glucose transport (GLUT) proteins and also incretin proteins from the GI system.

In the pancreas, clusters of cells that appear to form tiny islands among the exocrine cells accomplish the pancreatic endocrine functions. These clusters are known as the islets of Langerhans and are composed of four distinct cell types: alpha, beta, delta, and PP. The locations of the cells that produce these hormones are shown in Figure 31-2. Alpha cells secrete glucagon, beta cells secrete insulin, delta cells secrete somatostatin, and PP cells secrete pancreatic polypeptide hormone. Glucagon, insulin, somatostatin, and polypeptide hormones are released into the surrounding capillaries to empty into the portal vein, where they are distributed to target cells in the liver. The hormones then travel into general circulation to reach other target cells.

Insulin

Insulin is a potent anabolic hormone produced by the beta cells of the pancreas. Elevated levels of blood glucose stimulate insulin production. Insulin is the only hormone produced in the body that directly lowers blood glucose levels. Insulin is responsible for the storage of carbohydrate, protein, and fat nutrients. Insulin also augments the transport of potassium into the cells, decreases the mobilization of fats, and stimulates protein synthesis (Table 31-1). Box 31-1 defines the terms commonly used when discussing glucose and insulin balance. The major stimulant for insulin secretion is an elevation of serum glucose. The greater the rise in blood glucose, the more insulin the normal pancreas produces. Other hormones inhibit the release of insulin (Table 31-2).

TABLE 31-1

PANCREATIC ENDOCRINE CELLS, HORMONES, STIMULANT RELEASE FACTOR, TARGET TISSUE, AND RESPONSE OR ACTION

CELL HORMONE STIMULANT RELEASE FACTOR TARGET TISSUE RESPONSE OR ACTION
Alpha Glucagon ↓ Glucose Hepatocyte ↑ Glucose in bloodstream
    Exercise Myocyte ↑ Gluconeogenesis
    ↑ Amino acids   ↑ Glycogenolysis
    SNS stimulation   ↑ Fat mobilization
        ↑ Protein mobilization
Beta Insulin Glucose Skeletal cells ↓ Blood glucose
      Muscle cells ↓ Fat mobilization
      Cardiac cells ↑ Fat storage
        ↓ Protein mobilization
        ↑ Protein synthesis
        ↑ Glucogenesis
Delta Somatostatin Hyperglycemia Alpha cells ↓ Blood glucose
      Beta cells ↓ Glycogen secretion
        ↓ Insulin secretion
PP Pancreatic polypeptide Acute hypoglycemia Gallbladder ↑ Gallbladder contraction
      Smooth muscle ↓ Pancreatic enzyme

image

SNS, Sympathetic nervous system; ↑, increases; ↓, decreases.

TABLE 31-2

AGENTS THAT PROMOTE OR INHIBIT INSULIN RELEASE

INSULIN RELEASE (MAJOR STIMULANT: HIGH BLOOD GLUCOSE) INSULIN INHIBITION (MAJOR INHIBITOR: LOW BLOOD GLUCOSE)
Hormones  
Glucagon Somatostatin
Corticotropic hormone Norepinephrine
Thyrotropin Epinephrine
Somatotropin  
Glucocorticoids  
Incretins  
Medications  
Beta-adrenergic stimulators Beta-adrenergic blocking agents
Sulfonylurea Diazoxide
Theophylline Phenytoin
Acetylcholine Thiazide or sulfonamide diuretics

Blood Glucose

Blood glucose is reported in millimoles per liter (mmol/L), which is the System International (SI) unit of measure used throughout the world. In the United States, blood glucose is measured in milligrams per deciliter (mg/dL). The normal blood glucose range is 70 to 100 mg/dL (3.9 to 5.6 mmol/L). To convert mmol/L of glucose to mg/dL, multiply the mmol/L value by 18. To convert mg/dL of glucose to mmol/L, divide the mg/dL value by 18.

In patients who have symptoms of diabetes, pancreatic beta cell destruction has already occurred. In type 1 diabetes, all of the beta cells are nonfunctional. In type 2 diabetes, about 50% of the beta cells are destroyed by the time the patient exhibits signs and symptoms of diabetes. The destruction of the beta cells disrupts homeostatic ability to regulate blood glucose.

Glucagon

Glucagon, synthesized by alpha cells in the pancreas, has the opposite effect of insulin. Glucagon is released during hypoglycemia to induce hepatic glucose output. Because glucagon counter-regulates insulin levels and raises blood glucose levels, it is a potent gluconeogenic hormone. By means of gluconeogenesis, glucagon can form glucose from noncarbohydrate sources such as fat and protein when required. Glucagon release from the pancreas is stimulated by low blood glucose levels, starvation, exercise, or stimulation of the sympathetic nervous system (SNS), as listed in Box 31-2.4,5 Glucagon release protects the brain from the consequences of hypoglycemia.5

To meet short-term energy requirements, glucagon stimulates the release of glycogen stores from liver and muscle cells. Through a process called glycogenolysis, the glycogen stored in the liver is converted into a glucose form that can be used by the cells.5

For long-term energy needs, glucagon stimulates glucose release through the more complex process of gluconeogenesis. In gluconeogenesis, fat and protein nutrients are rapidly broken down into end products that are then changed into glucose.5

A normal blood glucose level is maintained in the healthy body by the insulin-to-glucagon ratio. When the blood glucose level is high, insulin is released, and glucagon is inhibited. When blood glucose levels are low, glucagon rather than insulin is released to raise the blood glucose level. The brain has a very limited supply of glucose, and glucagon release is essential to protect the brain from the effects of hypoglycemia.6

Somatostatin

Somatostatin is a hormone that is produced in the pancreatic delta cells. Somatostatin decreases glucagon secretion, and in high quantities, it decreases insulin release (see Table 31-1). Hyperglycemia stimulates the activity of the delta cells. It is theorized that the release of insulin enables somatostatin to control beta cell activity. Somatostatin may be involved in the regulation of the postprandial influx of glucose into cells.

Glucose Transporters

Human cells take up glucose by means of facultative glucose-transport proteins known by the term glucose transporter (GLUT). These proteins are specialized by tissue distribution and function as described in Table 31-3.7 At the cellular level, glucose crosses the cell plasma membrane through aqueous pores formed by GLUT transporters. At this time, 14 GLUTs have been identified.8 The GLUT number indicates the order in which the molecular sequence and GLUT tissue locations were identified.8 The functions of a few key GLUTs are described in more detail below.

TABLE 31-3

GLUCOSE TRANSPORTERS

Buy Membership for Critical Care Medicine Category to continue reading. Learn more here
GLUCOSE TRANSPORTER (GLUT) ANATOMIC LOCATIONS FUNCTION
GLUT1 Erythrocytes, endothelial cells of brain Basal glucose uptake
  Transport across blood–brain barrier  
GLUT2 Pancreatic beta bells, liver, kidney, small intestine High-capacity, low-affinity GLUT
    Can transport fructose
GLUT3 Brain cells, nerve cells