Endocrine Anatomy and Physiology

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 07/03/2015

Print this page

This article have been viewed 2293 times

Chapter 31

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.

FIGURE 31-1 Location of endocrine glands with the hormones they produce, target cells or organs, and hormonal actions.

Pancreas

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.

FIGURE 31-2 Macroscopic and microscopic structures of the pancreas and the islets of Langerhans.

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).

Box 31-1 Terms Used for Insulin and Glucose Imbalance

• Anabolism—constructive phase of metabolism in which the body converts simple substances into more complex compounds in the presence of energy

• Catabolism—destructive phase of metabolism in which the body breaks down complex substances to form simpler substances in the presence of energy

• Gluconeogenesis—formation of glucose from noncarbohydrate nutrients (e.g., fats, protein), which occurs in the liver

• Glycogen—storage form of glucose in liver and muscles

• Glycogenesis—formation of glycogen from glucose and adenosine triphosphate after a meal when both are plentiful

• Glycogenolysis—conversion of glycogen stored in the liver and muscles into usable glucose

• Osmolality—measurement of the number of particles in a solution or the concentration of a solution

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

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.

Carbohydrate Anabolism.

Glucose is admitted to the skeletal, cardiac, and adipose cells for use as energy in the presence of effective insulin facilitated by the glucose transporter 4 (GLUT4), as described below. The movement of glucose from the circulation into the intracellular compartment reduces the concentration of glucose in the bloodstream and helps preserve the blood’s osmolality. Simultaneously, glucose is available to the cell as its main energy source. Excess glucose in the form of glycogen is stored in the hepatic and muscle cells for use as fuel at a later time. In skeletal muscle, 90% of the glucose in the cell is converted to glycogen for longer-term storage.¹ Liver glycogen contributes up to 10% of total liver weight when fully replete.¹

Fat Anabolism.

Adequate, effective insulin levels affect fat metabolism. Dyslipidemias are strongly associated with type 2 diabetes. Type 2 diabetes is characterized by overproduction of large, triglyceride-rich, very-low-density lipoproteins (VLDLs).² Disorders of carbohydrate and fat metabolism are also associated with metabolic syndrome, a precursor to diabetes and cardiovascular disease.³

Protein Conservation.

Insulin and the GLUTs (see below) together facilitate the transfer of glucose across the cell wall. By having glucose (carbohydrate) available as the body’s fuel source, protein is spared from use as energy. Protein is then available for critical protein synthesis and for amino acid transport into the cells. Protein metabolism also benefits from an adequate insulin supply. Only in acute hyperglycemia of diabetic ketoacidosis (DKA) or in starvation states does the body use protein for energy sources.

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

Box 31-2 Effects of the Insulin-to-Glucagon Ratio on Carbohydrate, Fat, and Protein Metabolism

BALANCED INSULIN AND GLUCAGON	DECREASED INSULIN AND INCREASED GLUCAGON
↑ Use of glucose by cells	↓ Use of glucose by cells
↑Movement of potassium intracellularly	↓ Movement of potassium intracellularly
↑ Carbohydrate metabolism	↑ Blood glucose
↓ Gluconeogenesis	↑ Gluconeogenesis
↑ Glycogen storage	↓ Glycogen storage
↓ Glycogenolysis	↑ Glycogenolysis
↓ Lipolysis	↑ Lipolysis
↓ Fat mobilization	↑ Fat mobilization
↑ Fat storage	↓ Fat stores
↓ Protein mobilization	↑ Hepatic metabolism fats
↑ Protein synthesis	↑ Ketogenesis
	↑ Mobilization of protein
	↑ Proteolysis
	↑ Lipoprotein

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.

Pancreatic Polypeptide

The role of pancreatic polypeptide, synthesized by the PP cells within the islets of Langerhans, is not completely understood. Pancreatic polypeptide release can be stimulated by acute hypoglycemia or by an intake that is high in protein and low in carbohydrate. The effect of hypersecretion or hyposecretion of this hormone has not been identified. The hormone represses pancreatic enzyme secretion and relaxes the smooth muscle tissue of the gallbladder.

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