Clinical Note

In the absence of adrenal function, even relatively short periods of fasting may produce a catastrophic decrease in blood sugar (hypoglycemia) accompanied by depletion of muscle and liver glycogen. A drastically compromised ability to produce sugar from nonglucose precursors

(gluconeogenesis) forces these individuals to rely almost exclusively on dietary sugars to meet their carbohydrate needs. Their metabolic problems are further complicated by decreased ability to utilize alternate substrates such as fatty acids and protein.


TABLE 1 Some Effects of Glucocorticoids


Central nervous system

Cardiovascular system

Gastrointestinal tract

Liver Lungs

Pituitary Kidney



Immune system (see text)

Connective tissue

Taste, hearing, and smell

" in acuity with adrenal cortical insufficiency and # in Cushing's disease

# Corticotropin releasing hormone (see text)

# ADH secretion

Maintain sensitivity to epinephrine and norepinephrine

" Sensitivity to vasoconstrictor agents

Maintain microcirculation

" Gastric acid secretion

# Gastric mucosal cell proliferation

" Gluconeogenesis

" Maturation and surfactant production during fetal development

# ACTH secretion and synthesis


Needed to excrete dilute urine

" Resorption

# Formation

# Fatigue (probably secondary to cardiovascular actions)

" Protein catabolism

# Glucose oxidation

# Insulin sensitivity

# Protein synthesis

# Mass of thymus and lymph nodes

# Blood concentrations of eosinophils, basophils, and lymphocytes

# Cellular immunity

# Activity of fibroblasts

# Collagen synthesis

Glucocorticoids promote gluconeogenesis by complementary mechanisms:

1. Extrahepatic actions provide substrate. Glucocorti-coids promote proteolysis and inhibit protein synthesis in muscle and lymphoid tissues, thereby causing amino acids to be released into the blood. In addition, they increase blood glycerol concentrations by acting with other hormones to increase lipolysis in adipose tissue.

^ protein degradation ^ protein synthesis ^ glucose utilization ^ sensitivity to insulin

^ protein degradation ^ protein synthesis ^ glucose utilization ^ sensitivity to insulin

glucose glycogen storage j lipolysis r y |gluconeogenesis by

{ glucose utilization (Lt^S -- glyCer0l f ^ of enzymes f.. \ y A amount of enzymes sensitivity to insulin [ --------T '

adipose tissue

FIGURE 12 Principal effects of glucocorticoids on glucose production and metabolism of body fuels. ", increased; #, decreased.

2. Hepatic actions enhance the flow of glucose precursors through existing enzymatic machinery and induce the synthesis of additional gluconeogenic and glycogen-forming enzymes along with enzymes needed to convert amino acids to usable precursors of carbohydrate.

Nitrogen excretion during fasting is lower than normal with adrenal insufficiency, reflecting decreased conversion of amino acids to glucose. High concentrations of glucocorticoids, as seen in states of adrenal hyperfunction, inhibit protein synthesis and promote rapid breakdown of muscle and lymphoid tissues that serve as repositories for stored protein. These effects result in increased blood urea nitrogen (BUN) and enhanced nitrogen excretion.

Glucocorticoids defend against hypoglycemia in yet another way. In experimental animals glucocorticoids decrease utilization of glucose by muscle and adipose tissue and lower the responsiveness of these tissues to insulin. Prolonged exposure to high levels of glucocorti-coids often leads to diabetes mellitus (Chapter 41); about 20% of patients with Cushing's disease are also diabetic, and virtually all of the remainder have some milder impairment of glucose metabolism. Despite the relative decrease in insulin sensitivity and increased tendency for fat mobilization seen in experimental animals, patients with Cushing's disease paradoxically accumulate fat in the face (moon face), between the shoulders (buffalo

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