Endocrine System Hormones Quiz

Growth Hormone (GH)

• GH has various effects: sodium retention, decreased insulin sensitivity, lipolysis, protein synthesis (anabolic), bone growth stimulation, and IGF-1 secretion stimulation.
• GH and insulin are both anabolic hormones promoting protein synthesis, but insulin also promotes triglyceride and glycogen synthesis, unlike GH.

IGF-1 Functions

• IGF-1 mimics insulin's actions, has anti-lipolytic activity, and promotes protein synthesis.

GH Actions Summary

• Direct: Stimulates protein synthesis.
• Indirect: Promotes protein synthesis via IGF-1, stimulates bone growth, increases muscle protein synthesis, increases glucose production and gluconeogenesis in the liver, decreases insulin's effect on glucose uptake, increases lipolytic agent (e.g., epinephrine, glucagon) action, and raises free fatty acid and ketone levels.

GH Secretion Stimulators

• Hypoglycemia
• Stress
• Exercise
• Protein meals (amino acids like arginine)
• Sleep (onset)
• Androgens and estrogens

GH Levels Across Lifespan

• Highest during adolescence, second-highest in childhood, lower in adults, and lowest in the elderly.

Low GH Effects

• Reduced lean body mass, smaller protein mass, reduced bone mass.

GH Inhibitors

• Free fatty acids
• Cortisol
• Glucose
• REM sleep
• IGF-1

GH Effects on 16-Year-Old Boy

• GH increases both protein and glucose production.

Catabolic Hormones Overview

• These hormones (glucagon, epinephrine, cortisol) have a clear catabolic effect.

Glucagon

• Secretion: Pancreatic alpha cells, triggered by low glucose (fasting).
• Actions (Liver): Stimulates gluconeogenesis and glycogenolysis.
• Actions (Fat Tissue): Stimulates lipolysis.
• Synthesis: Processed from a large precursor molecule.
• Different cells produce different products due to varying enzymes.
• Pancreatic alpha cells produce: glucagon, MPGF, GPRP, GRPP
• Intestinal L cells produce: GLP-1 and other molecules

Glucagon Action Summary

• Stimulates glycogenolysis in the liver
• Stimulates gluconeogenesis
• Stimulates lipolysis
• Generates ketones
• Mobilizes energy stores

Increasing Glucose Output from the Liver

• Activates protein kinase A
• Stimulates glycogen breakdown
• Inhibits glucose metabolism
• Maintains glucose levels by releasing from glycogen, preventing further decrease

Increasing Lipolysis in Fat Tissue

• Activates hormone-sensitive lipase
• Accelerates triglyceride breakdown into glycerol and free fatty acids

Glucagon Secretion Stimulators

• Amino acids
• GI hormones (CCK, gastrin)
• Cortisol
• Exercise
• Infection
• Fasting

Glucagon Secretion Inhibitors

• Glucose
• Free fatty acids
• Ketones
• Secretin
• Insulin
• Somatostatin (inhibits glucagon and insulin)
• Alpha-adrenergic stimulation
• Beta-adrenergic stimulation (stimulates glucagon)

Epinephrine

• Production: Adrenal medulla
• Actions: Glycogenolysis (liver and muscle), stimulates gluconeogenesis, decreases glucose uptake, stimulates lipolysis, stimulates ketogenesis, mobilizes energy stores.

Epinephrine Release Stimulators

• Anxiety, fear, pain, hypoglycemia, hypotension, hypovolemia, hypothermia, hypoxia, exercise

Epinephrine Receptor Effects

• Beta-1 (Heart): Increases heart rate, stroke volume, cardiac output, blood pressure
• Alpha-1 (Vascular smooth muscle): Vasoconstriction
• Beta-2 (Skeletal muscle): Vasodilation
• Beta-2 (Liver): Glycogenolysis
• Alpha (Liver): Gluconeogenesis
• Beta-2 (Adipose Tissue): Lipolysis
• Beta-2 (Skeletal Muscle): Glycogenolysis
• Alpha (Pancreas): Inhibits insulin
• Beta-2 (Pancreas): Stimulates glucagon

Cortisol

• Stimulation Factors: Pain, low glucose, low blood pressure, low volume, low temperature, low oxygen, exercise
• Actions (Liver): Enhances norepinephrine and glucagon on gluconeogenesis
• Actions (Adipose Tissue): Promotes lipolysis
• Actions (Skeletal Muscle): Facilitates protein breakdown and glycogenolysis
• Glucocorticoid effects: Inhibit calcium uptake in the gut, bone formation, collagen synthesis, and IGF-1 actions on bone and muscle.

Glucocorticoids Net Effects

• Inhibits growth
• Decreases stature in children
• Causes osteoporosis and muscle atrophy in adults

Combined Catabolic Effects (Glucagon, Epinephrine, Cortisol) During Fasting

• Hypoglycemia triggers glucagon and epinephrine release.
• Glucagon and epinephrine stimulate gluconeogenesis and glycogenolysis to increase glucose production.
• Cortisol enhances glucagon and epinephrine effects by synthesizing enzymes and has a slower effect.
• Increases glycogen storage, breaks down skeletal muscle protein.

Cortisol Excess (Cushing's Syndrome)

• Hyperglycemia, insulin resistance, protein wasting, poor wound healing, truncal obesity, hypertension, hypervolemia, hypernatremia, hypokalemia, increased infection susceptibility, reduced inflammatory response, euphoria.

Cortisol Deficiency (Addison's Disease)

• Hypoglycemia, low blood pressure, poor response to angiotensin II, low volume and sodium, high potassium, depression, skin hyperpigmentation (due to elevated ACTH and MSH).

Hormonal Changes in Different Metabolic States

• Fed State: Increased glucose, insulin, glucagon (due to amino acids), and baseline epinephrine, GH, and cortisol; net effect: absorption and storage.
• Fasting: Decreased glucose, insulin, increased glucagon, epinephrine, GH, and cortisol; net effect: mobilization of stored fuel.
• Extended Fasting: Decreased glucose, insulin, increased glucagon, epinephrine, GH, and cortisol; ketones become a fuel source.
• Starvation: Very low glucose, insulin, suppressed glucagon, increased epinephrine, GH, and cortisol.