Hormones That Affect Blood Sugar and Stress
By: Diana Pham & Anny Tang
Islets of Langerhans (discovered by Paul Langerhans)
 region of pancreas containing endocrine (hormone-producing) cells; 1-2% of pancreas mass
Glucagon

Released from alpha cells when blood sugar is low

Converts glycogen into glucose via glycogenolysis

Glycogen is a secondary long term energy storage form in animals; it’s a polysaccharide stored in liver and muscle cells). Adipose tissue is the primary long term energy storage form.
Insulin

Released from beta cells when blood sugar is high

Converts glucose into glycogen via glycogenesis (a form of dehydration synthesis)

Forces 2/3 of cells (mainly muscle and fat cells) to take in blood sugar via GLUT4 transporters

Insulin binds to cell surface receptors, inducing the translocation of GLUT4 transporters to the plasma membrane where transporters will move glucose into cells via facilitated diffusion

Glucose entering cells are phosphorylated into Glucose 6 Phosphate to trap sugar in cell
Diabetes

Chronic disease affecting more than 2 million Canadians

Hyperglycemia: condition whereby blood glucose levels are very high as there is insufficient insulin to move glucose into cells to be used for metabolic purposes

Fats and proteins are metabolized as energy sources, which is problematic

Can be kept under control via diet and exercise, which increases GLUT4 transporters available in blood to force glucose into cells
Stress
 Somatic response to stressors (causes that upset your body’s balanced or stable mental state)

Provides you with better alertness and reflexes to prevent dangers from harming yourself in emergency situations
Short Term Stress Response
 Sympathetic nervous system turns on “Flight or Fight Response”

Brain perceives threat

Hypothalamus sends nerve signals to adrenal medulla (inner central part of adrenal gland)

These signals trigger adrenal medulla’s secretion of two catecholamine hormones: Adrenaline/epinephrine and Noradrenaline/norepinephrine
Adrenaline

First messenger hormone that works on the liver

Binds to G-protein-coupled receptors in liver which triggers adenylatcyclase cascade (cAMP cascade)

Increasing rate of glycogenolysis, resulting in blood sugar increase
Noradrenaline

Inhibits insulin production by interacting with G-protein-coupled-receptors, forming cascade to activate insulin inhibiting G proteins, thus lowering cAMP levels

This causes glycogen to be converted into blood glucose in the liver, resulting in blood sugar rise
Effects of Adrenaline and Noradrenaline

More blood glucose for metabolic processes, increased breathing and heart rates

Increased muscle contraction rate so blood flow can be redirected from digestive system and kidneys to vital organs such as heart, brain, lungs, and liver (for glycogen breakdown)

Better alertness and reflexes for fight or flight


Parasympathetic nervous system turns on relaxation response to prevent damage to hippocampus cells (this requires conscious effort)
Long Term Stress Response

Brain perceives threat

Hypothalamus releases CRH (corticotropin -releasing hormone) to anterior lobe of pituitary gland

Anterior lobe releases ACTH (adrenocorticotropic hormone) which is carried to adrenal cortex

endocrine cells in cortex synthesize and secrete corticosteroids

Regulated by negative feedback (lots of corticosteroids suppresses CRH and ACTH release)
Corticosteroids

Steroid hormones that bind to receptors present in almost all vertebrate animal cells

Two types: mineralocorticoids (ie. aldosterone) and glucocorticoids (ie. cortisol)
Cortisol

Formally called hydrocortisone

Bound to corticosteroid-binding globulin (a plasma protein)  binds to glucocorticoid receptor in the cytoplasm when glucose synthesis is needed  hormone-receptor complex moves into nucleus  binds to DNA response element  adjusts transcription of genes and cell’s phenotype

Helps regulate metabolism of proteins, fats and carbohydrates, especially sugar
Effects of Cortisol

Positive: o Quick burst of energy for survival reasons o Heightened memory functions o Lower sensitivity to pain o Helps maintain homeostasis in the body

Negative: o Blood sugar imbalances (may leads to hyperglycemia) o Over production of cortisol

Cushing’s syndrome o Higher blood pressure o Impaired cognitive performance and memory loss
Metabolism

Thyroid Gland: o Thyroxine (T
4
) and triiodothyronine (T
3
) hormones

regulate body metabolism, growth o and differentiation of tissues
Hypothyroidism: low T
4
secretion

slow metabolism

excess glucose is converted to fats o Hyperthyroidism: overproduction of T
4

fast metabolism causes weight loss, elevated body temp, nervousness

heredity Graves’ disease o Permissiveness: increases for epinephrine’s effect on target cells o hypothalamus

thyroid-releasing hormone (TRH)

pituitary

thyroid-stimulating hormone (TSH)  thyroid gland  releases T
4
 metabolism  high T
4
 inhibits TRH and stops TSH production

Parathyroid Gland: o Maintain homeostasis by responding directly to chemical changes in their immediate surroundings (example: low calcium level
 release of parathyroid hormone (PTH)
 causes kidneys and gut to retain Ca 2+ and promote Ca 2+ release from bones
 high levels of Ca 2+ inhibit PTH)

Growth Hormone: o Increases fatty acid levels in the blood by breakdown fats in adipose tissue o Causes a switch in cellular fuels from glucose to fatty acids, helps adjust blood sugar in times of prolonged fasting

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