Hormones and Mineral Homeostasis- Function Flashcards
Central sensor and regulator of energy homeostasis
Brain is central sensor and coordinates the actions of multiple hormonal signals
- Allows for feeling of hunger and fullness and the energy output
Brain communication when food is available
- Meal ingested
- GI tract increases GLP-1 which sends signal to the brain of fullness, AND GLP-1 goes through the blood to tell the pancreas to increase insulin
- Insulin also tells brain that they are well-fed. Leads to decrease of lipolysis, gluconeogenesis and increase in lipogenesis in the liver and glycogen production and glucose uptake by the muscle
Brain communication when food unavailable
- No food available, so GI produces Ghrelin and tells brain that they are hungry
- Ghrelin tells WAT to increase lipid synthesis and decrease FA oxidation (this happens at a tissue level and will always be present to some extent)
- Ghrelin goes into the bloodstream and tells pancreas to decrease insulin and therefore increase glucagon
- Glucagon increases lipolysis in WAT and increases gluconeogenesis and glycogenolysis in the Liver (decreases glycolysis)
Why does lipid synthesis happen even when food supply limited?
- Because all hormones are always present at a low level. So ghrelin will always be working at the tissue level and increasing some lipid synthesis.
- Net effect will be combination of a lot of hormones so Glucagon will overpower it and more lipolysis will occur
Thermogenesis
- Shivering- from the muscle
- Non-shivering
Brain communication during cold stress
- Brain secretes TRH, and pituitary secretes TSH
- TSH acts on thyroid gland
- Thyroid gland released T3 and T4 which act on BAT
- Thyroid hormones and SNS fibers from the brain (releasing Norepinephrine) at BAT results in non-shivering thermogenesis
**Muscle shivering is caused by the release of irisin by muscle
Nocturnal fasting
- Decrease in insulin
- Increase in glucagon, leptin, cortisol, growth hormone
- Glycogenolysis, lipolysis, ketogenesis, gluconeogenesis
Short fasting
- Decrease in insulin
- Increase in glucagon, CATs, cortisol, growth hormone
Prolonged fasting
- Increase NPY, glucagon, CATs, cortisol, Growth hormone, rT3
- Decrease in insulin, IGF01, T3, testosterone
- Increase in ammonia formation and excretion
Main hormones involved in mineral homeostasis
- Aldosterone- (Adrenal cortex- zona glomerulosa)
- Calcitonin- (thyroid gland parafollicular or C-cells)
- Parathyroid hormone- (Parathyroid gland principal or Chief cells)
- Vitamin D (calciferol)- (skin, liver, gut)
Vitamin D
In mineral homeostasis, vitamin D is considered a hormone and exhibits receptor mediated actions
Aldosterone
- The most potent endogenous mineralocorticoid
- Can also bind to the glucocorticoid receptors but the potency of the action is a lot less than the mineralocorticoid activity
Target cells
- Epithelial cells in the collecting tubules of the kidney (main site of action), epithelium of the stomach, colon, sweat glands, and the ductal cells of salivary glands
- Contain the corticosteroids (Aldosterone)
Counter regulation of calcitonin and parathyroid hormones
- Counter regulation example
- Calcitonin released when blood calcium levels are high, and it acts to lower blood calcium levels
- PTH released when there is a drop of blood calcium levels, which mobilizes calcium from bone by activating osteoclast cells
Parathyroid and thyroid C- cells with different calcium levels
- Hypercalcemia- thyroid C-cells have vesicles docked to membrane releasing calcitonin
- Hypocalcemia- Thyroid C-cells are not releasing calcitonin but Parathyroid chief cells have vesicles docked releasing parathyroid hormone
