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Thyroid and other hormones (Thyroid hormones (Function (Increase basal…
Thyroid and other hormones
Thyroid hormones
Related compounds
T4 (thyroxine): 2 tyrosine + 4 bound iodine
T3 (triiodothyronine): 2 tyrosine + 3 bound iodine
Thyroid gland
Two lateral lobes connected by the isthmus
Composition
Follicle (glandular) cells that produce glycoprotein thyroglobulin
Colloid (thyroglobulin + iodine) fills the lumen of the follicles and is the precursor of the thyroid hormone)
Parafollicular cells secrete calcitonin
Synthesis
1.Thyroglobulin (containing 70+ tyrosine) is synthesized and discharged into the follicle lumen
2.Iodides (I–) are actively taken into the cell, oxidized to iodine (I2), and released into the lumen
3.Iodine attaches to tyrosine, mediated by peroxidases, producing monoiodotyrosine (MIT) and diiodotyrosine (DIT) – still part of thyroglobulin
4.MIT & DIT link together to form T3 and T4 – still linked to thyroglobulin
5.TH stored in follicles – sufficient to provide 2-3 months’ need
6.Colloid is endocytosed and combined with a lysosome
7.T3 and T4 are cleaved from thyroglobulin and diffuse into the bloodstream
Iodide
Required for TH synthesis: 20% used to form TH and 80% excreted by kidneys
Transported from blood into glandular cells via Na/I symporter; expression and activity regulated by TSH
Transported from glandular cells into follicle via Cl/I antiporter (Pendrin)
Transport
T4 and T3 are transported by thyroxine-binding globulins (TBGs)
Both binds to target receptors but T3 is 10x more potent
Peripheral tissues convert T4 to T3
Regulation
Negative feedback regulation of TH release
Rising TH levels --> negative feedback inhibition on release of TSH
Hypothalamic thyrotropin releasing hormone (TRH) can overcome the negative feedback during pregnancy or exposure to cold
Need thyroid hormone for fetus to properly develop
Cold: Thyroid hormone produces heat
Function
Increase basal metabolic rate & heat production (calorigenic effect)
Increases number & activity of mitochondria
Increases activity of Na-K-ATPase
Increases glucose availability to cells
Increases glucose uptake by cells
Enhances glycogenolysis
Enhances gluconeogenesis
Enhances absorption from GI tract
Increases insulin secretion
Mobilizes lipid
Decreases triglycerides
Increases free fatty acids in plasma
Decreases cholesterol (increases cholesterol secretion in bile for excretion)
Excessive TH causes protein loss (catabolism)
Increases the need of vitamins
Increased GI motility and secretion
Increases pulse pressure, minimal effect on mean arterial pressure
Increases secretion of several other hormones (due to increase of need by tissues)
Insulin, parathyroid hormone, adrenocorticotropic hormone (ACTH), glucocorticoid
Increases blood flow
Increased metabolism --> increased metabolic end products and heat --> vasodilation --> cardiac output
Directly stimulates the heart
Increases heart and contractility (strength)
Excites the CNS
Maintains mental abilities
Excessive TH causes nervousness, anxiety, paranoia, insomnia
Excessive TH causes fine tremor in muscle (increases reactivity of the spinal cord neuronal circuitry to control muscle tone)
Promotes development
Critical for brain development in fetus and neonate
Bone development in childhood
Parathyroid hormone
Functions
Maintain plasma calcium level
Stimulates osteoclasts to digest bone matrix
Enhances reabsorption of Ca2+ and secretion of phosphate by the kidneys
Promotes activation of vitamin D by the kidneys; increases absorption of Ca2+ by intestinal mucosa
Negative feedback control: Rising Ca2+ in the blood inhibits PTH release
Adrenocortical Hormones
Mineralocorticoids (Aldosterone)
Function
Regulate electrolytes (primarily Na+ and K+) in extracellular fluid
Increase Na and decrease K (way to maintain Na in blood)
Most potent mineralcorticoid
In kidneys
Na+ reabsorption
K+ secretion
Water retention
Regulation
Renin-angiotensin system
Decreased blood pressure stimulates kidneys to release renin --> formation of angiotensin II (potent stimulator of aldosterone release)
High plasma concentration of K+ directly stimulates release aldosterone
ACTH causes small increases of aldosterone during stress
Atrial natriuretic peptide (ANP blocks renin and aldosterone secretion, to decrease blood pressure)
Glucocorticoids (Cortisol)
Maintain glucose homeostasis
Critical in resisting stress and inflammation
Cortisol (hydrocortisone) is the predominant glucocorticoid secreted by the adrenal gland
Function
Maintain glucose homeostasis
Stimulate gluconeogenesis in liver
Decrease glucose use by most cells
Mobilize fatty acids from adipose tissue
Redistribute lipid --> central obesity (buffalo torso)
Cause "Adrenal Diabetes"
Increase insulin release
Decrease tissue sensitivity to insulin
Mobilize amino acids from many tissues to liver
Muscle --> muscle weakness
Bone --> osteoporosis
Anti-inflammation
Stabilize lysosomal membrane --> decrease release of pro-inflammatory molecules from injured cells
Decrease permeability of capillaries
Decrease migration and phagocytosis of white blood cells
Suppress immune response
Improve healing due to inflammation
Stresses that increase glucocorticoid release
Trauma
Infection
Heat or cold
Sympathomimetic drugs
Surgery
Restrain
Debilitating diseases
Four F's
Gonadocorticoids (Sex hormones)
Most are androgens (male sex hormones) that are converted to testosterone in tissue cells or estrogens in females
May contribute to
Onset of puberty
Appearance of secondary sex characteristics
Sex drive
Steroidogenesis: Uses CYP (Cytochrome P450)
Adrenal Glands
Paired, pyramid-shaped organs atop the kidneys
Structurally and functionally, they are two glands in one
Adrenal medulla: Nervous tissue; part of the sympathetic nervous system
Adrenal cortex: Three layers of glandular tissue that synthesize and secrete corticosteroids
Cortex: Inside (mostly makes steroid hormones)
Medulla: Outside (mainly makes epinephrine and some norepinephrine)
Glomerulosa: Globs
Fasciculata: Bundles of cells
Reticularis: Network-like
Diseases
Thyroid
Hypothyroidism
Fatigue
Feeling cold
Dry, course skin
Weight gain
Constipation
Slow pulse rate
Myxedema
Goiter
Hyperthyroidism
High excitability
Intolerance to heat
Increased sweating
Weight loss
Diarrhea
Muscle weakness
Nervousness or other psychic disorders
Fatigue but cannot sleep
Tremor of the hands
In infants: Cretinism
Grave's disease
Adrenocortical
Imbalances of glucocorticoids
Hypersecretion (Cushing's Syndrome)
Depresses cartilage and bone formation
Inhibits inflammation
Depresses the immune system
Promotes changes in cardiovascular, neural, and gastrointestinal function
Hyposecretion (Addison's disease)
Deficits in both glucocorticoids and mineralocorticoids
Decrease in glucose and Na+ levels
Weight loss, severe dehydration, and hypotension