Integrative Physiology Ch. 7 - Introduction to the Endocrine System
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| Endocrinology | The study of hormones
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| Chemical hormones | A chemical secreted by a cell or group of cells into the blood for transport to a distant target, where it exerts its effect at very low concentrations
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| Processes that usually fall under hormonal control include: | Growth/development, metabolism, regulation of the internal environment (temp., water balance, ions), and reproduction
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| Hormones act on their targets in one of three basic ways | (1) by controlling the rates of enzymatic reactions; (2) by controlling the transport of ions or molecules across cell membranes; or (3) by controlling gene expression and the synthesis of proteins
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| The first documented association between endocrine structure and function was probably… | …castration which illustrated the link between the testes and male sexuality. It was a common practice in both Eastern and Western cultures because it decreased male sexuality and made them infertile
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| Classic hormones | Hormones of the pancreas, thyroid, adrenal glands, pituitary, and gonads – discrete endocrine glands that can be easily identified and surgically removed
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| Hormones may be secreted by… | …Isolated (diffuse) endocrine cells; by neurons (neurohormones); and by cells of the immune system (cytokines)
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| Key for gland/hormone summary: [P], [A], [S] | [P] = peptide, [A] = amino acid-derived, [S] = steroid
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| Posterior pituitary: hormones | Oxytocin [P]; vasopressin (ADH)
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| Posterior pituitary: Primary targets | Oxytocin: breast and uterus; vasopressin: kidney
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| Posterior pituitary: Main effects | Oxytocin: milk ejection, labor and delivery, behavior; vasopressin: water reabsorption
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| Anterior pituitary: hormones | (Note: All [P]) Prolactin; GH; ACTH; TSH; FSH; LH
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| Anterior pituitary: primary targets | Prolactin: breast; GH: liver and many tissues; ACTH: adrenal cortex; TSH: thyroid gland; FSH: gonads; LH: gonads
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| Anterior pituitary: main effects for prolactin, GH, ACTH, TSH | Prolactin: milk production; GH: growth factor secretion, growth, and metabolism; ACTH: cortisol release; TSH: thyroid hormone synthesis
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| Anterior pituitary: main effects for FSH, LH | FSH: egg or sperm production, sex hormone production; LH: sex hormone production, egg or sperm production
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| Thyroid gland: hormones | Triiodothyronine and thyroxine [A]; calcitonin [P]
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| Thyroid gland: primary targets | Triiodothyronine and thyroxine: many tissues; calcitonin: bone
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| Thyroid gland: main effects | Triiodothyronine and thyroxine: metabolism, growth, and development; calcitonin: plasma calcium levels (minimal effect in humans)
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| Heart: hormones | Atrial natriuretic peptide [P]
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| Heart: primary targets | Atrial natriuretic peptide: kidneys
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| Heart: main effects | Atrial natriuretic peptide: increases Na+ excretion
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| Liver: hormones | Angiotensinogen [P]; insulin-like growth factors [P]
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| Liver: primary targets | Angiotensinogen: adrenal cortex, blood vessels; insulin-like growth factors: many tissues
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| Liver: main effects | Angiotensinogen: aldosterone secretion, increases blood pressure; insulin-like growth factors: growth
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| Pancreas: hormones | Insulin, glucagon, somatostatin, pancreatic polypeptide [all P]
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| Pancreas: primary target | Insulin, glucagon, somatostatin, pancreatic polypeptide: many tissues
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| Pancreas: main effects | Insulin, glucagon, somatostatin, pancreatic polypeptide: metabolism of glucose and other nutrients
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| Adrenal cortex: hormones | [All S:] aldosterone; cortisol; androgens
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| Adrenal cortex: primary targets | Aldosterone: kidney; cortisol: many tissues; androgens: many tissues
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| Adrenal cortex: main effects | Aldosterone: Na+ and K+ homeostasis; cortisol: stress response; androgens: sex drive in females
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| Adrenal medulla: hormones | Epinephrine, norepinephrine [A]
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| Adrenal medulla: primary target | Epinephrine, norepinephrine: many tissues
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| Adrenal medulla: main effects | Epinephrine, norepinephrine: Fight or flight response
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| Secretion | The movement of a substance from the intracellular compartment either to the extracellular compartment or to the external environment
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| Ectohormone | The term given to hormones that are secreted into the external environment
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| Pheromones | Specialized ectohormones that act on other organisms of the same species to elicit a physiological or behavioral response. E.g. ants release pheromones to attract fellow workers to food sources
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| Sex pheromones | Pheromones that are used to attract members of the opposite sex for mating purposes. They can be found throughout the animal kingdom, in animals from fruit flies to dogs
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| Do humans have pheromones? | The question is still a matter of debate. Some studies hint that axillary (armpit) sweat glands secrete hormones that might serve as sex pheromones. A study showed females preferred the smell of more genetically diverse men
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| Candidate hormones | Molecules suspected of being hormones but not fully accepted as such (e.g. not sufficiently that it travels long distances to target cells) are called candidate hormones
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| How to identify candidate hormones by their names | They’re usually identified by the word “factor”, e.g. growth factor
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| Growth factors | A large group of substances that influence cell growth and division. Many have been proven to act as paracrine or autocrines, but they haven’t been proven yet as hormones.
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| Another example of a candidate hormone | The lipid-derived signal molecules, eicosanoids
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| What complicates the classification of signal molecules | A molecule may act like a hormone when secreted from one location but as a paracrine or autocrine signal when secreted from another location
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| The concentration range at which hormones are able to act | In the nanomolar (10^-9 M) to picomolar (10^-12) range (very small concentrations)
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| Are all chemical signals transported in the blood to distant targets considered hormones? | No, some don’t meet the low concentration requirement: that is, they need to be too high in concentration to act to be considered a hormone. E.g., histamine isn’t a hormone for this reason
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| All hormones bind to target cells and initiate biological responses. These responses are known as the _____ of the hormone | Cellular mechanism of action
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| What happens to hormones that are circulating in the blood if they’re taken up by a cell? | They’re degraded into inactive metabolites by enzymes primarily found in the liver and kidneys, and then excreted in either the bile or the urine
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| Half-life of a hormone in circulation | Indicates the rate of hormone breakdown in circulation; it is defined as the amount of time required to reduced the concentration of the hormone by one half
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| How do cells terminate the action of hormones already bounded to receptors? | Enzymes that are always present in the plasma can degrade peptide hormones bound to cell membrane receptors. Also, some cells bring in the hormone-receptor complex into the cell via endocytosis and then digested
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| How do cells terminate the actions of hormones that have made it into the cell’s ICF? | Intracellular enzymes metabolize them
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| Three main chemical classes of hormones and brief descriptions | Peptide/protein hormones: composed of linked amino acids; steroid hormones: derived from cholesterol; and amino-acid derived hormones: modifications of single amino acids, either tryptophan or tyrosine
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| Most hormones are of which chemical class of hormones? | Peptide/protein hormones
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| Peptide hormones | Huge size variability: ranging from three amino acids to larger proteins and glycoproteins. How to identify them? By exclusion: if they’re not steroid hormones nor amino acid derivatives, they’re peptide hormones
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| Preprohormones | The initial, inactive peptide that comes off the ribosome at the beginning of hormone production.
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| What happens to the preprohormone immediately upon being produced by the ribosome? | A signal sequence directs the protein into the lumen of the rough ER
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| What happens to the preprohormone as it moves through the ER and Golgi? | In the ER, the signal sequence is removed creating a smaller, still inactive *prohormone*. In the Golgi, the prohormone is packaged into secretory vesicles along with proteolytic enzymes
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| What do the proteolytic enzymes in the secretory vesicles do to the prohormone? | Post-translational modification
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| Post-translational modification | The proteolytic enzymes chop the prohormone into active hormone and other fragments
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| What happens to the secretory vesicles that are filled with the hormone? | They are stored in the cytoplasm of the endocrine cell until the cell receives a signal for secretion. At that time they’ll move to the cell membrane to be released via calcium-dependent exocytosis
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| Co-secretion | All of the peptide fragments created from the prohormone are released together into the ECF, in a process known as co-secretion
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| Interesting discovery relating to the prohormone for thyrotropin-releasing hormone (TRH) | It contains multiple copies of its hormone
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| Interesting discovery relating to proopiomelanocortin | It splits into three active peptides plus an inactive fragment
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| Can the inactive fragments of proteolyzed prohormones be clinically useful? | Yes, for example proinsulin is cleaved into active insulin and an inactive fragment known as C-peptide. Clinicians measure the levels of C-peptide in the blood of diabetics to monitor how much insulin the patient is producing
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| Solubility of peptide hormones in water and the significance? | Peptide hormones are water soluble and therefore generally dissolve easily in the ECF for transport throughout the body
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| Half life of a peptide hormone and the significance? | Relatively short: in the range of several minutes. Thus if the organism wants to sustain the effect of the hormone for a while it must be secreted continually
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| Are peptide hormones able to enter their target cell? | They’re lipophobic so they’re usually unable to enter the target cell.
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| How do peptide hormones create a response in a cell? | They bind to surface receptors to activate a signal transduction system. Many peptide hormones work through cAMP messenger systems. A few peptide hormones have tyrosine kinase activity or other pathways
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| What kind of changes to peptide hormones create? | The response is usually rapid because second messenger systems usually modify existing proteins. Changes include opening or closing membrane channels and modulating metabolic enzymes or transport proteins
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| Which second messenger systems have longer-lasting effects? | If the second-messenger system activates genes and directs synthesis of new proteins then the effects are longer-lasting. Some peptide hormones do this, most don’t.
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| Note: endothelium vs. epithelium | Endothelium is just simple squamos epithelium that lines organs and blood vessels INSIDE the body. Just remember that the thin lining of tissues INSIDE the body is usually endothelial
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| Where are steroid hormones made (as opposed to peptide hormones)? | Unlike peptide hormones, which are made in tissues all over the body, steroid hormones are made only in a few organs: three types are made in the adrenal cortex, sex steroids are produced in the gonads; and placenta in pregnancy
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| Where is the adrenal cortex | It makes up the outer portion of the adrenal glands, which are each located atop each kidney
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| Unique characteristics of cells that produce steroid hormones | They have unusually large amounts of smooth ER, the organelle where the steroid hormones are produced.
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| Are steroid hormones stored in advance in secretory vesicles like peptide hormones? | Since steroids are lipophilic and diffuse easily across cell membranes, they can’t be trapped in secretory vesicles. Instead, the cells secrete steroid hormones as it is needed.
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| How are steroid hormones secreted by the cell? | When a stimulus activates the endocrine cell, precursors in the cytoplasm are rapidly converted to active hormone. The hormone concentration in the cytoplasm rises, and the hormones move out of the cell via diffusion
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| How do steroid hormones reach their targets? | They must bind to carrier proteins to travel through the ECF and reach their target? Why? Because unlike peptide hormones, steroid hormones are not soluble in the ECF.
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| What proteins are used as carriers? | Some steroid hormones have specific carriers, such as corticosteroid-binding globulin. Others simply bind to plasma proteins, such as albumin.
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| Describe the half-life of steroid hormones | The binding of a steroid to a carrier protein protects the hormone from enzymatic degradation and results in an extended half-life. E.g. cortisol’s half-life is 60-90 minutes while epinephrine’s is measured in seconds
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| Can steroid hormones diffuse into their target cells? | Yes, but only UNBOUND steroids can be diffused through membranes, so the steroids must release from their carriers first. (Carriers—since they’re soluble in water and can diffuse through the plasma—are lipophobic)
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| Where are steroid receptors found? | Inside the cytoplasm or nucleus of the target cells.
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| Where is the ultimate destination of steroid receptor-hormone complexes? Once they reach their destination, what do they do? | The nucleus, where the complex acts as a transcription factor, binding to DNA and either activating or repressing (turning off) one or more genes.
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| Any hormone that alters gene activity is said to have a _____ effect on the target cell | Genomic effect
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| Response time for the biological effects to occur for released steroid hormones that have genomic effects | There is usually a large lag-time between hormone-receptor binding and the first measurable effects. The lag can be as much as 90 minutes. Thus, steroids with genomic effects do not mediate reflex pathways requiring rapid responses
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| Steroids with nongenomic responses | Several hormones including estrogens and aldosterone have cell membrane receptors linked to signal transduction pathways on cell membranes, just as peptide hormones do. These responses are very rapid.
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| Review: what is the parent compound for all steroid hormones? | Cholesterol – it’s modified by enzymes to make various steroid hormones
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| Example of three steroid hormones and where they’re derived from | Aldosterone: adrenal cortex. Cortisol: adrenal cortex. Estradiol (an estrogen): ovary
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| Amino acid-derived hormones | Small molecules created from either tryptophan or tyrosine, both notable for the ring structures in their R-groups. Only melatonin (made by pineal gland) is derived from tryptophan, all others are derived from tyrosine
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| Structural differences between catecholamines and thyroid hormones | Catecholamines have one tyrosine molecule; thyroid hormones have two AND iodine atoms
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| Catecholamines | Epinephrine, norepinephrine, and dopamine – they’re neurohormones that bind to cell membrane receptors the way peptide hormones do.
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| Thyroid hormones | Produced by the thyroid gland in the neck, behave more like steroid hormones, with intracellular receptors that activate genes
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| Review: all reflex pathways have the same components: | Stimulus, input signal, integration of the signal, output signal, and response
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| The output signal in endocrine and neuroendocrine reflexes. Example of output signal and related integrating center | A hormone or neurohormone. E.g., insulin is the output signal and the pancreatic cells constitute the integrating center (they have to integrate various reflexes from the nervous system and blood to “decide” output)
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| The simplex reflex control pathways | Pathways in which an endocrine cell directly senses a stimulus and responds by secreting its hormone. In this type of pathway, the endocrine cell acts as both sensor (receptor) and integrating center
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| Examples of hormones that operates via the simple endocrine reflex | Parathyroid hormone (PTH – secreted by the parathyroid glands), insulin, glucagon, as well as some hormones of the diffuse endocrine system
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| Parathyroid endocrine cells: where are they and what do they do? | Clustered in four small glands that lie behind the thyroid gland. They monitor and control plasma (via their hormone, PTH) Ca^2+ concentration with the aid of G protein-coupled Ca^2+ receptors on their cell membrane.
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| Parathyroid endocrine cells: how do they do it? | When a lot of Ca^2+ receptors are bound to Ca^2+, PTH secretion is inhibited. If Ca^2+ is low, PTH is secreted. PTH travels through the blood to act on bone/kidney/intestine, initiating Ca^2+ absorption responses in cells
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| How does the nervous system lead to the secretion of hormones? | Either via efferent neurons (e.g. from the brain to the pancreas to secrete insulin) or via specialized groups of neurons that secrete neurohormones (e.g. in the brain or adrenal medulla, etc)
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| Two endocrine structures incorporated into the anatomy of the brain | Pituitary gland and pineal gland
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| Example of efferent neurons leading to hormone secretion | Stretch receptor in the digestive tract causes afferent neuron to send signal to brain which then sends signal to pancreas via efferent neuron to secrete more insulin. Note: now pancreas has two different pathways to integrate
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| The human nervous system produces three major groups of neurohormones: | (1) Catecholamines, made by modified neurons in the adrenal medulla; (2) hypothalamic neurohormones secreted from posterior pituitary; (3) hypothalamic neurohormones secreted from anterior pituitary
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| Note: another (non-major, I guess) endocrine gland located in the brain and its related neurohormone | The pineal gland which produces and secretes melatonin
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| Pituitary gland | A lima-bean sized structure extending downward from the brain, connected to it by a thin stalk and cradled in a protective pocket of bone
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| Anatomy of pituitary gland: infundibulum | The stalk that connects the pituitary to the brain
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| Anatomy of pituitary gland: sphenoid bone | The type of bone that’s surrounding and protecting the pituitary gland
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| Composition of pituitary gland | It’s comprised of two different tissue types that merged during embryonic development: the anterior pituitary (located closer to the front of head) and the posterior pituitary (located closer to the back of head)
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| Anterior pituitary | A true endocrine gland of epithelial origin, derived from embryonic tissue that formed the roof of the mouth. The anterior pituitary is AKA the adenohypophysis and its hormones are adenohypophyseal secretions
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| Posterior pituitary | An extension of the neural tissue of the brain. It secretes neurohormones made in the hypothalamus. It is AKA the neurohypophysis.
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| The two neurohormones stored and released in the posterior pituitary: | Oxytocin and vasopressin – both of which are small peptide hormones
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| Where are the two neurohormones which are stored/secreted in the posterior pituitary initially synthesized? | In the cell bodies of neurons in the hypothalamus, a region of the brain that controls many homeostatic functions. Each of the two hormones are made in a different cell type
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| After oxytocin and vasopressin are synthesized in the hypothalamus, how do they make their way down into the posterior pituitary? | Hypothalamic neurohormones are synthesized in the same manner as any other peptide hormone. But after synthesis, the secretory vesicles are transported down long neuronal extensions into the posterior pituitary
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| How are hypothalamic neurohormones released into circulation? | When a stimulus reaches the hypothalamus, and electrical signal passes from the neuron cell body to the distal (distant) end of the cell in the posterior pituitary, and the vesicle contents are released into the circulation
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| How many amino acids is each of the posterior pituitary neurohormones comprised of? | Nine amino acids
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| Vasopressin | AKA antidiuretic hormone, or ADH, regulates water balance in the body.
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| Oxytocin | In women, oxytocin released from the posterior pituitary controls the ejection of milk during breast-feeding and contractions of the uterus during labor and delivery
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| Another, more general, role of oxytocin in the body | Some neurons release oxytocin as a neurotransmitter or neuromodulator onto neurons in other parts of the brain. Some postulate that autism may be related to defects in the normal oxytocin-modulated pathways of the brain
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| Hormones secreted by the anterior pituitary | prolactin (PRL), thyroid stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH)
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| What controls secretion of all hormones of the anterior pituitary? | Hypothalamic neurohormones
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| Trophic hormone; which hypothalamic and anterior pituitary hormones are trophic? | A hormone that controls the secretion of another hormone. Trophic hormones in the body: all hypothalamic hormones, all except one of the anterior pituitary hormones
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| Naming scheme of hypothalamic hormones | Even though they’re all trophic hormones, for historical reasons they’re given the names “releasing” (-RH) and “inhibiting” (-IH) hormones. E.g. “growth hormone-inhibiting hormone”.
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| Which anterior pituitary hormone is not a trophic hormone? | Prolactin, which directly targets the breast
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| How do the pathways containing the trophic anterior pituitary hormones work? Note: these are regarded as “complex” pathways | The hypothalamus secretes a hypothalamic hormone “releasing” or “inhibiting” hormone whose target is endocrine cells of the anterior pituitary; the anterior pituitary then secretes a hormone that targets an endocrine gland
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| Once the anterior pituitary hormone reaches the endocrine gland in the body… | …the endocrine gland will secrete a hormone that will eventually reach a non-endocrine target. E.g. upon being stimulated by ACTH, the adrenal cortex will secrete cortisol which will target many non-endocrine tissues
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| How does negative feedback occur in the hypothalamic-anterior pituitary pathway? | Instead of the response acting as the negative feedback signal, the hormones themselves are the feedback signal. Each hormone feeds back to suppress hormone secretion by integration centers earlier in the reflex pathway
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| Long-loop negative feedback | When secretion of one hormone in a complex pathway increases or decreases, the secretion of other hormones also changes because of feedback loops that link the hormones in the same pathway
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| Short-loop negative feedback | Pituitary hormones feed back to decrease hormone secretion by the hypothalamus. E.g., ACTH exerts short-loop negative feedback on the secretion of CRH
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| Portal system | A specialized region of the circulation consisting of two sets of capillaries directly connect by a set of larger blood vessels
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| Three portal systems in the body: | One in the kidneys, one in the digestive system, and one in the brain
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| Hypothalamic-hypophyseal portal system | The portal system though which hypothalamic trophic hormones are transported directly to the pituitary.
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| The advantage of having hypothalamic hormones secreted into the portal system? | A much smaller amount of hormone can be secreted to elicit a given level of response because the blood volume flowing through is so small. The same amount of hormone in a normal blood vessel would be too dilute
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| Why is it advantageous to have a smaller volume of blood flowing through the hypothalamic-hypophyseal pituitary portal system? | Higher concentration. A small number of neurosecretory neurons in the hypothalamus can control the anterior pituitary
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| Overall processes the pituitary gland controls in the body | Metabolism, growth, and reproduction
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| Prolactin (PRL) | One anterior pituitary hormone. It controls milk production in the female breast, along with other effects. In both genders it seems to play a role in the regulation of the immune system.
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| Growth hormone (GH), AKA somatotropin | Effects metabolism of many tissues in addition to stimulating hormone production by the liver which are then sent to tissues like the bone and soft tissue to promote growth
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| Gonadotropins | Includes the follicle-stimulating hormone and luteinizing hormone. They have effects on the testes and ovaries
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| Thyroid-stimulating hormone (TSH) | Controls hormone synthesis and secretion in the thyroid gland
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| Adrenocorticotropic hormone (ACTH) | Acts on certain cells of the adrenal cortex to control synthesis and release of the steroid hormone cortisol
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| Three types of hormone interaction | Synergism, permissiveness, and antagonism
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| Synergism | When two or more hormones interact at their targets so that the combination yields a result that is greater than additive. E.g. epi = 5mg glucose /100 ml blood; glucagon = 10mg/100ml; epi + glucagon = 22mg/100. Note: chart pg 234
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| Synergism is AKA… | …potentiation, as in “epinephrine potentiates glucagon’s effect on blood glucose”
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| Mechanism behind synergism | Not always clear, but often linked to overlapping effects on second messenger systems
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| Permissiveness | One hormone cannot fully exert its effects unless a second hormone is present.
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| Example of permissiveness | Maturation of the reproductive system is controlled by gonadotropin-releasing hormones, gonadotropins, and steroid hormones. If thyroid hormone isn’t present, maturation is delayed. Thyroid hormone has a permissive effect
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| Mechanism behind permissiveness | Not well understood
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| Antagonism | When two molecules are working against each other, with one diminishing the effectiveness of the other.
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| Example of antagonism | Competitive inhibitors, where two molecules compete for the same receptor. Used in pharmacology; e.g. the estrogen receptor antagonist tamoxifen, which is used to treat breast cancers that are stimulated by estrogen
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| Functional antagonists | Two hormones that have opposing physiological actions. E.g. glucagon and growth hormone both raise glucose levels whereas insulin decreases it, thus they’re antagonistic to each other
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| Do hormones that are antagonistic toward each other compete for the same receptors? | Not necessarily. They may act through different metabolic pathways, or one may decrease the number of receptors for the opposing hormone.
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| Three basic patterns of endocrine pathology: | (1) hormone excess, (2) hormone deficiency, and (3) abnormal responsiveness of target tissues to a hormone
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| Hypersecretion | If a hormone has been secreted too much and now exists in excessive amounts. As a result the effect of the hormone will be exaggerated
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| Causes of hypersecretion | Numerous causes including benign tumors (adenomas) and cancerous tumors of the endocrine glands. Occasionally nonendocrine tumors secrete hormones
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| Exogenous | Coming from the outside of the body.
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| Endogenous | Coming from inside the body
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| A condition that is iatrogenic means… | It means the condition has been physician caused. E.g. if an exogenous hormone (from a medical treatment) resulted in a state of hormonal excess in the patient, the cause is regarded as iatrogenic
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| What happens if a patient is given too much exogenous cortisol? | The cortisol will feedback negatively to the hypothalamus and stop the production of CRH. As a result cortisol production would shut down. If the adrenal cortex is starved of cortisol long enough, the glands will atrophy
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| Atrophy | Loss of cell mass; in the previous example with excess endogenous cortisol, the endocrine cells of the adrenal glands shrink and lose their ability to manufacture ACTH, i.e. the adrenal gland atrophies
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| Can atrophied glands regain function after the administration of exogenous sources of a hormone? | They may be very slowly or even totally unable to gain back function. Therefore patients on hormone therapy must be tapered off the treatment very slowly to give their glands time to recover
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| Hyposecretion | Too little hormone is secreted, causing symptoms of hormone deficiency.
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| Example of Hyposecretion | Insufficient diet in iodine will make the thyroid unable to manufacture the iodinated thyroid hormone
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| Most common cause of hyposecretion | Atrophy of the gland due to some disease process
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| How is negative feedback pathways affected in hyposecretion? | The opposite to that of hypersecretion. The absence of negative feedback causes more trophic hormones to be produced.
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| Example of the negative feedback affect in hyposecretion | The adrenal cortex atrophies in tuberculosis and cortisol production decreases. The hypothalamus and anterior pituitary will then secrete more CRH and ACTH in an attempt to stimulate the adrenal gland into making more cortisol
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| Abnormal tissue responsiveness | When the hormones exist in normal concentrations but the tissue isn’t responsive. This can be due to receptor or second messenger problems
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| Down regulation | If hormones secretion is abnormally high for a long time, target cells may down-regulate (decrease the number of) their receptors in an effort to diminish their responsiveness to excess hormone
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| Hyperinsulinemia | Classic example of down-regulation. Sustained high levels of insulin cause target cells to remove insulin receptors from their cell membrane. Signs of diabetes, even though insulin levels may be high, will result
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| Receptor abnormalities | Abnormal tissue responsiveness can result when there are mutations in the receptors that cause them to be absent or nonfunctional
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| Testicular feminizing syndrome | Androgen receptors are nonfunctional in the male fetus because of a genetic mutation. As a result the androgens produced by the developing fetus are unable to influence development of the genitalia.
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| Signal transduction pathway abnormalities | Abnormal tissue responsiveness can also result when there are problems in the signal transduction pathway, e.g. defects in the G protein
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| Pseudohypoparathyroidism | Low parathyroid hormone results even though blood levels of the hormone are normal or elevated. This is due to a defect in the G protein that links the hormone receptor to the cAMP amplifier, adenylyl cyclase
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| UNDERSTAND FIGURE ON PAGE 237 | UNDERSTAND FIGURE ON PAGE 237
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| Primary pathology | If a pathology (deficiency or excess) arises in the last endocrine gland in a reflex, the problem is considered to be a primary pathology
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| Example of primary pathology | If a tumor in the adrenal cortex begins to produce excessive amounts of cortisol, the resulting condition is called primary hypersecretion
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| Secondary pathology | If a dysfunction occurs in one of the tissues producing trophic hormones, the problem is secondary pathology.
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| Example of secondary pathology | The pituitary is damaged because of head trauma and ACTH secretion diminishes. The resulting cortisol deficiency is considered to be secondary hyposecretion of cortisol
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| Etiology of a disease | The cause of a disease
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| How common are hypothalamic pathologies? How common are pathologies in the anterior pituitary? | Hypothalamic: rare. Anterior pituitary: about 2/3 of all cortisol hypersecretion syndromes.
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| Two possible explanations in a primary disorder | Endogenous hypersecretion of the hormone or exogenous administration of the hormone
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| What happens if there is an adrenal tumor that is secreting a hormone, e.g. cortisol, in an unregulated fashion | The normal control pathways are totally unaffected. The excess cortisol shuts off hypothalamic and anterior pituitary cortisol production via negative feedback, but the tumor is not reliant upon their signals
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| Evolutionary conservation of hormone function | As scientists sequence the genomes of diverse species, they are discovering that in many cases hormone structure and function have changed amazingly little from primitive vertebrates through the mammals
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| How is modern insulin produced | Genetic engineering: the human gene for insulin is inserted into a bacterium which then synthesizes the hormone, providing us with a plentiful source of human insulin
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| E.g. of a hormone that we don’t use any more and is evolutionarily “on its way out” | Calcitonin which is found in fish and plays a major role in their metabolism, is also in humans and apparently has no role
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| Some endocrine structures that are important in lower vertebrates are vestigial in humans, meaning… | …that in humans these structures are present as minimally functional glands.
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| Example of vestigial structure in humans | E.g. melanocyte-stimulating hormone (MSH) from the intermediate lobe of the pituitary controls pigmentation in reptiles and amphibians. Adult humans only have a vestigial intermediate lobe with no measurable MSH
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| Comparative endocrinology | The study of endocrinology in nonhuman organisms. E.g. melatonin was discovered via research in tadpoles.
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| Melatonin | The “darkness hormone” secreted at night as we sleep. It is the chemical messenger that transmits information about light-dark cycles to the brain center that governs the body’s biological clock
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| Grave’s disease | Autoimmune disorder in which the body produced antibodies that mimic TSH and bind to the receptor in the thyroid. The thyroid gland then is fooled into overproducing the hormone.
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| Graves’ disease effect on relevant hormone levels in the blood | TRH and TSH are both low and thyroid hormones (thyroxine) are elevated because it’s a primary hypersecretion pathology
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| Hypothalamic-anterior pituitary pathway, target: breast | PRFs (prolactin releasing factors) AND dopamine (inhibits) -> prolactin (non-trophic) -> [[breast tissue]]
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| Hypothalamic-anterior pituitary pathway, target: thyroid gland | TRH (thyroid releasing hormone) -> TSH (thyroid stimulating hormone) -> [thyroid gland] -> thyroid hormones -> [[many tissues]]
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| Hypothalamic-anterior pituitary pathway, target: adrenal cortex | CRH (corticotropin-releasing hormone) -> ACTH (adrenocorticotropin) -> [adrenal cortex] -> cortisol -> [[many tissues]]
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| Hypothalamic-anterior pituitary pathway, target: Liver | Somatostatin (inhibits) AND GHRH (stimulates) -> GH (growth-hormone) -> [liver] -> IGFs (insulin-like growth factors) -> [[many tissues]]
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| Hypothalamic-anterior pituitary pathway, target: endocrine cells of the gonads | GnRH (gonadotropin-releasing hormone) -> FSH (follicle stimulating hormone) OR LH (luteinizing hormone) -> [gonads] -> Androgens OR estrogens/progesterone -> [[germ cells of gonads]] and [[many tissues]]
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| Insulin release requires phosphorylation by: | PKC and PKA in addition to the calcium influx in order to exocytose the secretory vesicles filled with insulin
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| Translocation | The process of moving the protein throughout the ER. Hence “cotranslational translocation” which occurs in the ER
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| Summary of synthesis/secretion of peptide hormones | RER: cotranslational translocation -> Golgi: prohormone processing -> cytosol: storage in immature secretory granules (hydrophilic so can be stored); exocytosis via mature granules (way after synthesis, stored long term)
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| Proinsulin -> insulin + c-peptide (note: proinsulin cannot function, only insulin can. This process is therefore required) | Pro-insulin is a single “curly-Q”-looking unit. During post-translational modification a large portion called “C-peptide” is snipped off and all that remains are two strands linked by multiple disulfide bonds (cysteines) = insulin
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| What enzymes are involved in snipping proinsulin to insulin? | Prohormone convertases that live in the secretory pathway. They recognize pairs of bases of amino acids and cleave them, *especially Lys-Arg*
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| Prohormone for ACTH | Pro-opiomelanocortin which is snipped to: ACTH, gamma-lipotropin, beta-endorphin, and an inactive fragment
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| Preprohormone for TRH | Snipped to *6 copies* of TRH as well as some other peptides and a signal sequence
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| Parent of steroids | Cholesterol
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| Where are steroids made | Adrenal cortex and testes/ovaries
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| Glucocorticoid is important for | Mobilizing glucose stores in the body during fasting
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| Aldosterone does what? | Controls sodium reabsorption – too much reabsorption will result in too much in the blood, more fluid being retained and ultimately increased pressure
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| Summary of the synthesis/secretion of steroids | Cholesterol is shuttled first to the mitochondria where it’s converted to an intermediate. The intermediate is sent to the ER where it’s modified. Then sent back to mitochondria. Then immediately synthesized, diffuses through membrane
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| A cell that makes steroids is called a… | …steroidogenic cell.
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| Difference between steroidogenic and peptide-synthesizing cells | Peptide cell has lots of rough ER, golgi, and dark secretory granules. Steroidogenic cells = more smooth ER, lots of lipid droplets (cholesterol), and no secretory granules.
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| How are steroids transported through circulatory system? | Carriers since they’re lipophilic
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| How can steroid hormones affect its target? | Bind straight to DNA; bind to receptor in nucleus; bind to receptor in cytosol; or bind to cell surface receptor
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| How does steroid hormone glucocorticoid bind to its target? | Binds directly to receptor located ON DNA!
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| From where are catecholamines and thyroid hormones derived? | Tyrosine
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| Compare half life of peptide hormones to steroids | Peptide: short, steroid: long (especially when it directly affects gene expression)
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| Three catecholamines | Dopamine, norepinephrine, epinephrine
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| Two thyroid hormones | Thyroxine, triiodothyronine
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| Overall structural difference between thyroid hormones and catecholamines | Thyroid hormones have two ring structures
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|
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| Conversion of tyrosine to dopamine | Hydroxylation of benzene ring (add another hydroxyl group) by enzyme *TYROSINE HYDROXYLASE* and de-carboxylation of carbon next to amine
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|
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| Conversion of dopamine to norepinephrine | Convert H on C next to benzene to OH by the enzyme DOPAMINE BETA-HYDROXYLASE
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|
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| Conversion of norepinephrine to epinephrine | Convert primary amine to secondary amine by turning one of the H’s into a methyl group
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|
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| Why the name “catecholamine”? | A benzene with two hydroxyls next to each other is the basis for the molecule “catechol”. And of course there’s an amino on the opposite side of the molecule.
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|
||||
| What do you call a cell that can produce catecholamines? | Catecholaminergic cells
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|
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| What do you call pathways that are dominated by catecholamines? | Catecholaminergic pathways
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|
||||
| Recap: what do you call cell that can produce peptide hormones? | Peptinergic cells
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||||
| What happens if a neuron continuously secretes norepinephrine? | After it runs out it will response by producing more tyrosine hydroxylase thus creating more dopamine thus creating more norepinephrine. A form of up regulation if you will
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| The most stored catecholamine in neurons | Norepinephrine
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|
||||
| Unique part about thyroid hormones | The multiple iodines – it’s the only place in the body where you use iodine
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|
||||
| Summary of the synthesis of neurotransmitters (e.g. in adrenal medullary cell or any other catecholaminergic cell) | Tyrosine -> dopamine -> stored in hydrophilic granules -> secreted long after creation via exocytosis
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| Compare catecholamines and thyroid hormones to peptide and steroid hormones | Catecholamines are like peptide hormones; thyroid hormones are like steroid hormones
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| One of the peptide hormones stored in the adrenal medulla | Enkephalin – opiate peptide that mimics opium. Mood modulator and pain reducer. Narcotic analgesic. It’s secreted along with epinephrine every time you have a fight/flight response. They’re coordinately secreted from same vesicles
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| Difference between catecholamine and peptide hormone | Dopamine is pumped INTO vesicles from cytosol – there’s no golgi or ER involved. VERY IMPORTANT.
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|
||||
| For thyroid hormones, what is stored in the secretory vesicles? Add note | Precursors. The fact that these are stored in secretory vesicles is the only difference between that of steroid hormones
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|
||||
| Transcriptome | The population of all mRNAs
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|
||||
| Is the anterior/posterior pituitary part of the brain? | Anterior = no, it’s not made of neurons. The posterior = yes.
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| Somatotrophs | Cells that release growth hormones
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|
||||
| Effects of glucocorticoids from chronic stress | Increased blood sugar and proteins/fats broken down for energy
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|
||||
| Effects of mineralcorticoids (e.g. cortisol) from chronic stress | Retention of sodium and water, increased blood pressure and blood volume
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|
||||
| Effects of catecholamines from short term stress response | Increased heart rate, increased bp, convert glycogen to blood glucose, dilation of bronchioles, decreased digestion, decreased urine, increased alertness
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|
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| HPA axis | Hypothalamic-pituitary-adrenal axis
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|
||||
| All hypothalamic hormones are _____ hormones | Peptide
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|
||||
| How many peptides make up TRH and what are they? | 3: Glutamic acid – histidine – proline
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|
||||
| Why is the small size of TRH significant | It makes it resistant to changes in pH and temperature
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|
||||
| Unique aspect of peptide hormones in the brain such as TRH | Their C-terminus is not a carboxylic acid, it’s an amide; the OH is replaced by NH2
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|
||||
| Enzyme discovered by professor | PAM, it requires O2 and Cu as cofactors
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|
||||
| High levels of cortisol do a good thing and a bad thing | Decrease inflammation and suppress immune system
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|
||||
| Cells that CRH binds to in anterior pituitary | Corticotrophs
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|
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