Jackson Lectures 1 Flashcards

1
Q

• preprohormone is synthesized on ——–; includes extra

A

ribosomes, amino acids and foldings.

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2
Q

• prohormone formed by cleaving

A

extra amino acids in the RER; packaged into secretory vesicles in the Golgi apparatus.

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3
Q

Some cholesterol is produced by de novo synthesis from

A

acetyl CoA.

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4
Q

Cholesterol esterase releases

A

cholesterol from stores

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5
Q

Steroid acute regulatory protein (StAR) facilitates

A

intracellular transport of cholesterol by binding to cholesterol and transporting it through the watery cytoplasm to the mitochondria where is crosses both outer and inner membranes

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6
Q

Cholesterol is converted to steroids by

A

P450 enzymes in the mitochondria – these are cytochrome P450 enzymes that add –OH or cleave C-C. Steroids shuffled to SER for further enzyme modification

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7
Q

Synthesis of steroids is regulated by regulating the

A

peptide hormone that stimulates their synthesis, the synthesis of steroidogenic enzymes, and/or the number of steroidogenic cells

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8
Q

Catecholamines or catecholaminergic hormones are synthesized in the

A

adrenal medulla and hypothalamus (in neurons or cells derived from neural crest cells)

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9
Q

norepinephrine (NE) (noradrenaline) produced in –

A

adrenal medulla (catecholamine)

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10
Q

epinephrine (E) (adrenaline) produced in

A

adrenal medulla (catecholamine

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11
Q

dopamine (DA) - produced in

A

hypothalamus (catecholamine)

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12
Q

catecholamines are common neurotransmitters so other neurons make them, particularly those of the

A

autonomic nervous system

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13
Q

NE, E and DA are

A

hydrophillic, polar

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14
Q

Eicosanoid hormones – group of locally-acting hormones derived from

A

arachidonic acid.

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15
Q

Eicosanoid hormones Are known for

A

local effects and are responsible for most inflammatory mediators

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16
Q

Aspirin inhibits enzymes that produce

A

prostaglandins

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17
Q

Most hormones are secreted in

A

short bursts with the timing of the bursts controlled by an upstream signal.

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18
Q

No hormone is released in between

A

vesicular release or the next round of steroid synthesis (because they can’t be stored).

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19
Q

Some secretion is.

A

circadian

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20
Q

The circadian pattern is typically due to

A

increases and decreases in pulse frequency, but can also be associated with changes in pulse amplitude.

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21
Q

*Patterns of secretion may be controlled by three factors

A
  1. plasma concentrations of a nutrient, e.g. GH and glucose; calcium regulating hormones
  2. neural control, e.g. neurons have rhythmic firing pattern; psychological stress responses
  3. hormonal control, e.g. GnRH → LH → T; common pattern
22
Q

• carrier or binding proteins are synthesized in the

A

liver, and the use of carriers affects the availability of hormone

23
Q

• [free hormone] is a function of

A

[binding protein]

24
Q

• binding proteins also protect the hormone from

A

degradation and clearance;

25
Q

small hydrophilic hormones can also use

A

binding proteins to minimize rate of clearance

26
Q

Some degradation of hormones occurs in the blood due the action of circulating

A

enzymes. Catecholamines and peptides are highly susceptible to enzymatic degradation – rate is related to molecular size and association with binding proteins.

27
Q

• Steroid and thyroid hormones are less susceptible to degradation in the blood due to the fact that they

A

attach to binding proteins.

28
Q

• Receptors for hydrophilic hormones are on cell surface/in plasma membrane. These hormones are too

A

large and/or too lipophobic to pass through membrane

29
Q

• ionotropic responses open

A

ion channels; Ca2+ , Na+ and K+

30
Q

• metabotropic responses alter

A

cell activity; phosphorylate proteins including second messengers; move things around (receptors, vesicles)

31
Q

• Receptors for lipophilic hormones are

A

intracellular and/or nuclear (steroid and thyroid hormones)

32
Q

Steriods/thyroid hromone: • Receptor + ligand forms a

A

DNA-binding protein → regulates transcription

these responses are delayed – protein synthesis takes time

33
Q

there are some membrane receptors for steroid hormones that control

A

rapid, non-genomic responses

34
Q

• The anterior pituitary gland or adenohypophysis develops from an

A

outpocketing of the oral ectoderm that pinches off from the roof of the mouth and lies above the palate.

35
Q

Two hormones are released from the posterior pituitary –

A

oxytocin and vasopressin

36
Q

Oxy and vaso are synthesized in the neuronal cell bodies in the

A

supraoptic and paraventricular nuclei (see green neurons in Fig 11.13 above), and secretory vesicles are stored in the axon terminals within the posterior pituitary.

37
Q

• Oxytocin stimulates

A

smooth muscle contraction- one of the few things that involves positive feedback

38
Q

Vasopressin (or antidiuretic hormone) has actions in the

A

kidney and blood vessels to regulate blood pressure.

39
Q

The adenohypophysis is NOT an extension of the hypothalamus, but it is regulated by

A

hormones secreted by hypothalamic neurons

40
Q

Hypothalamic neurons secrete

A

hypophysiotropic (or releasing) hormones; hypophysiotropic hormones are typically named for the pituitary hormone(s) they regulate.

41
Q

Hypothalamic neurons: axon terminals lie in the

A

median eminence; at the base of the median eminence are portal blood vessels/capillaries

42
Q

Some things to remember about hypophysiotropic hormones

A
  • often found elsewhere in the nervous system; they’re not all peptides!
  • the hypothalmo-pituitary portion of the endocrine system is often referred to as the neuroendocrine system; hypothalamus + pituitary + target = an axis
  • the complexity of the system provides multiple control sites, and permits amplification of the initial signal
43
Q

Anterior pituitary secretes at least eight hormones

A

follicle stimulating hormone (FSH)

  1. luteinizing hormone (LH)
  2. growth hormone (GH) (somatotropin)
  3. thyroid stimulating hormone (TSH or thyrotropin)
  4. prolactin (PRL)
  5. adrenocorticotropic hormone (ACTH or corticotropin)
    7 and 8. β - lipotropin and β- endorphin which are products of the pro-opiomelanocortin (POMC) gene. POMC is a precursor polypeptide synthesized in corticotrophs that is cleaved to yield multiple peptides with varied actions and target tissues. One of those situations – ACTH released, you get these.
44
Q

7 and 8. β - lipotropin and β- endorphin which are products of the

A

pro-opiomelanocortin (POMC) gene.

45
Q

. POMC is a precursor polypeptide synthesized in

A

corticotrophs that is cleaved to yield multiple peptides with varied actions and target tissues. One of those situations – ACTH released, you get these.

46
Q

o Long-loop negative feedback is

A

self-regulation by product/hormone of ultimate target tissue, e.g. cortisol and ACTH/CRH

47
Q

o Short-loop negative feedback occurs when the hormone from

A

2nd gland in the axis affects the action of the 1st gland, e.g. LH and GnRH

48
Q

Thyroid synth: all the words!!!

A
  1. Iodide is transported across the basal side of the follicle cells via a Na+ / I- transporter. This is called iodide trapping, and is really only found in the Thyroid. It has to come from diet because body cannot make iodide.
  2. Iodide diffuses down its concentration gradient across the apical membrane into the colloid of the follicle. Pendrin is the protein transporter that helps get I- into colloid (Na/I- transporter).
  3. The follicle cells also synthesize a large, tyrosine-rich protein called thyroglobulin (TG), and the enzyme thyroid peroxidase. Both proteins are exocytosed across the apical membrane into the colloid.
  4. In the colloid (which is extracellular fluid), iodide is oxidized by thyroid peroxidase, and linked to thyroglobulin. Binding I- to TG maintains the concentration gradient needed in step 2 to continuously sequester I- in the colloid. Iodinating tyrosine residues on TG. Can have one or two iodides attached to TG to have di-iodoTG
    If one I- is added to a tyrosine residue the resultant molecule is monoiodotyrosine (MIT); iodinating two sites on a tyrosine produces diiodotyrosine (DIT).
  5. DITs combine with either other DITs to form tetra-iodothyronine (T4, or thyroxine), or an MIT to form tri-iodothyronine (T3). T3 and T4 remain attached to TG, and are stored in the colloid. T2 is not energetically favorable. This is how they are stored in the colloid and do not diffuse across. This ensures that you always have a store of hormones that can be released when needed. YOU HAVE TO HAVE IODIDE TO SYNTHESIZE thyroid hormone.
  6. In response to TSH, droplets of colloid containing TG + T3/T4 are pinocytosed into the follicle cells.
  7. The droplet fuses with a lysosome containing enzymes that cleave T3 and T4 from the TG
  8. T3 and T4 are released in the cytoplasm by lysosomal hydrolysis.
  9. T3 and T4 diffuse into capillaries. Amino acids from the degraded TG are recycled into new TG
49
Q

TH has

A

negative feedback actions that regulate its own secretion at the level of the hypothalamus and pituitary.

50
Q

Most of T3 and T4 will attach to

A

binding proteins, some will be free-floating.

51
Q

T3 —– times more active than T4

A

10