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Biochemistry > Week 16- Unit 4 > Flashcards

Week 16- Unit 4 Flashcards

1
Q

What are the alternative counter-regulatory hormones to focus on (5) ?

A
  1. Somatostatin
  2. Growth Hormone
  3. Catecholamines (norepinephrine and epinephrine)
  4. Glucocorticoids (cortisol - steroid hormones)
  5. Thyroid Hormone
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2
Q

What are the “peptide hormones” ? (4)

What do they all signal through?

A

Insulin
Glucagon
Somatostatin
Growth Hormone

-signal through binding of a cell membrane receptor

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3
Q

The Catecholamines ( nor and epinephrine) are _______ type hormones, they also signal through _______ ______ specifically the ___ or ____ adrenergic receptors.

A

Amine

Membrane receptors

Alpha or Beta Adrenergic

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4
Q

Glucocorticoids (cortisol) are ______ that signal through _______ receptors that function as ________ ________.

A

steroid

intracellular

transcription factors

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5
Q

Thyroid hormone is different from all the other hormones as it is a ________ type hormone but signals similar to the _______ types by binding to an ________ receptor and functioning as a transcription factor.

A

Peptide

Steroid

Intracellular

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6
Q

Insulin is secreted from ______ cells of the ______. It will suppress glucagon release from ______ cells.
(anabolic processes)

A

Beta
Pancreas

Alpha

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7
Q

Glucagon is secreted from _______ and _____ cells in pancreas. It can also stimulate the release of insulin in such a way that helps regulate ______ and ______ to maintain blood glucose. Without this regulation, Glucagon can precipitate __________ such as in diabetic ketoacidosis.

A

Alpha and L cells

GNG
Glycogenolysis

Hyperglycemia

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8
Q

Somatostatin is an general _______ for the release of other hormones. It is secreted as a ______ molecule much like insulin and glucagon, meaning it is secreted in _____ form that requires cleavage of the active peptide.

A

Inhibitor

Pro-molecule

Peptide

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9
Q

Somatostatin is secreted from several sites, mainly what 4 areas?

A

Hypothalamus
D cells of pancreatic islets
Central Nervous system
Gastric/intestinal mucosa

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10
Q

Somatostatin is secreted in response to what 3 MOLECULES mainly?

A

Glucose, Arginine, Leucine

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11
Q

What HORMONES can stimulate the release of Somatostatin ?

A

Glucagon
VIP
Cholecystokinin (CCK)- in Duodenum

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12
Q

Somatostatin will signal via a ______, activating an ______ G-protein which will then _______ adenylate cyclase. This will _______ cAMP.

A

GPCR

inhibitor

inactivate

decrease

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13
Q

Besides the main GPCR inhibitory pathway for signaling, Somatostatin can also activate several ______, _______ and _______.

A

Phosphatases
MAPK cascades
Ca+2 (calcium mediated signaling)

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14
Q

Somatostatin’s primary action is to decrease ______ will suppress the release of many hormones including what 4 ?

A

cAMP

Growth Hormone
TSH
Insulin
Glucagon

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15
Q

Somatostatin will also ______ gastric emptying by impacting the secretion of gastric and pancreatic _______.

A

Decrease

enzymes (required for digestion)

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16
Q

Glucagon can stimulate the release of both _____ and _____ in the pancreas.

A

Somatostatin (Delta cell)

Insulin (Beta cell)

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17
Q

Insulin will inhibit the release of ______ but does not necessarily effect the release of ______.

A

glucagon

Somatostatin

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18
Q

The action of Somatostatin being able to ____ both glucagon and insulin in a regulatory feeback look is necessary so Blood glucose can ______ again to stable levels before ______ is released again into the body.

A

inhibit

rise

insulin

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19
Q

Growth Hormone is a water _____ polypeptide with a very _____ half-life in circulation of ___ to ___ minutes.

A

soluble
Short

20 to 50

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20
Q

Growth hormone (GH) is composed of a _____ polypeptide chain in a spiral with ____ ____ bonds.

A

single

2 disulfide

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21
Q

Growth hormone is release from the ______ _____ gland. Starting at the ______ any number of stimuli can impact the release of _____ that will travel to the location of GH release.

A

Anterior pituitary

Hypothalamus

Growth Hormone Releasing Hormone (GHRH)

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22
Q

What are 4 examples of factors that can stimulate release of GHRH from they hypothalamus?

A 
Sleep Rhythms
Low blood glucose
High blood AA
Stress
Exercise
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23
Q

After it is released from the Hypothalamus, GHRH binds to the ______ _____ of cells in the ______ ______. This results in the release of _____ by way of any number of second messengers including cAMP or Ca+ mediated signaling.

A

plasma membrane

Anterior Pituitary

Growth Hormone

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24
Q

After release from the anterior pituitary, Growth Hormone will travel in the blood to the ______ and interact with receptors similar to ______ _____ receptors. This will stimulate the release of ______ from the liver.

A

Liver

Jak-STAT

Insulin-like Growth Factor 1 (IGF-1)

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25
Q

IGF-1 will be similar to insulin by binding a plasma membrane _____ _____ for signaling. It regulates itself for feedback at several different levels.

A

Tyrosine kinase

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26
Q

Growth Hormone will feedback and inhibit the release of ______ in the Hypothalamus.
Similarly, _____ will feedback and inhibit its release from the Hypothalamus as well.

A

GHRH

IGF-1 (from liver)

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27
Q

IGF-1 can directly inhibit the release of _____ at the Anterior Pituitary gland. It will inhibit the release of _____ from the Hypothalamus, and then it will also STIMULATE the release of _______ from the Hypothalamus.

A

GH

GHRH

Somatostatin (will travel to inhibit release of GH at anterior pituitary)

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28
Q

The primary physiologic factors effecting stimulation of release of Growth Hormone depend on fuel availability. If Blood Glucose is _____ after meals , it will stimulate release of GH and GH helps reduce Glucose _____ and increases ______.

A

Low (GH helps increase blood glucose)

uptake

GNG

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29
Q

GH is released in response to ____ blood glucose and ______ blood levels after meals. The other three main stimulating factors are ?

A

low
AA

Sleep, Stress, Exercise

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30
Q

What will suppress the GH secretion at the physiological level after meals ?

A

High blood glucose after meals

High blood Fatty Acids

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31
Q

Release of GH can also be stimulated with pharmacological means such as addition of _______ or it can be inhibited by the introduction of _______.

A

GHRH

Somatostatin

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32
Q

Pathological states such as Starvation where energy is extremely low, will elicit the _____ of growth hormone release. This helps influence the pathways of ____ and _____ as a means of providing energy.

A

Stimulation

GNG
Lipolysis

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33
Q

Pathological states such as Obesity, Hypothyroidism, Hyperthyroidism will ______ growth hormone secretion.

A

suppress

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34
Q

For a GH receptor, they ______ upon ligand binding. However the receptors themselves lack _____ activity, so they are associated with _____ family of kinases.

A

dimerize

kinase

Jak2

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35
Q

The Jak2 (JAK) family of kinases that associate with GH receptor will phosphorylate the receptor after dimerization from ligand binding, this will then phosphorylate and activate ________, _______, or ______ signaling that all can have a cellular effect.

A

STAT (1,3,&5)
MAPKs
Phosphoinostitol kinases (PI3K)

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36
Q

GH as a physiological effect can be considered a means of _____ energy. It leads to a “muscle building” environment.

A

increasing

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37
Q

GH will effect the Adipose by ______ lipolysis by increasing the sensitivity of the tissue to _________. This will then in turn stimulate lipolysis by phosphorylation of ________.
This is a means of decreasing fat storage—>lean athletic physique.

A

increasing

epinephrine

Hormone sensitive lipase

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38
Q

In the Skeletal muscle, GH will increase ______ uptake and oxidization by the muscle.
This generates _____.
GH also increases ______ transport and uptake which will lead to increased _____ _____.

A

Free Fatty Acid (FFA - came from adipose)
ATP

AA

Protein Synthesis

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39
Q

In the liver, GH will ______ GNG and decreases ______ uptake to maintain blood levels, then increasing glycogen synthesis (even though counter intuitive, it is making energy and storing it too)

A

increase (GNG)

Glucose

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40
Q

In the liver, GH will also increase _______ uptake that will be oxidized to Acetyl CoA which increases substrate for ______.

A

FA

Ketogenesis

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41
Q

In the liver, because GH will decrease glucose uptake and increase ketogenesis (FA uptake too), this will contribute to ______ blood glucose levels and increased energy reserves.

A

elevated

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42
Q

Most importantly , GH will stimulate the release _____ and _____ that illicit the indirect effects of GH release on the body.

A

IGF-1
IGF-2

(2 Isoforms)

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43
Q

What cells in the Anterior Pituitary Gland will release Growth Hormone?

A

Somatotrophs

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44
Q

IGF can function in both an ______ and ______ way after being produced after the binding of GH to its Jak-STAT family Receptor on the liver.

A

Endocrine

Paracrine

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45
Q

IGF can act as a paracrine by binding to its own receptor on the ______. This receptor is similar to a ____ ___ (insulin like receptor with endogenous activity)

A

Liver

Tyrosine Kinase

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46
Q

The cascade initiated by IGF binding its own receptor in a Liver cell (paracrine) will cause a ________ response. This allows the cell to grow.

A

Mitogenic

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47
Q

As an autocrine, IGF will be similar to activites of ______ and it also has an influence on bones (long bones) on _____ or growth of the bone.

A

Insulin

Sulfation (needed for bone growth)

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48
Q

Growth Hormone will ______ glucose uptake in the Muscle, and _____ protein synthesis.

A

decrease

increases

49
Q

Defects in GH are rare, but Excessive release of GH will cause _______ or Giantism.

A

Acromegaly

-Begins in young children or adolescents

50
Q

What usually causes Acromegaly?

A

Tumor of somatotrope cells (secrete the GH from Anterior Pituitary)

51
Q

Synthesis of Catecholamines like epinephrine and norepinephrine (stress induced) is initiated with ______ as the precursor.

A

Tyrosine

52
Q

What organ will release Catecholamines like norepinephrine and epinephrine?

A

Adrenal Medulla

53
Q

What 4 things may cause Catecholamine release from the adrenal medulla?

A

Exercise
Hypoglycemia
Pain
Hypoxia (lack of oxygen)

54
Q

The major role of Catecholamines is to rapidly increase energy by increasing ______ in the adipose and ______ in the liver and muscle. They will also counteract the effects of _____.

A

Lipolysis

Glycogenolysis

Insulin (inhibits activity)

55
Q

Epinephrine can enhance the activity of glycogenolysis in the liver using an _______ _______.

A

Alpha-agonist receptor

56
Q

Binding of the Epinephrine to the Alpha-agonist receptor in the liver will activate ______ Which cleaves the membrane bound _____.

A

G-Protein

PIP2

57
Q

What will the PIP2 be cleaved into in the beginning of Epinephrine induced activity on the liver cell?

A
  1. IP3

2. DAG

58
Q

What does IP3 do in the epinephrine liver cell pathway?

A

stimulate release of Ca+ from the Endoplasmic Reticulum . This will then activate Calcium calmodulin

59
Q

What will DAG do in the epinephrine pathway in the liver cell?

A

Activates Protein Kinase C which will phosphorylate Glycogen synthase to make it inactive
(leads to Glycogenolysis)

60
Q

During exercise, Glucose in the muscles can be converted to ______ or to Pyruvate which is then transaminated to _______ and both shuttled to the liver for use as substrate for _____.

A

Lactate

Alanine

GNG

61
Q

Glucocorticoids are all synthesized by starting with _________ and are for long term survival.

A

Cholesterol

62
Q

Synthesis and secretion of Glucocorticoids is controlled by ________signaling.

A

neuroendocrine

any number of factors upon the Hypothalamus to signal release down the line

63
Q

What two neurotransmitters will signal the brain to release ______ after they are signaled themselves by the Hypothalamus .

A

Acetylcholine
Serotonin
(monoamines above)

CRH

64
Q

AcetylCholine and serotonin will target cells in the _____ ______ to release ______.

A

Paraventricular nucleus

CRH (cortisol releasing hormone)

65
Q

CRH (cortisol releasing hormone) is released and will target cells specific in the pituitary gland, these cells will release ______ into general circulation.

A

ACTH - this will then travel and target the Adrenal gland to initial synthesis of Cortisol

66
Q

Cortisol release from the Adrenal glands will provide a negative feedback loop by inhibiting the release of ____ from Hypothalamus and the _____ from the Pituitary.

A

CRH

ACTH

67
Q

What is the rate limiting step in the synthesis of Cortisol from Cholesterol?

A

First step in synthesis pathway when Cholesterol is converted to :
Pregnenolone

68
Q

In the muscles, Glucocorticoids will ______ protein degradation, ____ protein synthesis, and ______ glucose utilization.

A

Increase degradation

Decrease synthesis

Decrease utilizaiton

69
Q

In the Adipose, Glucocorticoids will increase ________ for their fuel avaliability.

A

Lipolysis of TG

70
Q

Glucocorticoids can increase the synthesis of ____________ in the Liver, this is the enzyme that is required for GNG.

A

PEP-carboxykinase

71
Q

Glucocorticoids will _______ GNG and _____ glycogen storage. This occurs so that when_______ is released, there can be rapid entry of Glucose into the blood.

A

enhance

increase

epinephrine

72
Q

Glucocorticoids (cortisol) will cause the normally opposed GNG and Glycogen synthesis to increase together by increasing _________ like AA, and increasing transcription of _________.

A

precursors (AA from muscles)

PEPCK (PEP carboxykinase)

73
Q

Increases in Cortisol levels can result in the symptoms of _____ ____ and ______ _____.

A

Weight Gain

Central Adiposidy

74
Q

Patient A - 41 year old female presents with High blood cortisol level, fatigue, weakness, lethargy, gained 40lbs in 2 months (central obesity and neck obesity) . Her physical examination was remarkable for ______ _______ with weight of 211 lbs.

A

Cushingoid appearance

75
Q

In Patient A, Cortisol levels were elevated but ACTH was reduced. What does this suggest about the location of the defect?
Is the elevated cortisol a primary or secondary defect?

A

Location = Tumor in Adrenal Gland (high cortisol but low ACTH)

Primary Defect

76
Q

In Patient A, the tumor in the adrenal gland will increase Cortisol output, this will cause negative feedback and inhibit _____ at the pituitary gland, and _______ at the Hypothalamus level.

A

ACTH release

CRH release

77
Q

T4 is also called ?

T3 is also called?

A

(3,5,3,5)Tetra-iodothyronine

(3,5,3)Tri-iodothyronine

78
Q

The two secreted Thyroid hormones called :
T4 -is also called ?

T3 -is also called?

A

(3,5,3,5)Tetra-iodothyronine

(3,5,3)Tri-iodothyronine

79
Q

The majority of Thyorid hormone is bound, and it is only the small portion of free hormone that has ______ activity This free form is able to cross membranes freely and bind intracellular receptors.

A

Biological

80
Q

Both T3 and T4 contain the skeleton of _______ residues. From here they are modified by the addition of _____ to the rings.

A

Tyrosine

Iodine

  • T3 has 3 iodines
  • T4 has 4 iodines
81
Q

T3 and T4 production required the first synthesis of __________ and then are only released once it has been degraded.

A

Thyroglobulin

82
Q

Synthesis of T3 and T4 starts with a ______ _____ that moves Na+ and Iodine into the Thyroid follicular cell.

A

Sodium-iodide symport

83
Q

The movement of Iodine into the cell requires energy , so the symport is coupled to a _______

A

Na+-K ATPase

-pump to keep a electrochemical concentration gradient

84
Q

Once in the cell, the Iodine is oxidized by ______ _______. This enzyme is located at the apical brush border.

A

thyroid peroxidase

85
Q

The oxidation of Iodine once in the cell by thyroid peroxidase will form an ________ (I+). This will be what moves out of the cell into the Colloid space and reacts with ______residues.

A

Iodinium Ion

Tyrosine

86
Q

Where is the Thyroglobulin protein stored that the Iodinium ion (I+) will react with?

A

Colloid space

87
Q

To make T4 , you have a couping of 2 ___________

A

Di-Idonatedtyrosine (DIT)

88
Q

To make T3 you have a coupling of ______ and ______.

A

DIT

MIT (monoiotosine-tyrosine residue)

89
Q

Once the T3 and T4 are synthesis, they can be stored by staying bound to the _______ and remain in the _____ space.

A

Thyroglobulin (Tgb)

Colloid

90
Q

The release of Thyroid hormone is different from other peptides as it is not released in a pro-form to be cleaved for activation, rather , the Tgb+T3 or T4 goes back into the cell through _______ from the colloid space.

A

Pinocytosis

91
Q

Once the Tgb+T3 (T4) is in the cell again and out of the Colloid space, it is degraded by Lysosomes proteases , what then occurs?

A

The Tgb is degraded by lysosomes but the T3 and T4 are now free to be released into circulation out of the cell.

92
Q

T4 is in ______ concentrations in the blood . However ______ is though to be the more biologically active form in the body.

A

higher

T3

93
Q

T3 has a much shorter half-life between ____ and ____ days.

T4 has a half-life of about ______

A

1 and 1.5 days

7 days

94
Q

One thing to note is that T3 and T4 are not found in appreciable amounts in ______ ______. It will mainly travel through blood bound to ____.

A

blood circulation

Tgb

95
Q

A contributing factor that T3 and T4 are not readily in blood is because of what feature of seroids?

A

they can cross cell plasma membrane very easily and leave the circulation

96
Q

Thyroid Hormones in the body are primarily controlled by _________ _______.

A

Thyroid-secreting hormone

TSH

97
Q

TSH is released from the _____ in a circadium patter (wave like ).

A

Pituitary

98
Q

What does the Hypothalamus release to target the Pituitary for release of TSH?

A

Thyroid Release Hormone (TRH)

99
Q

Thyroid secreting hormone (TSH) from the anterior pituitary will reach the _____ and activate many different processes. It acts on a _______ ____ on the thyroid.

A

Thyroid

G-Protein coupled receptor

100
Q

In the presence of TSH, then ____ and ____ will be released. These can impact the peripheral tissue, and specifically ____ will feedback and inhibit the activity of ____ and _____.

A

T3 and T4

T3

TRH
TSH

101
Q

TSH is secreted from the Pituitary Gland and will bind a _______ receptor on the surface of the Thyroid ______ cells.

A

G-coupled Protein

Follicular

102
Q

The activation of the G-protein coupled receptor by TSH will increase what 3 things?

A
  1. Expression for synthesis for Tgb
  2. Activity of Iodine Transporter increases (calcium mediated boost)
  3. Expression of Thyroid peroxidase (required for oxidation of Iodine before added to Tgb)
103
Q

As the T3 and T4 bound to Tgb translocates through the cell through pinocytosis, ______ and ______ will digest the Tgb leaving T3 and T4 to diffuse outside cell.

A

Proteases

Peptidases

(from lysosomes)

104
Q

What is the primary negative feedback regulating thyroid hormone release from the thyroid?

A

T3 will provide negative feedback at the pituitary gland preventing TSH from being released

105
Q

T3 and T4 can be taken up by cells and will function as _____ _____ to illicit gene expression and ____ ______.

A

Transcription factors

Protein synthesis

106
Q

The physiological changes caused by Thyroid hormones in the liver include:

  • ________ Glycolysis
  • ________synthesis
  • Conversion of cholesterol to ____ salts
  • TAG _______
  • _____Hepatic Glucose secretion during fasting
A

Increased
CHolesterol

bile

synthesis increses

increases (increases sensitivity to epinephrine)

107
Q

The same bipolar impact of Thyroid hormones on the liver is seen in adipose, it can both:

  • Increase Lipolysis by_______
  • Increase Lipogenesis by ______
A
  • increases sensitivity to epinephrine (more break down of FA)
  • direction determined by insulin and glucose levels
108
Q

In the skeletal muscle, thyroid hormone will:
Increase glucose ______.
Stimulate protein ______.
Enhance Glycogenolysis by _______

A

uptake

synthesis

increasing sensitivity to epinephrine

109
Q

In the pancrease, Thyroid Hormone will _______ sensitivity of beta cells to release ______. Thyroid hormone is actually _______ for sufficient release of insulin from the pancreas.

A

increase

Insulin

required

110
Q

Thyroid Receptor (TR) is bound to DNA and in the abscence of T3/T4 functions as a ________ on gene expression. It can dimerize with different receptors (Homo dimers with same or Heterodimers with retinoic).

A

repressor

111
Q

Binding of T3 to its Thyroid receptor on sitting on the DNA will cause a conformational change that activates the _______ _____. This is done through activation of a _____ ____.

A

Transcriptional complex

Histone Acetylation domain (HAC- domain)
-allows for opening of DNA and accessibility for transcription

112
Q

Cortisol has its receptor in the ______ and its receptor will require ligand binding before translocation to the ______.

A

cytosol

nucleus (sit on DNA)

113
Q 
11 Year old female- Patient B- presents with high weight loss, heat intolerance, decline in grades at school, family hx for thyroid disease in both grandmothers.
Test results:
T3= very high at 374
TSH =low
T4 = elevated 
This was confirmed as \_\_\_\_\_\_ disease.
A

Graves disease

-hyperthyroidism with thyrotoxicosis

114
Q 
In Patient B with Graves disease:
T3= very high
TSH = low
T4 = high
Why is the TSH low? Where is the defect?
A

TSH is low because there is inappropriate release of T3 from the Thyroid which is then inhibiting TSH release from Pituitary

Defect is in the Thyroid

115
Q

To explain the heat intolerance in Graves disease:

Cold stimulus will signal Hypothalamus to release ________.. This will signal via _______ receptors on ________ cells.

A

Norepinephrine
-(Catacholamine)

G-coupled protein

Brown fat cells

116
Q

To explain the heat intolerance in Graves disease:

The G-protein receptor activation will increase _________ which functions as an _________.

A

Thermogenin

Uncoupler

117
Q

Thermogenin is an _______ and will dissipate the proton gradient and Heat is released as the gradient is not coupled to synthesis of _____.

A

uncoupler (protein)

ATP

118
Q

At the same time the Epinephrine is stimulating Thermogenin activity in brown fat cells, it is stimulating _____ break down and making a lot of _____ and ____. This can be rapidly oxidized in ETS and since its uncoupled releases excess heat.

A

Triglyceride

NADH

FADH(2)

119
Q

To explain the heat intolerance in Graves disease:
Elevated ____ will enhance the signaling of _______ in brown fat. This leads to an abnormal increase in FA oxidation and abnormal thermogenin production all leading to high heat production in ETS.

A

T3

Norepinephrine (NE)
-T3 increases cell sensitivity to E and NE

Biochemistry (20 decks)

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