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Biochem > Hormones and Integrated Metabolism > Flashcards

Hormones and Integrated Metabolism Flashcards

1
Q

Neuronal Signaling VS. Hormonal Signaling

A

Neuronal Signaling:
- release transmitters that act on nearby cells (small distance)

Hormonal Signaling:
- hormones are carried by bloodstream to nearby cells or other organs (long distance)

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2
Q

What is the challenge in detecting hormones? What was developed as a way to measure hormones?

A
  • Challenge in detecting: Hormones are produced in small amounts -> hard to purify in appreciable quantity
  • RIA (radioimmunoassay): more sensitive way to measure hormones using radiolabeled antibodies
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3
Q

Features of Hormone-Receptor Interactions

A
  • Specific Interactions
  • High affinity: only low amounts of hormone are needed
  • Different types of cells have different receptors
  • Different cells with same receptor can have different downstream effects
  • Similarly structured hormones can bind different receptors
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4
Q

What are the three classes of hormones based on pathway from release to target?

A

Classification based on path from release -> target

1) Paracrine: released into extracellular space to neighboring target (ex: eicosanoids)
2) Endocrine: released to blood, carried to target cells (ex: insulin, glucagon)
3) Autocrine: affects the cell where they are produced
- Binds to surface receptors

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5
Q

What are the five types of “downstream” events that happen following hormone binding?

A

1) Secondary messenger (cAMP, IP3) is released inside the cell: allosterically regulates enzymes
2) Tyr kinase receptor is activated
3) Hormone-gated ion channel is open or closed -> causes changes in membrane potential
4) Adhesion receptor (ligands, adhesions) sends info to the cytoskeleton -> promote movement/growth
5) Steroid (that’s bound to receptor protein in nucleus) alters gene expression -> acts as a transcription factor b/c it can go through nuclear membrane

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6
Q

Extracellular and Intracellular Hormones

A

Extracellular: Cell surface receptors
- Can be metabotropic or ionotropic
- Hormone binds to receptor on outside of cell and acts though the receptor (doesn’t enter cell)

Intracellular: Nuclear receptors
- Steroid or Thyroid hormone enters cell, acts in the nucleus

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7
Q

What are the 8 classes of hormones based on chemical structure?

A

Plasma membrane receptors; 2nd messengers:
1) Peptide: Insulin, Glucagon
2) Catecholamine: Epinephrine
3) Eicosanoid: Prostaglandin E2

Nuclear receptors; transcriptional regulation:
4) Steroid: Testerone
5) Vitamin D: Calcitriol
6) Retinoid: Retinoic acid
7) Thyroid: T3

Cytosolic receptor and cGMP:
8) Nitric Oxide

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8
Q

What hormones are made from peptide and amine? (Insulin, Epinephrine)

A

Insulin: peptide hormone
Epinephrine: amine hormone

  • Binds to receptors that span the membrane (on outside) and cause conformation change that produces a 2nd messenger -> results in signal amplification
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9
Q

How is Insulin (peptide hormone) produced? Where is insulin stored?

A
  • Synthesized on ribosome of beta cells as preproinsulin and processed into insulin
  • Stored in secretory vesicles in beta cells
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10
Q

Why is Insulin made? What receptors do Insulin bind to?

A

Insulin is made in response to increased blood glucose levels. It binds to receptors in the muscle, brain, liver, adipose tissues, other tissues.

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11
Q

What is the role of insulin in muscles, liver, and adipocytes?

A
  • In muscle: facilitates glucose uptake
  • In liver: promotes glycogen synthesis
  • In adipocytes: promotes glycerol synthesis and inhibits breakdown of fats
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12
Q

What products does POMC (Pro-Opiomelanocortin) make? (peptide pro-hormones can make multiple products)

A
  • Has at least 8 different cleavage sites
  • Produces at least 10 different peptide hormones
  • Mutations in POMC are associated with obesity
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13
Q

What hormones are made from catecholamine?

A

Epinephrine and Norepinephrine
- Synthesized in adrenal glands from L-tyrosine (AA)
- Concentrated in storage vesicles and released
- Binds to extracellular receptors to generate secondary messengers

(Tyrosine -> Dopamine -> Norepinephrine -> Epinephrine)

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14
Q

What hormones are made from Eicosanoid?

A

Prostaglandins, Thromboxanes, Leukotrienes
- Not made in advanced: made when needed from arachidonic acid via phospholipase A2
- They are paracrine hormones (act nearby)
- Role in inflammation, smooth muscle contraction and platelet function

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15
Q

What hormones are made from Cholesterol?

A

Steroids: Cortisol, Testosterone, Estradiol
- binds to carrier proteins, travel through bloodstream
- enters the cell nucleus and binds to nuclear receptors (acting as transcription factor) to alter gene expression

(Cholesterol -> Progesterone -> Steroids)

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16
Q

What type of receptor does Vitamin D hormone bind to?

A

Nuclear receptor
- Vitamin D is obtained from good or sun exposure
- Active form of Vitamin D: calcitrol
- Affects the transcription of genes that regulate Ca2+ and the balance between Ca2+ deposition and removal from bone

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17
Q

What causes Rickets?

A

Lack of vitamin D

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18
Q

What type of receptors do Retinoid hormones bind to?

A

Nuclear receptors
- Retinoid hormones come from vitamin A1 (retinol) which is from b-carotene
- All cells have at least 1 form of retinoid receptor
- Hormone-receptor complex regulates genes that have roles in cell growth and differentiation

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19
Q

What type of receptors do Thyroid hormones bind to?

A

Nuclear receptors

Thyroglobulin (precursor) makes T4, which is converted to T3
- T3: has 3 iodines at Tyr residues
- T4: has 4 iodines at Tyr residues

Receptor-Hormone complex increases expression of enzymes that yield energy

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20
Q

What type of receptor does Nitic Oxide interact with?

A

Intracellular receptor

NO: free radical made from arginine and O2, by the enzyme NO synthase
- acts locally (near point of its release)
- enters target cell and activates guanylyl cyclase to increase cGMP -> activation of cGMP-dependent protein kinase, relaxation of contractile protein in smooth muscle of blood vessels (lowers blood pressure)

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21
Q

What are the major endocrine glands?

A
  • Brain: hypothalamus, pituitary
  • Thyroid, Parathyroid
  • Adipose (fat) tissue
  • Adrenals (on top of kidneys)
  • Pancreas
  • Ovaries/Testes
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22
Q

What is Top Down vs. Bottom Up hormone signaling?

A

Top-Down signaling:
- signals start in the brain and sent out to the body (ex: oxytocin, cortisol, etc)

Bottom-Up signaling:
- signals start from somewhere in the body and send messages to the brain (ex: epinephrine (adrenaline), insulin)

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23
Q

What is the hypothalamus?

A

It is the coordination center of the epinephrine system. It is located in the forebrain.
- Receives and integrates nerve signals from the CNS
- Synthesizes peptide hormones: oxytocin, vasopressin
- Synthesizes factors that regulate the function of the anterior pituitary

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24
Q

What is the pituitary?

A

The release of hormones from the pituitary targets other glands.

1) Posterior pituitary (neurohypophysis): goes into blood vessels
- has ends of axons from the hypothalamus
- holds short peptide hormones made in hypothalamus
2) Anterior pituitary (adenohypophysis): receives signals from bloodstream
- endocrine organ that receives releasing factors from the hypothalamus via blood vessels
- makes tropins (long peptide hormones)
- activates second targets: adrenal cortex, thyroid, ovaries/testes

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25
Q

What hormones do the Posterior Pituitary make?

A

Oxytocin and Vasopressin: both play roles in social behavior

  • Oxytocin promotes: contraction of uterus during labor, milk release from mammary gland
  • Vasopressin promotes: water reabsorbion in kidneys (maintain salt balance), constriction of blood vessels (increases blood pressure)
26
Q

What is the Hypothalamic Cortisol Cascade?

A

Cortisol = stress hormone

Fear, infection, hypoglycemia, etc sends signals to the hypothalamus. The cortisol end-product feedback and can inhibit these steps (negative regulation)

  • Hypothalamus release: corticotropin-releasing hormone
  • Anterior pituitary: corticotropin (ACTH)
  • Adrenal gland: Cortisol
27
Q

What happens if the cortisol signaling happens for a long time? (Chronic Stress)

A

In instances of chronic stress, it can lead to adrenal fatigue. The adrenal gland doesn’t release as much cortisol, which dampens responses and results in higher susceptibility

28
Q

How does the liver adapt to changing metabolic conditions?

A
  • Portal vein: carries nutrients to the liver
  • Hepatocytes: turn nutrients into fuel
  • Hepatocyte enzymes turn over quickly (adapt quickly to change) -> increase or decrease with changes in diet and needs of other tissues
29
Q

What hormones do pancreatic cells secrete (located in the islets of Langerhans in pancreas)?

A
  • a cells: glucagon
  • b cells: insulin
  • d cells: somatostatin
30
Q

What does insulin stimulate in muscles/fat and the liver?

A

Insulin stimulates conversion of excess glucose to glucogen and/or TAGs

  • In muscle/fat: stimulates glucose uptake (glycolysis happens when G6P is high and makes acetyl-CoA)
  • In fat: stimulates TAG assembly
  • In liver: stimulates glycogen synthase, inactivates glycogen phosphorylase, stimulates fatty acid synthesis from excess acetyl-CoA
31
Q

How does glucose regulation of insulin secretion happen?

A

Glucose enters B-cells via GLUT2, which enters glycolysis causing ATP to increase. ATP binds to ATP-gated K+ channels, which causes K+ channels to close and depolarize the plasma membrane. Depolarization of the plasma membrane triggers the opening of voltage-gated Ca2+ channels, Ca2+ in cytosol triggers the release of insulin into the bloodstream

32
Q

What is the target of Sulfonylurea drugs?

A

ATP-Gated K+ Channels
- K+ channel: octamer of 4 SUR1 (sulfonylurea receptor) subunits and 4 Lir6.2 subunits
- Sulfonylurea drugs close the K+ channel and stimulate insulin secretion -> used to treat type 2 diabetes to overcome insulin resistance

33
Q

How does glucagon raise glucose in the blood?

A

Glucagon does the opposite of Insulin.
It works via cAMP-mediated cascades in the liver.
- Activates glycogen phosphorylase and inactive glycogen synthase
- Inhibits glycolysis, stimulates PEPCK for gluconeogenesis
- Inhibits pyruvate kinase

34
Q

How does glucagon affect adipose tissue to spare glucose for the brain?

A

Via cAMP cascades
- activates TAG hydrolysis (phosphorylates perilipin and activates hormone-sensitive lipase) -> results in fatty acid transport to other tissues -> glucose is spared for the brain

35
Q

How does Epinephrine stimulation of cAMP cascades differ from glucagon?

A
  • stimulates glucagon secretion and inhibits insulin secretion
  • breaks down muscle and liver glycogen
  • stimulates glycolysis -> stimulates lactate formation
36
Q

What happens with glucose after a meal?

A
  • Glucose increases -> Insulin stimulates glycolysis and glycogen synthesis
  • After few hours: Glucose drops, Glucagon secreted, Glucose is released
37
Q

What are the effects of prolonged fasting?

A

Muscles are used for fuel.
- Liver deaminates or transaminates amino acids
- FA is oxidized to acetyl-CoA but oxaloacetate is depleted to make glucose -> leads to ketone bodies being formed

38
Q

Difference between regular state and fasting state

A
39
Q

What does Cortisol (stress hormone) do?

A
  • Promotes FA and glucose release in response to emotions, pain, infection, etc
  • Changes types and levels of enzymes (act as transcription factors)
  • Counteracts effects of insulin
  • Continued release of cortisol leads to adrenal fatigue: less cortisol release
40
Q

What are the two types of Diabetes Mellitus?

A

Type 1: due to insufficient production of insulin
- due to autoimmune destruction of insulin producing b cells in pancreas
- onset: early in life

Type 2: due to insulin resistance
- due to cells not responding to insulin
- onset: late adulthood
- associated with obesity

41
Q

What are the symptoms of diabetes?

A
  • Elevated blood sugar levels -> In response, the body tries to dilute the glucose which leads to excessive urination and thirst
  • In type 1: fat breakdown is accelerated which leads to high production of ketone bodies
    (some ketones are ketoacids -> raise blood H+ -> ketoacidosis
  • Untreated diabetes = dramatic weight loss
42
Q

Monitoring glucose levels

A

High fasting blood glucose level: 126 or higher
- warning sign for diabetes

Low fasting blood glucose level: <50-40
- warning sign of hypoglycemic conditions

After a meal (postprandial): levels are usually higher (up to 145mg/100mL)

43
Q

What are the long-term effects of elevated blood sugar?

A
  • proteins can be glycosylated
  • hemoglobin is abundant
  • increases the risk of cardiovascular disease, renal failure, and damage to small blood vessels/nerves
44
Q

What hormones do Adipose tissue release?

A

Adipose tissue: endocrine organ
- releases adipokines (peptide hormones) that carry info about fuel stores to brain
- includes Leptin and adiponectin

45
Q

What is leptin?

A

Considered an adipokine (peptide hormone)
- protein made by adipose tissue (fat cells) and sent to the brain
- appetite suppressant -> reduces appetite

In the brain: DB gene encodes the leptin receptor (sense that leptin is sent from adipose tissue)

  • Inhibits NPY (appetite-stimulating hormone), stimulates a-MSH (appetite-suppressing hormone)
46
Q

What are the two appetite-related hormones that leptin affects?

A

1) Neuropeptide Y (NPY): orexigenic (appetite-stimulating) hormone
- sends signals to eat and levels of NPY rise in starvation
- NPY is inhibited by leptin and insulin

2) a-MSH (a-melanocyte-stimulating hormone): anorexigenic (appetite-supressing) hormone
- sends signal to stop eating
- release of a-MSH is stimulated by leptin

47
Q

How does leptin increase transcription of the gene that yields a-MSH?

A
  • Receptor dimerizes when leptin binds
  • JAK phosphorylates 2 Tyr in receptor dimer
  • STATS dimerize, move to the nucleus, and stimulates transcription
  • Leptin increases transcription of the gene for the precursor to a-MSH
48
Q

How does Leptin increase thermogenesis via the sympathetic nervous system?

A
  • Stimulates release of norepinephrine cascade via b3-adrenergic receptors
  • Increases UCP1 gene transcription, which increases thermogenesis
49
Q

In what type of individuals does leptin resistance occur in?

A

Obese individuals
- Leptin is usually elevated in cases of obesity -> something downstream in leptin response must be defective

50
Q

How does insulin inhibit appetite?

A

Insulin inhibits appetite by interacting with the hypothalamus. Insulin binds with the insulin receptors in the orexigenic neurons, which inhibits the release of NPY and stimulates a-MSH.

51
Q

Cross-talk between insulin and leptin?

A
  • Leptin makes liver and muscle more sensitive to insulin
  • Common 2nd messenger may enable leptin and insulin to trigger same downstream pathways
52
Q

What hormones are a-MSH and NPY associated with?

A

a-MSH: leptin (adipose), insulin (pancreas)

NPY: ghrelin (stomach, hunger signal)

53
Q

What is Adiponectin made of? Where are its receptors located?

A

Made of adipose tissue, receptors located in the brain
- Makes other organs sensitive to insulin

54
Q

How does adiponectin make other organs sensitive to insulin? What else does it inhibit?

A
  • Works via the AMP-activated kinase pathway: AMPK phosphorylates and inactivates acetyl-CoA carboxylase (that usually makes malonyl CoA, which inhibits FA import into mitochondria) -> FAs free to enter mitochondria for oxidation -> increases FA oxidation, increases insulin sensitivity and decreases glucose production
  • AMPK pathway inhibits cholesterol synthesis
55
Q

What are PPARs (Peroxisome Proliferator-Activated Receptors)?

A
  • In peroxisomes
  • Binds FAs or derivates, then binds to RXR (retinoid X receptor and becomes transcription factors that alter expression of genes for fat/carb metabolism
56
Q

What are the three types of PPAR and it’s functions?

A

1) PPARα (alpha): in liver and muscle
- regulates FA oxidation and mitochondrial uncoupling
2) PPARγ (gamma): in liver and adipose tissue
- regulates genes for lipid synthesis and storage
- activated by thiazolidinediones
3) PPARβ/δ (beta/delta): liver, heart, skeletal muscle
- regulates genes for uptake/oxidation of FA and for ketone body formation
- activated by FA and eicosanoids

57
Q

What is Ghrelin?

A

Short-term orexigenic peptide that’s secreted in the stomach
- ghrelin receptors: in brain, heart, adipose tissue
- works via GPCRs to increase sensation of hunger -> injection of ghrelin increases appetite

58
Q

What is Prader-Willi syndrome associated with?

A
  • High levels of ghrelin
  • Insatiable appetite
59
Q

What is PYY3-36?

A

An appetite-suppressing hormone secreted from small intestine/colon
- secreted in response to food entering stomach
- inhibits release of NPY -> leads to reduced hunger

60
Q

Type 2 Diabetes and Metabolic Syndrome: symptoms?

A
  • Hallmark: resistance to insulin
  • Other symptoms: obesity, high TAGs, low HDL, high blood pressure, elevated blood glucose, other signs of inflammation
61
Q

How does the “Lipid Burden” Hypothesis explain how obesity can lead to type 2 diabetes?

A

In those who are obese, adipocytes become packed and unable to accommodate more TAG. Since adipocytes are unable to deposit TAG, this leads to FA in the blood. Excess FA enters the muscle and liver, creating TAG lipid droplets which cause these organs to lose sensitivity to insulin. This causes blood glucose levels to rise -> Type 2 Diabetes

62
Q

What are treatments for type 2 Diabetes?

A
  • Diet/Exercise
  • Insulin
  • AMPK activator: Metformin (glucophage)
  • PPAR activators (increase adiponectin)
  • Sulfonylureas: stimulating insulin binding ATP-gated K+ channels
  • Prevent degradation of GLP-1 (peptide that stimulates insulin secretion)

Biochem (6 decks)

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