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FHB II > Endocrine Lecture 5 > Flashcards

Endocrine Lecture 5 Flashcards

1
Q

Pancreas:

Exocrine vs Endocrine Pancreas

A

Exocrine pancreas: majority of cells, acinar cells secrete digestive enzymes “pancreatic juice” into pancreatic duct

Endocrine pancreas: consists of 3 major cell types clustered in groups called the islets of Langerhans

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2
Q

Explain the following endocrine pancreas cell types:

Explain which hormones they secrete and how abundant are they?

Beta Cells

Alpha Cells

Delta Cells

Epsilon Cells

A

Beta Cells (most abundant, 75%) secrete insulin

Alpha cells (20%) secrete glucagon

Delta cells (5%) secrete somatostatin (SS14)

Epsilon Cells (<1%) secrete ghrelin

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3
Q

What are the major and minor pancreatic hormones

A

Major Hormones: insulin (energy storage…anabolic hormone), glucagon (energy mobilization…catabolic hormone)

Minor: somatostatin, amylin, ghrelin

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4
Q

Explain the arrangement of alpha and beta cells in humans

Beta cells are clustered in the “____” while alpha cells are “______”

_____ effects between beta and alpha cells

A
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5
Q

Explain the flood flow pattern within the islet of langerhans

Arterioles that feed the islet come straight into the _____ (beta cells respond to _____)

Cells on outside are then___

A

Arterioles that feed into the islet come straight into the center (beta cells respond to blood glucose)

Cells on outside are then hit with hormones from beta cells (so insulin directly affects alpha and delta cells but the outside do not affect the inside cells)

Insulin rich blood flows from the center to the periphery islet

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6
Q

Insulin Synthesis:

Half life of insulin is _____

Insulin and ____ are released together

___ half life is _____: making it a good indicator of pancreatic function

Cleavage of _____ is critical for the insulin to be able to interact with its receptor

A

Insulin synthesis:

Half life of insulin is 3-8 minutes

Insulin and C peptide are released together

C peptide half life is 35 minutes: making it a good indicator of pancreatic function

Cleavage of C peptide is critical for the insulin to be able to interact with its receptor

(Note: endogenous insulin is what has C peptide, if you inject someone with EXogeneous insulin, it will NOT have c peptide)

You can measure C peptide in blood to see if someone is making endogenous insulin or not

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7
Q

Explain the seven steps of insulin release (look at the sheet)

A
  1. Glucose is high in the blood outside the beta cell and the beta cell senses it
  2. Glucose gets transported inside the beta cell by GLUT-2 (low affinity transporter, only active when glucose is high)…. glucose gets phosphorylated by GK, and the metabolism of G6P generates ATP

3/4. The ATP generated from the glucose 6 metabolism closes K+ channels

5/6: increased K inside the cell causes cell membrane to depolarize, opening voltage gated calcium channels

  1. Calcium influx causes exocytosis of insulin containing vesicles
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8
Q

Describe the basis of the biphasic response of insulin release following ingestion of a meal

A

Biphasic Insulin Response:
Insulin release is biphasic in response to glucose

5% of vesicles are available for immediate release - docked at membrane

95% are “stored” or reflext newly synthesized insulin

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9
Q

Insulin Receptors:

Receptor Tyrosine Kinases

Insulin binds receptor at ____ subunit

_____ is autophosphorylated

Autophosphorylation of receptor recruits IRS (insulin receptor substrates)

IRSs activate intracellular signaling cascades (explain the two intracellular cascades for insulint)

A

Insulin Receptors:

Receptor Tyrosine Kinases

Insulin binds receptor at alpha subunit

Beta subunit gets autophosphorylates

Autophosphorylation of receptor recruits IRS (insulin receptor substrates)

IRSs activate intracellular signaling cascades:

  1. AKt - metabolic actions
  2. MAPK: mitogenic actions
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10
Q

Insulin Receptors:

AKt pathway: muscle and adipose tissue

What is the glucose transporter for muscle and adipose tissue?

A

AKt pathway: all anabolic effects

GLUT 4 translocation in muscle and adipose tissue to get glucose into skeletal muscle and adipose tissue (GLUT 4 is insulin dependent)

AKT promotes anabolism so it promotes glycolysis, protein synthesis

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11
Q

Explain the following glucose transporters

GLUT 1

GLUT2

GLUT3

GLUT4

GLUT5

A

GLUT1: brain vasculature, insulin independent

GLUT2: pancreatic beta cells, liver, intestine, insulin indendent, but low affinity, only works when glucose is high

GLUT3: neurons, major transporter in brain

GLUT4: only one that is insulin dependent, in skeletal muscle and adipose tisse

GLUT5: sperm

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12
Q

Insulin: Physiological Effects on Adipose Tissue:

Primary action is energy ______

promotes _____ production

release of ___ from _____

inhibits lipolysis

glucose enters adipose tissue via which transporter

A

Insulin: Physiological Effects on Adipose Tissue

Primary action is energy storage

Promotes TG production

release of FFA from chylomicrons, glycolysis (for energy to make TG)

inhibits lipolysis

Glucose enters via GLUT 4

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13
Q

Insulin: Physiological Effects on Muscle

Primary action is ______

Muscle: promotes ____ and ____ production, and protein ______

Glucose enters through _____ (transporter)

A

Insulin: Physiological Effects on Muscle:

Primary action is energy storage

Muscle: promotes glycogen and TG production, protein synthesis

Glucose enters through GLUT 4

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14
Q

Insulin: physiological effects on liver:

Liver: promotes ___ and ____ production

____ glucose production output via:

  • inhibits _____ (enzyme)
  • stimulates ______ synthesis (enzyme)

Glucose enters liver via _______ (transporter)

A

Insulin: Physiological Effects:

Primary action: energy storage:

Liver - promotes glycogen and TG storage, reduces glucose production output:

  • inhibits glucose 6 phosphatase
  • stimulates glucokinase synthesis

Glucose enters liver via GLUT 2

note: the creation of TG in the presence of high glucose creates “fatty liver”

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15
Q

Glucagon Synthesis:

Products from the Pancreatic A cell include?

PRoducts from intenstinal L cell include?

  • ______ (GLP-1 and GLP-2) are important in clinical use
  • synthesizes from the same prohormone as glucagon
  • tissue specific enzymatic activity
  • Intestinal GLP is timulated by ______
A

Glucagon Synthesis:

Products from pancreatic a cells: active glucagon and inactive copeptides

Products from intestinal L cell: inactive glucagon-GRPP but active GLP-1 and GLP-2

Incretins (GLP-1 and GLP-2) are important clinical use

Synthesized from same prohormone as glucagon

Tissue specific enzymatic activity

Intenstinal GLP is stimulated via CARBS

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16
Q

Glucagon Release:

Major counterregulatory hormone to insulin - most things that stimulate insulin will ____ glucagon

Released in response to ___ glucose levels

What two things (other than low glucose) stimulate glucagon?

A

Glucagon Release:

Major counterregulatory hormone to insulin - most things that stimulate insulin will inhibit glucagon

Released in response to low glucose levels

AAs stimulate release (protein meals)

Catecholamines stimulate release (exercise)

17
Q

Insulin Release: Other modulatory pathways:

GLP-1 (incretins):

  • Produced in ___ by ___ cells
  • Released in response to high ____

Potentiate insulin release by increasing intracellular calcium

Degraded by ____ enzyme

Drug target for T2DM

A

GLP-1: (incretins:

-Produced in intestine by L cells in response to high carb meal

Potentiate insulin release by increasing intracellular calcium

Degraded by DPP-4 enzyme

Drug target for T2DM

18
Q

Protein/AA - metabolism generates ATP which can increase intracellular calcium _______ insulin released from protein alone

NE/EPI directly ___ insulin release from beta cell through activation of ______ receptors (decreases cAMP and prevents increase in intracellular Ca)

Action at ______ receptor is minor and contributes primarily to basal release

A

Protein/AA: very little insulin release from protein alone

NE/Epi (catecholamines) directly inhibit insulin release through activation of alpha-2 adrenergic receptors

Action at beta-2 is minor and contributes to basal release

19
Q

Glucagon Actions:

Primary action: _______

Main targets are _____ and ____

There are NO glucagon receptors in ______

Glucagon is ____ of insulin

A

Glucagon Actions:

Primary actions: energy mobilization

Main targets: liver and adipose tissue

There are NO glucagon receptors in skeletal muscle

Opposite effects of insulin

20
Q

Somatostatin (SS14)

  • produced by ____ in pancreatic islet
  • stimulated by ______ meals
  • _____ by insulin
  • how is it used to treat insulin producing tumors

Amylin:

  • released with ______
  • synergistic with insulin in regulation of blood glucose
  • circulating amylin is ___ with obesity
A

Somatostatin (SS14)

  • produced by delta cells in pancreatic islet
  • stimulated by high fat, high carb meals
  • inhibited by insulin (just how it works paracrine wise)
  • SS14 is used to treat insulin producing tumors because it will supress insulin release

Amylin:

  • released with insulin and C peptide in secretory vesicles
  • synergistic with insulin in regulation of blood glucose
  • circulating amylin increased with obesity, HTN
21
Q

What is used to treat insulin producing tumors

A

Insulin producing tumors:

treated with SS14 (supress insulin release)

22
Q

Ghrelin:

most circulating ghrelin is produced in the stomach

  • Stimulates food intake at the hypothalanus
  • _____ Gh release

______ relationship between ghrelin and obesity

Produced in ____ cells of islet

Paracrine action on beta cells:

____ insulin

A

Ghrelin: the stomach gremlin stimulating to your brain that you are hungry and food deprived

Stimulates food intake at the hypothalamus

STIMULATES GH release

inverse relationship between ghrelin and obesity

Produced in EPSILON cells of islet

Paracrine action on beta cells: ghrelin will inhibit insulin release (makes sense because you are already low in blood sugar, don’t need to be any lower)

23
Q

When you haven’t eaten in a while:

what is released first

what is then released after 6 hours

A

When you haven’t eaten in a while and your blood glucose starts to go down

Glucagon - primary

Then cortisol and growth hormone are released 6 hours later (defense against prolonged hypoglycemia)

24
Q

Catecholamines : ____ plasma glucose levels, increased during exercise and stress

Catecholamines: Epi:

  • ______ insulin release
  • ______ glucagon release
  • ____ hepatic glucose output
  • ______ glucose uptake in skeletal muscle
A

Catecholamines: raise plama glucose levels

Catecholamines; EPI:

  • inhibit insulin release (a2 receptor)
  • stimulate glucagon release
  • increase hepatic glucose output
  • decrease glucose uptake in skeletal muscle
25
Q

When insulin is present:

AA from proteins stimulate _____ which stimulates ____ (liver)

IGF-1 then stimulates protein uptake in ______

GH opposes insulin lipogenesis

A

When insulin is present:

AA from proteins stimulate GH which stimulates IGF-1

IGF-1 then stimulates protein uptake in muscle, proliferation of visceral organs

GH opposes insulin lipogenesis (this is why you don’t get fat every single time you eat)

26
Q

Prolonged Fasted State:

Brain needs constant supply of glucose

Initial source of glucose:

____ from fat stores (release of FFAs, breakdown liver glycogen, breakdown of protein)

Then a metabolic shift happens, where ____ are used as main energy source for the brain (this is due to ____)

Reduced reliance on glucose as fuel source

A

Prolonged Fasted Staet:

Brain needs constant supply of glucose:

Initial source of glucose is breaking down glycogen from liver, then breakdown fat stores (80%) and also start to break down proteins

BUT, those AA’s from the breakdown of proteins will stimulate GH, and GH will then cause a metabolic shift, stop breaking down protein so readily and switches to ketone bodies

Metabolic switch: ketone bodies used as energy source for brain

27
Q

Metabolic Syndrome:

What are the four components of being diagnosed with metabolic syndrome

A

Metabolic Syndrome:

Visceral obesity

Insulin resistance (fasting glucose above 100)

dyslipidemia

Hypertension

28
Q

The primary hormone released by adipocytes is called ______

What is SREBP-1C?

What is PPARy?

A

Primary hormone released by adipocytes is called LEPTIN

SREBP-1C is activated by insulin and lipids to promote TG synthesis

PPARy: is a nuclear receptor that regulates TG storage

29
Q

There is a _____ relationship between plasma leptin and total fat

A

There is a DIRECT relationship between leptin and total fat

30
Q

******(there will be a question on the test about this)

Leptin’s overall goal is to decrease food intake (body telling you that you have enough to eat)

Leptin does that by _______ apetite stimulators

and ______ apetite inhibitors

Therefore leptin ______ Neuropeptide Y and AGRP

Leptin _______ aMSH and CART

A

Leptin’s overall goal is to decrease food intake

Leptin does that by inhibiting apetite stimulator and stimulating apetite inhibitors

Leptin INHIBITS Neuropeptide Y and AGRP (apetite stimulators)

Leptin STIMULATES/activates aMSH and CART

FHB II (14 decks)

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