Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > 4.1 Food intake and pancreas > Flashcards

4.1 Food intake and pancreas Flashcards

1
Q

historical view of regulation of food intake
- what are the 2 hypothesis?

A
  1. lipostatic hypothesis (Kennedy, 1953), adipose tissue produces a “lipostatic” factor (chemical) –> regulates food intake –> how much fat should body accumulate –> based on animal hibernation
  2. glucostatic hypothesis (insulin was already discovered) (Mayer& Thomas 1967): fluctuations in glycaemia lead to stimulation/inhibition of food intake
    - every food intake regulation is to serve the homeostatic glucose concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

physiological regulation of food intake is a complex _________ process that is regulated by many _______ and _______ factors
- other influencing factors include (7)

A
  • complex homeostatic process
  • many endocrine and metabolic factors
  • visual, olfactory, taste sensation, emotions, memory, life conditions (stress), culture/customs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which gastrointestinal hormone was first discovered? then which one?
- these hormones impact ______ ______ –> which impact metabolism, which impacts everything in life

A
  • secretin! (1902), then gastrin
  • impact food intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

name hormones (+ functions ish) produced in:
- stomach (2)
- duodenum (4)

A

STOMACH:
- ghrelin (hunger + growth hormone release)
- gastrin (acid secretion)
DUODENUM:
- cholecystokinin (gall bladder contraction, GI motility, pancreatic exocrine secretion)
- secretin (pancreatic exocrine secretion)
- gastrointestinal peptide (GIP) (incretin activity)
- motilin (GI motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

name hormones (+ functions ish) produced in:
- pancreas (3)
- small intestine/colon (4)

A

PANCREAS:
- insulin and glucagon (glucose homeostasis)
- pancreatic polypeptide (gastric motility and satiation)
- amylin (glucose homeostasis + gastric motility)
COLON:
- GLP-1 (incretin activity + satiation)
- GLP-2 (GI motility and growth)
- oxyntomodulin (satiation + acid secretion)
- PYY (satiation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define pancreatic exocrine secretion + incretin activity
(both are functions of GI hormones)

A

PANCREATIC EXOCRINE SECRETION:
- helps digestion and absorption
INCRETIN ACTIVITY:
- any chemical signal that modulates glucose homeostasis by regulating insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what (2) are crucial in central regulation of feeding/food intake? their functions ish
- in one of those regions, there is integration of (4)
- which 2 nuclei connects the 2?

A
  • hypothalamus (regulatory center) + brain stem (fundamental central nervous system –> controls fundamental living processes of body)
  • hypothalamus –> integration of brain neurotransmitters, peripheral neurohumoral afferents, adipocyte-derived signals, GIT peptides
  • nucleus tractus solitarius and PVN –> connects brain stem with hypothalamus (serotoninergic neurons)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 5 “things”/centers that have a role in feeding regulation? (apart from hypothalamus, brainstem and nucleus tractus solitarius)

A
  1. ventromedial hypothalamus (VMH) –> satiety center = tells you when you’re full
    - lesion leads to hyperphagia (ie animals that don’t have VMH don’t have control of how much they eat, so they overeat)
  2. lateral hypothalamus nucleus –> hunger center = tells you to find food
    - lesion leads to anorexia
  3. suprachiamic nucleus (SCN) –> light entrainment regulates circadian rhythm –> timing –> lesions in humans lead to hight hyperphagia and obesity
  4. PVN and ARC –> integrate signals from hypothalamus-pituitary-thyroid (HPT) axis and HP-adrenal axis
  5. vagus nerve (direct neuronal regulation) –> satiety signals to brain stem after ingestion of a meal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

all neuronal and hormonal regulation feed through which 2 neurons?
- these 2 neurons receive & integrate ___(2)______ input from what?
- describe both neurons
- what nucleus are they from?

A

a-MSH and NPY neurons! –> receive and integrate hormonal & metabolic input from peripheral organs
- a-MSH –> regulate neurons that stimulate anorexia (stop eating) and catabolism (spend energy/metabolize more)
- NPY neurons –> regulate neurons that stimulate orexia (food intake) and anabolism (store energy/metabolize less)
- arcuate nucleus!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which hormones from adiposity signal, satiety signal and hunger signal are anorexigenic vs orexigenic hormones?

A

ADIPOSITY SIGNALS
- leptin (more adipose tissue = more leptin) –> main anorexigenic hormone: stimulates a-MSH (supports lipostatic homeostasis) and inhibits NPY
- insulin (from pancreas): anorexigenic –> inhibits NPY
SATIETY SIGNALS:
- PYY and GLP-1 (from gut): anorexigenic –> both inhibit NPY
HUNGER SIGNALS:
- ghrelin (stomach): orexigenic –> stimulates NPY neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • what is the active ingredient in marijuana? mainly signals through what receptor?
  • what are the 2 endocannabinoid hormones? –> both have what as a precursor?
  • what are the 2 receptors for endocannabinoids? through which signalling pathway?
  • receptors are mainly expressed where?
  • how to regulate [hormone] at tissue level?
A
  • THC –> CB1 receptor
  • anadamide (AEA) and 2-arachidonoylglycerol (2-AG) –> both come from arachidonic acid
  • receptors: CB1 and CB2 –> GPCR with Gai (inhibits cAMP)
  • CB1 –> highly expressed in CNS
  • CB2 –> highly expressed in PNS
    *but both are expressed in both
  • local/tissue metabolizing enzymes for endocannabinoids –> metabolize AEA & 2-AG are local level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

endocannabinoid system:
- overall effect depends on what?
- net effect of system? on metabolism

A
  • depends on type and amount of CB1 vs CB2
  • net effect of anabolism! store energy and decrease catabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens when CB1 is inhibited?
- hypothalamus (1)
- adipose tissue (2)
- muscle (2)
- liver (1)
- GI tract (1)
THUS, OVERALL EFFECT OF ENDOCANNABINOID SYSTEM?

A

HYPOTHALAMUS:
- decrease food intake
- weight loss + reduced waist circumference
ADIPOSE TISSUE:
- increase adiponectin (opposite of leptin) + decrease lipogenesis
- reduces visceral fat + improved lipidemia + insulin sensitivity
MUSCLE:
- increase glucose uptake and increase o2 consumption (= glycolysis)
- enhances insulin sensitivity
LIVER:
- decrease lipogenesis
- improved lipidemia and insulin sensitivity
GI TRACT:
- increase satiety
- weight loss (increase catabolism)
OVERALL EFFECT:
- inhibit CB1 = weight loss = increase catabolism
- endocannabinoid system –> anabolic effects!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 2 cell types in exocrine pancreas?
- secreted into what?

A
  1. acinar cells –> secretion of digestive enzymes (proteases, amylases, lipases)
  2. duct cells –> secretion of NaHCO3
    - secreted into duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

endocrine pancreas consists of what?
- 5 types of cells that secrete what hormone?
- hormones are secreted into what?

A
  • islets of Langerhans (3 million islets, 1-2gm)
    1. a-cells –> glucagon
    2. b-cells –> insulin –> most abundant cells and most studied
    3. d-cells –> somatostatin
    4. e-cells –> ghrelin (comes from stomach as well)
    5. f-cells (PP cells) –> pancreatic polypeptide
  • hormones secreted into blood! –> endocrine pancreases has rich blood supply!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explain blood supply to pancreas
- artery vs vein

A
  • hepatic artery (branching from aortic artery (main artery in body)) brings blood in
  • splenic and mesenteric veins bring blood out to portal vein
    *portal vein connects and collects all blood from GI tract –> leads to liver for metabolic processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • is endocrine or exocrine portion of pancreas more vascularized?
  • blood first supplies what?, then travels to what (2)
A
  • endocrine is 5 to 10 times more vascularized/ more blood flow) than to exocrine pancreas
  • blood first goes to middle and supplies centrally located b cells (detect glucose levels). then blood travels to peripheral a (glucagon) and d cells (SST)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  • islets of langerhans are homogenous or heterogenous?
  • within islets, groups of b cells function ________ –> how?
  • do b cells always proliferate?
  • avg lifespan of b cells?
  • b-cells differentiate from what?
  • what is another way b-cells are formed?
A
  • heterogenous! –> multiple cell types and sizes
  • within islets, groups of b-cells function together as a unit –> through gap junctions
  • proliferation of b cells is minimal after 5 years of age in humans (but doesn’t mean no new cells are formed)
  • avg lifespan = 25 years
  • neogenic niche (stem cells) at periphery of islets –> differentiate into b cells when needed
  • transdifferentiation of a and d cells under extreme b-cell loss
19
Q

explain complex interplay of insulin, glucagon and somatostatin within islets of langerhans

A
  • insulin inhibits glucagon
  • glucagon directly stimulates insulin BUT indirectly inhibits insulin by stimulating SST
  • SST inhibits insulin and inhibits glucagon and inhibits pancreatic polypeptide
20
Q

what is the main regulator for insulin secretion?
what are 3 other regulators?

A

glucose!
- neural, endocrine and paracrine factors

21
Q

insulin vs glucagon
- type of hormone?
- structure?

A

INSULIN
- peptide hormone –> 51 aa
- post-translational modifications: 1 gene –> produces a, b and c –> C-peptide is cleaved off –> a and b peptide chains are connected by 2 disulphide bridges
GLUCAGON:
- smaller peptide hormones: 29 aa
- produced as preproglucagon –> processed to proglucagon and glucagon
- single chain

22
Q

where is insulin metabolized? vs where is C-peptide metabolized?
- C peptide is a measure of what?

A
  • insulin is metabolized in liver
  • C-peptide is metabolized in kidney
  • C-peptide is a better measure of b-cell function/insulin secretion from islets than insulin itself
23
Q
  • beta cells contain ______-_______ granules of __________
  • half life of granules?
  • younger granules (2) vs older granules (1)
  • granules contain insulin ______ stabilized by (2)
A
  • 5000-8000 granules of insulin
  • half-life = 5 days
  • YOUNGER: deeper in cytoplasm, but more mobile than older ones
  • OLDER: degraded intracellularly –> intracellular degradation of insulin
  • insulin hexamer stabilized by calcium and zinc
24
Q
  • what is the main stimulatory of insulin synthesis and release? ____a_____
  • enters through what
  • which enzyme serves as ___a____ sensors
A
  • glucose!
  • through GLUT2
  • hexokinase/glucokinase = glucose sensors (primary mechanism by which rate of insulin secretion adapts to changes in blood glucose)
25
Q

what are the 6 steps in release of insulin from b-cells?

A
  1. uptake of glucose by type 2 facilitated glucose transporter (GLUT2)
  2. aerobic glycolysis (glucokinase, Krebs Cycle…) and increase of ATP/ADP ratio
  3. increase ATP/ADP ratio = inhibition of ATP sensitive K+ channels –> reduction of K+ efflux = membrane depolarization
  4. opening of voltage gated Ca2+ channels (VDCC)
  5. increased intracellular Ca2+ triggers exocytosis of insulin containing granules
  6. opening of Ca2+ activated potassium channels (K-Ca) leads to repolarization of membrane (resetting)
26
Q

what 2 things helps/facilitate insulin exocytosis (among other things)?

A
  1. metabolic coupling factors generated during glucose metabolism facilitate exocytosis and/or proinsulin synthesis (ie FFA from circulation and intracellularly formed succinate)
  2. glucagon-like peptide (GLP-1 form intestine) or related peptides bind to GLP-1 receptors and trigger cAMP production. It potentiates amplification pathway, ion channels and exocytosis
27
Q
  • which nerve is the longest nerve in the body + serves as neural regulator for insulin secretion?
  • this nerve acts as ______ and _______ neuron
  • main neuronal coordinator of (3)
  • release of ___________ in the _________ stimulates insulin release
A
  • vagus nerve!
  • sensory and motor neuron (providing and receiving signals from peripheral organs)
  • appetite control + digestion + metabolism
  • acetylcholine (cholinergic) in the pancreas
28
Q

what are the major factors controlling release of insulin from b-cells?
- nutrients (4)
- GI hormones (5)
- Hormones (2 positive, 4 negative)
- autonomic nerves (2 pos, 1 neg)

A

NUTRIENTS:
+ glucose
+ amino acids
(+) keto acids
(+) TG/FA
GI HORMONES:
+ gastrin, CCK, GIP, GLP-1, Secretin
HORMONES:
+ Growth hormone
+ glucagon (?)
- Adrenaline
- cortisol
- somatostatin
- other peptides
AUTONOMIC NERVES:
+ cholinergic
+ b adrenergic
- a adrenergic

29
Q

what are the major factors controlling release of GLUCAGON from a-cells?
- nutrients (2 pos, 1 neg)
- GI hormones (3 pos, 2 neg)
- Hormones (2 positive, 2 negative)
- autonomic nerves (2)

A

NUTRIENTS:
+ hypoglycemia
+ amino acids (arginine, alanine
- FFA
GI HORMONES:
+ gastrin, CCK, GIP
- GLP-1, Secretin
HORMONES:
+ Growth hormone
+ Adrenaline
- insulin
- somatostatin
AUTONOMIC NERVES:
+ cholinergic
+ adrenergic

30
Q

metabolic functions (pathways ish + enzyme) of insulin:
- liver (6)
- adipose (4)
- muscle (4)

A

LIVER:
- increase glucose uptake (glucokinase)
- increase glycolysis (increase PFK1, pyruvate dehydrogenase complex)
- increase glycogenesis (glycogen synthase)
- increase lipid accumulation (Acetyl-coa carboxylase)
- decrease gluconeogenesis
- decrease glycogen breakdown (decrease glycogen phosphorylase)
ADIPOSE:
- increase glucose uptake (GLUT4)
- increase lipogenesis (Acetyl-coa carboxylase (for FA) + lipoprotein lipase (for TG))
- increase glycolysis (increase PFK1, pyruvate dehydrogenase complex)
- decrease lypolysis
MUSCLE:
- increase glucose uptake (GLUT4)
- increase glycogenesis (glycogen synthase)
- increase glycolysis (increase PFK1, pyruvate dehydrogenase complex)
- decrease glycogen breakdown (decrease glycogen phosphorylase)

31
Q

function and where?
- GLUT2
- GLUT3
- GLUT4

A

GLUT2:
- b-cell glucose sensor + transport out of intestinal and renal epithelial cells
- b cells of islets + epithelial cells of small intestine and kidneys
GLUT3:
- basal glucose uptake
- brain, placenta, kidneys, many other organs
GLUT4:
- insulin-stimulated glucose uptake
- skeletal and cardiac muscle, adipose tissue, other tissues

32
Q
  • insulin promotes glucose uptake in (2) by increasing _____ transporters on cell surface
  • insulin promotes glucose uptake in (1) by stimulating which enzyme and thus promoting what? –> therefore, what is maintained?
A
  • muscle and adipose tissue by increasing GLUT4 transporters
  • in liver –> stimulating glucokinase: promote phosphorylation of glucose to form glucose-6-phosphate –> concentration gradient of non-phosphorylated glucose needed for facilitated uptake via GLUT2 is therefore maintained
33
Q

glucose levels are regulated by _______ that affect ____a__ and ___b___
- a and b also affect blood glucose levels

A
  • hormones! that affect appetite control/ physiology of GI tract + cell metabolism
  • double way arrow btw blood glucose levels & appetite, and blood glucose & cell metabolism
34
Q

explain pathway for hormonal regulation of glycogenesis (insulin receptor) 4 ish steps

A
  1. insulin binds to insulin receptor
  2. phosphorylation –> IRS –> PI3K
  3. PI3K converts PIP2 to PIP3 –> activates PDK-1 and PKB
  4. PKB phosphorylates active GSK3 –> phosphorylated GSK3 = inactive
    4.1 if GSK3 is inactive –> CANNOT phosphorylate (on Ser residues) glycogen synthase a (active) to glycogen synthase b (inactive), thus glycogen synthase a remains active!
35
Q
  • which enzyme converts glycogen synthase b to glycogen synthase a? and vice versa?
  • what inhibits (2) and activates (2) the enzyme that converts inactive glycogen synthase to active?
A
  • GS a (active) –> GS b (inactive), by GSK3
  • GS b (inactive) –> GS a (active), by PP1
  • PP1 is inhibited by glucagon and epinephrine
  • PP1 is activated by insulin and glucose/glucose6-phosphate –> therefore stimulating glycogen synthase a for more glycogen synthesis
36
Q
  • which 2 molecules stimulate glycogenolysis? in which tissue?
    = explain pathway of glycogenolysis (6 steps)
A
  • epinephrine in myocytes
  • glucagon in hepatocytes
    1. epinephrine and glucagon –> activate Gsa
    2. Gsa activates adenyl cyclase: ATP to cAMP
    3. cAMP activates PKA
    4. PKA and Ca2+ activate phosphorylase b kinase
    5. phosphorylase b kinase activates glycogen phosphorylase b into glycogen phosphorylase a
    6. glycogen phosphorylase a + AMP convert glycogen to glucose 1-phosphate
37
Q

glucagon has 2 signaling pathways in liver
- explain

A
  1. glucagon –> GPCR –> Gq –> phospholipase C –> PIP2 to inositol 1,4,5 triphosphate –> Ca2+ –> inhibits glycolysis & glycogenesis + activates gluconeogenesis
  2. glucagon –> GPCR –> Gas –> adenylate cyclase –> cAMP –> PKA –> increase phosphorylase kinase –> activates glycogen phosphorylase a = increase glycogenolysis
    *PKA also stimulates gluconeogenesis
    - OVERALL: decrease glycolysis + decrease glycogenesis + increase gluconeogenesis + increase glycogenolysis = increase glucose!
38
Q

endocrine control of blood glucose
- 2 major hormones
- 6 other important hormones
- all those hormones act at the same time?
- which hormone is the only one that lowers blood glucose?

A
  • insulin + glucagon = major hormones
  • epinephrine + cortisol + growth hormone + thyroid hormone + secretin + CCK
  • all act at same time and form an integrated control system
  • INSULIN is the only hormone that lowers blood glucose
39
Q
  • which receptors does insulin has? vs glucagon and epinephrine?
  • insulin, glucagon and epinephrine –> regulation of enzyme activities by (2) –> switching btw _______ and _______ states –> activation cascade
A
  • insulin: RTK
  • glucagon and E: GPCR
  • regulation of enzyme activities by phosphorylation (kinases) and dephosphorylation (phosphatases)
  • switching btw active and inactive state
40
Q

SCHÉMA:A
regulation of blood glucose:
- post meal hormonal control by _________ –> what happens (in general terms) in gut, muscle, liver, adipose and nerve/other tissues?
- fasting state hormonal control by (3) –> what happens (in general terms) in gut, muscle, liver and adipose?

A

POST MEAL
- insulin!
1. carbs from meal –> from gut to blood glucose
2. from blood, glucose goes to:
- muscle –> forms glycogen!
- liver –> forms glycogen and TG
- adipose: forms TG
- nerve and other tissues for function
FASTING STATE:
- glucagon, adrenaline or glucocorticoids
1. muscle: protein –> aa –> to liver
2. adipose: TG –> FA –> to liver
3. liver:
- aa (from muscle) converted to glucose
- glycogen converted to glu
- FA –> ketone bodies!
- glucose goes to blood

41
Q

regulation of blood glucose:
- serum glucose in fasting stage: __-__ mM (generally < ____ mM or ______ mg/dL)
- rise to ___ mM after meal (glycosuria if exceeding ____ mM or _____ mg/dL)
- anabolic effects of insulin: 2 ish
- key target tissues of insulin (3)
- insulin promotes what?: essential for normal (2)

A
  • 3-5 mM (<6.1 mM or < 140 mg/dL)
  • rise to 7 mM after meal (glycosuria if >11.1 mM or 200 mg/dL)
  • synthesis of protein, lipid and glycogen + inhibition of their degradation (usage of glucose)
  • liver, muscle, adipose tissue
  • promotes cell growth! essential for normal growth and development
42
Q

regulation of blood glucose (continued):
- glucagon increases many anabolic/catabolic processes? particularly where?
- btw meals/fasting, the release of _______ from ______ is tightly regulated (most tissues rely predominantly on _______ as an energy source)
- other energy sources are (2)
- is insulin continuously secreted? or only after meal?

A
  • catabolic processes! particularly in liver! (production of glucose)
  • release of glucose is tightly regulated –> rely on glucose as energy source
  • fatty acids and ketones (muscle)
  • insulin is continuously secreted to enable peripheral tissues to uptake glucose
43
Q

muscle vs liver glucose metabolism (glucagon vs epinephrine ish)
- 5 differences
- 1 similarity
(SCHÉMA)

A

DIFFERENCES:
- muscle doesn’t have glucagon receptor! only responds to epinephrine VS liver responds to epinephrine AND glucagon
- muscle isoform pyruvate kinase is not phosphorylated by PKA
- muscle doesn’t produce F26BP
- increase glycolysis in muscle (glu-6-P converted to pyruvate) VS decrease glycolysis in liver (bc glu-6-P is exported to blood) (pyruvate is converted to glucose 6 P)
- increase gluconeogenesis in liver
SIMILARITIES:
- increase glycogenolysis in both: glycogen to glucose 6 phosphate

44
Q

fuel metabolism in prolonged fasting: 9 steps

A
  1. protein degradation yields glucogenic aa –> some parts of aa enter TCA cycle + release of NH3
  2. NH3 –> urea –> urea exported to kidney and excreted in urine
  3. TCA intermediate (oxaloacetate) is diverted to gluconeogenesis in liver
  4. glucose (produced from gluconeogensis) is exported via bloodstream to brain
  5. FA from adipose tissue are oxidized for fuel, producing acetyl-CoA
  6. lack of oxaloacetate prevent acetyl-coA entry into TCA cycle –> acetyl-CoA accumulates
  7. Acetyl-CoA accumulation favors ketone body synthesis
  8. ketone bodies are exported via bloodstream to brain, which uses them as fuel
  9. excess ketone bodies end-up in urine

Endocrinology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions