Download DIGESTION: GI Tract DIGESTION: Catabolism

DIGESTION: GI Tract
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Four Functions:
A.
B.
C.
D.
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Motility: Movement of substances
Secretion: Enzymes / digestive juices
Digestion: Physical catabolism of food
Absorption: nutrients into circulation
Innervation of the GI:
1. Parasympathetic
2. Sympathetic
One muscular tube: smooth vs. skeletal muscle
•
-
Peristalsis
segmentation
DIGESTION: Catabolism
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Start of digestion: Mouth- Salivary amylase
Absorption:
1. Sm. Intestine: vitamins and minerals
2. Lg. Intestine: water and salts
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Carbohydrates
Salivary Amylase
Mouth
long sugars
Pancreatic amylase Sm. Intestine
Other enzymes
Sm. Intestine
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double sugars
long sugars double sugars
double sugars
simple sugars
Proteins
Pepsinogen/Pepsin
Trypsinogen/Trypsin
Other Enzymes
Stomach
Sm. Intestine
Sm. Intestine
Proteins
AA chains
Proteins
AA chains
AA chains
single AAs
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DIGESTION: Catabolism
• Fats
Bile Salts
Lipases
Sm. Intestine(liver)
Sm. Intestine(pancreas)
Emulsification(droplets)
TGs
Fatty acid +
Monoglycerides
• Enhanced absorption in Small intestine by Villi
HORMONES
• Chemical released by one cell to travel to another
cell to exert an effect
- 1,25(OH)2VitD3, PTH, Oxytocin, EPO, Insulin
• Insulin: -Islet cells, stimulated by high levels of
blood glucose, purpose is to lower blood glucose
levels
Insulin levels
-Islet cells
Muscle cells
Fat Cells
Plasma levels of
Blood glucose
Liver
-Islet cells
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DIABETES MELLITUS
• ‘Open loop’ disease of glucose regulation
1) IDDM: no insulin production- Injections required
2) NIDDM: Functional insulin produced, effector
tissue problematic
• Effector tissues:
1. Muscle/Fat: Insulin receptor = Tyrosine Kinase
Signaling induces GLUT4 exocytosis, Glucose flux
into cell.
2. Liver: Insulin binding activates glycogenic enzymes
Liver does not have GLUT4, only GLUT2 (signaling
independent)
-cell glucose/insulin feedback
•
1.
2.
3.
4.
5.
6.
GLUT2-K(ATP)-V Gated Ca2+ Channels
Glucose flux into cell via GLUT2
Increase in [ATP]in
Decrease in GK(ATP)
Voltage increase
Opening of V-Gated Ca2+ channel, Ca2+ flux in
Release of vesicles containing insulin
PM GLUT4
Plasma
Glucose
Plasma
Insulin
Glycogenesis
Net flux of
glucose into
cells
Plasma
Glucose
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GLUCAGON
• Protein secreted by -islet cells of the pancreas
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•
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Release stimulated by low plasma glucose
Glucagon receptor on liver: GPCR cAMP release
Glucagon release leads to glycogen breakdown
sensor & comparator: -islet cells
• Actuating signals: glucagon levels
Plasma
Glucose
Plasma
Glucagon
Conversion of
glycogen to
glucose
Flux of glucose
out of liver
Plasma
Glucose
PITUITARY
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Pituitary is closely associated with hypothalamus
Pituitary stalk connects pituitary to hypothalamus
Posterior pituitary hormones: vasopressin and
oxytocin
Hypothalamus secretes ‘Releasing Hormones’
RHs travel through capillaries to the anterior
pituitary, binding receptors to cause release of a
hormone into blood stream
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RELEASING HORMONES
& HORMONES
Hypothalamus
TRH
Anterior Pituitary
TSH
Peripheral effects
release of thyroid
hormones (thyroxin)
GHRH
GH
Stimulate cell growth
(GHRs)
GnRH
LH, FSH
stimulate production of
sex hormones in the
gonads (Test., Est.,
Progest.)
HORMONE SPECIFICS
Two broad categories:
1. Lipid Soluble: Intracellular receptors
2. Non-lipid soluble: Plasma membrane receptors
Corresponding receptors
1. GPCR
cAMP flux: V2, Glucagon, RH
2. Ionotropic
3. Intracellular activity: Insulin Tyrosine Kinase
GLUT4 exocytosis
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BODY TEMPERATURE
• Mammals have a T > external and internal set point
• Sensors for body temp are central thermoreceptor
neurons in hypothalamus and peripheral
thermoreceptor neurons in skin
• Comparator uses input from both sets of sensors
and sends actuating signals:
– Body too hot: Increase sweat, increase flushing*
– Body too cool: decrease sweat, decrease flushing,
shivering.
• Long term: release of hormones to raise body metabolism
• Fever: higher set point
• *Flushing = flow of blood near skin in capillary beds
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