3 - Hormones and Metabolism Flashcards
1
Q
Gluconeogenesis
A
-
Glycogen / Lactate / AA / Glycerol
- –> Form Glucose in LIVER
- 90% of all glucose (not from diet) is generated in the LIVER
- Stimulated by decreasing blood glucose levels
2
Q
Negative Feedback of Glucose
A
- System senses Increase in Glucose
- Pancreas releases Insulin
- Insulin signals muscle/adipose tissue to intake glucose
- -> Reduction in glucose in blood
3
Q
Pancreas
A
- Controls Metabolism by producing:
- Digestive Enzymes (from acinar cells)
- Trypsin
- Chymotrypsin
- Elastase
- Amalase
- 2 Endocrine Hormones
- Insulin
- Glucagon
- Digestive Enzymes (from acinar cells)
4
Q
Acinar Cells
A
-
Exocrine cells of the Pancreas that secrete digestive enzymes
- Trypsin
- Chymotrypsin
- Elastase
- Amalase
- –> breakdown food in GI
5
Q
Delta Cells
A
In Islets of Langerhans of Pancreas
Produce:
SOMATOSTATIN
6
Q
Sigma Cells
A
In Islets of Langerhans of Pancreas
Produce:
GHRELIN
7
Q
Insulin’s 5 Main Functions
A
- Prevents release of Fatty Acids from Adipose tissue
- Promotes synthesis of Glycogen
- Accelerates transport of Glucose -> Muscle
- Accelerates synthesis of Triglycerols
- Inhibits synthesis of Glucose by _liver_
8
Q
Insulin
A
-
Peptide Hormone (Anabolic)
-
Pre-proinsulin -> ER
- cleaved -> Proinsulin -> secretory vesicles
- -> Insulin + C-Peptide
- cleaved -> Proinsulin -> secretory vesicles
-
Many of the AA’s are MUTATED
- genetic mutations everywhere are what cause different diseases
-
Pre-proinsulin -> ER
- Half life of insulin is about 5 minutes
- __degraded by the liver + kidney
9
Q
C-Peptide
A
-
@Secretory Vesicles
- Proinsulin -> Insulin + C-Peptide
-
Biomarker for insulin levels
- longer half life
- useful for monitoring pancreatic B-cell activity
- due to low rxn w/ insulin
- absence in synthetic preparations
10
Q
Pathway of Insulin Release
A
- Glucose -> Pancreatic B-Cell via GLUT2
-
Glycolysis in Cytosol -> Mito
- -> Increase in ATP/ADP ratio
- modulation of K+ channels
- Depolarization (more negative)
-
Ca2+ INFLUX
- INSULIN RELEASE
-
Ca2+ INFLUX
- -> Increase in ATP/ADP ratio
-
Glycolysis in Cytosol -> Mito
11
Q
GLUT2
A
Glucose Influx Transporter
Pancreatic Beta Cell
Liver
12
Q
How does Insulin INCREASE Glucose absorption into the cell?
A
- Insulin -> Insulin Tyrosine Receptor Kinase on Muscle + Adipocytes
-
IRS1 Phosphorylation -> P13Kinase
-
Phosphorylated AKT
-
Translocates GLUT4 to the membrane
- MORE TRANSPORTERS TO BRING GLUCOSE INTO THE CELLS
-
Translocates GLUT4 to the membrane
-
Phosphorylated AKT
-
IRS1 Phosphorylation -> P13Kinase
13
Q
GLUT4
A
Glucose Influx Transporter
Found on Muscle + Adipocytes
Upregulated by Insulin binding
14
Q
Insulin action on the LIVER
A
-
Stimulates GLYCOLYSIS
-
GLUT2 brings glucose into liver
- -> brings IN glucose -> glycogen
-
GLUT2 brings glucose into liver
-
Inhibits Gluconeogenesis
- inhibits formation of glucose
- Blood flow goes from Pancreas to Liver
- exposes Liver to large amounts of hormones
- Stimulates GLUCAGON synthesis
- major organ for pancreatic hormone inactivation
- exposes Liver to large amounts of hormones
15
Q
Insulin action on Adipocytes
A
Prevents release of
FREE FATTY ACIDS
16
Q
Insulin action on Muscle
A
- Accelerates influx of GLUCOSE into the muscle
- via GLUT4
- -> sets stage for glucose oxidation
17
Q
Glucagon
A
- Produced by Alpha-Cells of Islets of langerhans
-
Part of Precursor w/ other peptide hormones
- GLP-1 / GLP-2 / GRP
- STIMULATED by Low plasma Glucose
- Inhibited by Insulin & Somatostatin
- Mostly impacts the LIVER and not other tissues
18
Q
Glucagon’s 5 Main Functions
A
- Stimulates Amino Acid uptake
- Gluconeogenesis
- Glucose release
- Inhibits Glycolysis
- Inhibits FFA synthesis
19
Q
Somatostatin Production
A
- From Delta Cells of pancreatic islets
- Stimulated by increase in Glucose
- similar to insulin release
- Stimulated by increase in Glucose
- Produced as a larger precursor
- cleaved in the ER to form a mature 14 AA product that is released
- Inhibits Glucagon readily
- Inhibits Insulin from rising too rapidly
20
Q
GLP / GIP Receptor
A
- Found on Beta Cells of islet of langerhans
-
Sense Glucose levels
- -> stimulate release of Insulin
- Similar to UCN3 of Delta cells but secrete different hormones
21
Q
UCN3 Receptor
Urocortin3
A
- Found on Delta Cell on islet of langerhans
-
Sense Glucose
- Secrete SOMATOSTATIN
- sense the SAME signal as GLP/GIP but have a diffrentiation in signal transduction
22
Q
Somatostatin Function
A
PARACRINE REGULATION
acts on alpha/beta cells locally
- Inhibits* Glucagon Readily
- Inhibits* Insulin from RAPIDLY RISING
23
Q
Priority for the disposal of Dietary Fuels
A
- 1) Restore Glucose for Brain
- brain can use glycerol from liver
- while rest of body uses fatty acids
- 2) Replenish Glycogen in the liver
24
Q
Leptin
A
Decreases Food Intake
- Polypeptide hormone produced by ADIPOCYTES
- Binds to LEPR-B in the BRAIN
- translation of neuropeptide POMC
- Binds to LEPR-B in the BRAIN
- Links body energy (fat) to the central conrol of energy balance
- Leptin action is key for energy stores to be sensed by the CNS
- Does NOT benefit obesity due to
- LEPTIN RESISTANCE
25
Q
Leptin Actions
A
binding to LEPR-B -> translation of neuropeptide POMC->
Increases Energy Expenditures (use storage)
- Decreases Food Intake / Appetite*
- Reduces Body Weight*
26
Q
Leptin Pathway
A
- Increase in Intake = Energy Imbalance
- Intake > Expendature
-
Adipocytes secrete Leptin
- leptin binds to LEPR-B in BRAIN hypothalmus
- __translation of neuropeptide POMC
- __signal to Use Energy
- decrease Food Intake
- reduce Body Weight
- __translation of neuropeptide POMC
- leptin binds to LEPR-B in BRAIN hypothalmus
27
Q
ob + db gene discovery
A
- ob gene codes for LEPTIN
- db gene codes for Leptin Receptor ( LEPR-B )
- Cross between OBESE mice, each with each KO gene
- ob KO mouse lost weight
- leptin from db mouse transfered over and was able to bind to leptin receptors
- db KO mouse stayed obese
- receptor can not transfer from one mouse to another so the db mouse stayed obese
- ob KO mouse lost weight
