SI Powerpoint: Control of Metabolism

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Transcript SI Powerpoint: Control of Metabolism

SI Session
Metabolism
Spring 2010
For Dr. Wright’s Bio 6 Class
Designed by Pyeongsug Kim ©2010 [email protected]
Review your understanding of catabolism and anabolism.
Be able to discuss a mechanism by which each of the following affects blood glucose levels (i.e., does it
increase or decrease blood sugar, and HOW):
Insulin
Glucagons
Growth hormone/insulin-like growth factors
Epinephrine
Glucocorticoids
Thyroxine
Compare and contrast type I and type II diabetes mellitus with respect to:
Age of onset
Why blood glucose levels are high
Is insulin deficient?
Recommended treatment
Are beta islet cells damaged?
How does parathyroid hormone and/or vitamin D3 (1, 25-dihydroxyvitamin D3) affect:
Reabsorption of calcium from intestine
Reabsorption of calcium in kidneys
Resorption of bone
(Think: does it tend to put more calcium in the blood, or less?)
What are the consequences of having low blood calcium? (review question!)
Metabolism
: All body’s process that transform energy.
Designed by Pyeongsug Kim, ©2010
Chemical reactions in Metabolism:
• Anabolism
Reactants
A + B + energy
Product

C
Form larger molecules
+ energy
• Catabolism
Reactant
C


Products
A + B + energy
Breaking down into smaller molecules

+ energy
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*Generally….
High levels due to CATABOLISM.
Low levels due to ANABOLISM.
Stimulates glycolysis (Catabolism).
 increase blood glucose.
Stimulate glycogenesis(Anabolism).
 decrease blood glucose.
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The hormones affect Blood glucose levels:
Insulin
Glucagons
Growth hormone
Insulin-like growth factors
Epinephrine
Glucocorticoids
Picture from http://www.projectswole.com/diet/how-to-manipulate-insulin-for-fat-loss-and-muscle-gain/
Designed by Pyeongsug Kim, ©2010
Insulin (secreted by Pancreas (Beta cells)
↓ Blood glucose by stimulating…
-Cellular uptake of glucose
-Conversion of glucose to glycogen and fat.
↑Blood glucose
“-lysis”:
Breakdown to smaller molecules
“-genesis”: Making to a big molecules
In Beta cell
↑insulin secretion
Glycogenesis
_____________:
Glucose  Glycogen
In Alpha cell
↓Glucagon secretion
Cells uptake glucose
Lipogenesis
_____________:
Glucose  Triglyceride
↓Blood glucose
Liver/muscle: Glucose  Glycogen
Anabolism!!
Adipose tissue: Glucose Triglyceride
*Insulin is __________
anabolism of carbohydrate and lipids.
Designed by Pyeongsug Kim, ©2010
Glucacon (secreted by Pancreas (Alpha cells)
↑ Blood glucose by stimulating…
-Making glucose from glycogen and noncarbohydrates (triglyceride
and amino acids)
-Glycogenolysis(breakdown Glycogen into glucose) in the liver.
-Glucogenesis
“-lysis”:
Breakdown to smaller molecules
“-genesis”: Making to a big molecules
↑Blood glucose
Glycogenolysis
_____________: Glucose ← Glycogen
In Beta cell
↓ insulin secretion
Gluconeogenesis
_____________: Glucose ← Triglyceride(or noncarbohydrate)
In Alpha cell
↑ Glucagon secretion
↓ Cells uptake glucose
↑ Blood glucose
Liver/muscle: Glucose ← Glycogen
Catabolism!!
Adipose tissue: Glucose ← Triglyceride
Designed by Pyeongsug Kim, ©2010
From Dr. Wright’s Bio6 powerpoint
Designed by Pyeongsug Kim, ©2010
ANS system activity in metabolism
-Both sympathetic and parasympathetic nerves innervate
pancreas
-Sympathetic, along with epinephrine,
stimulates glucagon secretion
 increase blood glucose
-Parasympathetic
 stimulates insulin secretion
 ↑ gastrointestinal activity (digestion)
 decrease blood glucose
Designed by Pyeongsug Kim, ©2010
Growth hormone(GH)
-Secreted by A.pituitary glands.
-Controlled by GHRH(from hypothalamus)
-stimulates growth in children and adolescents.
-More secreted GH during stress and fasting in adults.
-increased when fasting, stress, low blood glucose and high
amino acid by skeletal muscle.
Picture from http://adolescents.wordpress.com/
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Insulin-like Growth factors (IGFs)
-”Somatomedians”
-Polypeptides(protein) produced by liver or many
tissues.
-mediators of some of GH actions.
Cell division
Cartilage and bone growth
Protein synthesis in muslce & other organs.
-Not mediated of GH actions.
Lipolysis
decreased glucose utilization.
Designed by Pyeongsug Kim, ©2010
Insulin-like Growth factors (IGFs)(Cont’d)
From Dr. Wright’s Bio6 powerpoint
Designed by Pyeongsug Kim, ©2010
Growth hormone(GH) (secreted by Anterior Pituitary glands)
↑ Blood glucose by stimulating…
- ↓cellular glucose uptake; Glycogenolysis in the liver
↓ Blood glucose
↑ amino acid in Blood
e.g. fasting
↑GnRH in Hypothalamus
In liver
↑Glycogenolysis
↑GH in Anterior pituitary
↓ Cells uptake glucose
↑ Blood glucose
Muscle and other organ: Protein← amino acids
↓ amino acid in Blood
Adipose tissue: fatty acids← Triglyceride
↑ fatty acids in Blood
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*Insulin is __________
anabolism of carbohydrate and lipids.
Hormones for catabolism of carbohydrates and lipids
Glucagon
Growth hormone(GH)
Epinephrine
Glucocorticoids,
Thyroxine
*However, GH and Thyroxine promotes protein synthesis
 anabolism of protein.
Designed by Pyeongsug Kim, ©2010
Epinephrine
Increase in stress.
Produced in adrenal medulla
↑ Blood glucose by stimulating…
-release glucose from liver (Glycogenesis)
-Gluconeogenesis(making glucose from noncarbohydates)
Glucocorticoids
-Produced in adrenal cortex
-Controlled by ACTH
-Increased during prolonged fasting or exercise
↑Blood glucose by stimulating…
- ↓cell glucose utilization
-Gluconeogenesis(making glucose from noncarbohydates)
↑Lipolysis
↑protein breakdown in muscle.
Designed by Pyeongsug Kim, ©2010
Thyroxine(T4) (secreted by thyroid follicles)
-Secreted in thyroxine by TSH.
-response to low ATP
-Increase cell respiration (to make more ATP)
↑ glucose utilization
increase metabolic heat as a result of cell
respiration.  Cold adaptation!!
-participate in body growth and CNS in
children.
↑ protein synthesis
↑ BMR(Basal metabolic rate)
-Both hypothyroidism and hyperthyroidism
 Cause muscle wasting(protein breakdown)
-No direct in lipid metaolism.
A person with hypothyroidism
cannot stand being cold.
Picture from http://abbeygracepink.com/?p=185
Designed by Pyeongsug Kim, ©2010
Thyroxine(T4) (cont’d)
-act on nearly every cell in the body.
-participate in catabolism of carbohydrates and lipids
-Tend to elevate blood glucose.
-participate in protein synhesis.
“T4 and T3 tend to ELEVATE PLASMA GLUCE and
potentiate the effects of other HYPERGLYCEMIC
hormones..ie.. NE, E, cortisol, glucagon, and GH”
Designed by Pyeongsug Kim, ©2010
Designed by Pyeongsug Kim, ©2010
Diabetes
onset
Symptoms
Proportion
Ketoacidosis?
Obesity
Beta cells damaged?
Insulin secreted?
Immunity to islets
MHC association
Treatment?
Type 1
< 20 years
Rapid
10%
Common
rare
Yes
Decreased
Yes
Yes
Insulin
Type 2
> 40 years
Slow
90%
Rare
common
No
May be increased
No
?
Diet, exercise,
medication
From Dr. Wright’s slide
Vitamin D3 (VD3)(1, 25-dihydroxyvitamin D3)
-Produce in the skin from sunlight
 so, fall VD3 production during winter
-PTH(parathyroid hormone) increase VD3 hormones
-Increase Ca2+ in blood by.....
Reabsorption of calcium from intestine
Reabsorption of calcium in kidneys
Reabsorption CaPO4 crystals of bone
In case of high calcium but normal phosphate
VD3 – ↑reabsorption of phosphate and
↑reabsorption of calcium in the kidney.
PTH - ↓reabsorption of phosphate and
↑reabsorption of calcium in the kidney.
See table 19.7 Endocrine regulation of Ca and phosphate balance
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Calcium levels regulated by hormone- ______________
calcitonin & PTH
________
Calcitonin
- inhibits dissolution of bone
- stimulates excretion of Ca2+ in urine
 therefore, (lower/rise) Ca2+ level in blood.
_____
PTH
-increase resorption in bone.
-increase absorption in small intestine.
-increase absorption in kidney.
 therefore, (lower/rise) Ca2+ level in blood.
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When blood Ca2+ level rises….
Negative feedback!
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When blood Ca2+ level falls….
Negative feedback!
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Consequences of having low blood calcium
-Result from inadequate amount of VD3 or low PTH
 ↓Reabsorption Ca2+ from bone, kidneys, and
intestine
 ↓ Blood Ca2+
 Bone demineralization to increase Blood Ca2+
Osteomalacia, Osteoporosis
rickets(in children)
Bone demineralization – loss calcium from the bone
Bone mineralization – deposit calcium into the bone
Designed by Pyeongsug Kim, ©2010