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Week 14 - Regulation of Metabolism and Diabetes


Terms in this set (110)

Absorptive State 0-4 hours post consumption

nutrients entering blood from GI tract and used


Absorptive State
for energy and synthesis of macromolecules

Cellular Energy Production


Absorbed Glucose Glycogenesis
Triglycerides Synthesis

Cellular Energy Production cellular uptake and conversion to ATP, CO2, H2O
(Glucose)

Cellular Energy Production Almost all cells


(Glucose) Location

Which cell uses most Nervous System


glucose?

Glycogenesis (Glucose) form glycogen form glucose

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Where is Glucose Stored? Liver (100g), Skeletal Muscle (400g)

If liver and skeletal muscle stored as triglycerides


can not store more glucose,
where does it go?

Triglycerides Synthesis Liver and adipose tissue


(Glucose) Location?

Triglycerides Synthesis glucose becomes α-glycerol and fatty acids


(Glucose) Process?

What happen to Triglycerides packaged and shipped out in a VLDL


formed in the liver?

VLDL (very low density lipoprotein lipase that breakdown FA + Glycerol to


lipoprotein) be transported to adipose cells

How are lipids absorbed in as chylomicrons


the body?

rebuilt into triglycerides once arrived to adipose


Fate of Absorbed Lipids
tissue

Cholesterol Absorption transported in LDL and HDL

Absorbed AA converted into proteins in muscle

component of plasma membrane to increase


Cholesterol Function
stability

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Where does excess AA go? liver to be deaminated into NH3 and α-ketoacid

What happens to α-ketoacids converted into FAs or ATP (enter Krebs Cycle)
in liver?

What determines metabolism insulin


during absorptive state?

What secretes Insulin? beta cells from pancreatic Islets of Langerhans

What does insulin cause? muscle, liver, adipose to enter the absorptive state

Increase in GLUT4, AA transport


Insulin Muscle Effects
increase glycogen synthesis

increase glycogen synthesis


Insulin Liver Effects increase lipogenesis
decrease gluconeogenesis

increase GLUT4
Insulin Adipose Effects increase lipogenesis
decrease lipolysis

Increase plasma glucose


decrease plasma AA
Insulin Secretion Stimulus
incretins (feed-forward response)
SNS/Epi inhibits and PNS activate

increase in blood glucose concentrations


Postprandial Hyperglycemia
following a meal

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>4 hours after eating


Post-Absorptive State
GI tract empty of resources

Euglycemia good blood sugar

Why is Euglycemia so Brain only runs on glucose and needs a consistent


important? supply

How does the liver/muscle Glycogenolysis


add glucose to the blood?

Glycogenolysis breakdown of glycogen to glucose

make glucose from lactate (muscle), glycerol


Gluconeogenesis
(Adipose), AA (muscle)

Where does Gluconeogenesis liver


occur?

glucose consumption decrease (stop using


Glucose Sparing Glycolysis) by the rest of the body so NS has a
consistent supply

During Post Adsorptive State, Fatty acids (can NOT be used by nerves), Ketones
where do the cells get their (can be used by nerves)
energy?

What are Ketones important decrease protein catabolism


for?

Glucagon Secreted by? alpha pancreatic ells

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Glycose Counter-Regulatory System that adjust the body when glucose not
System around during post-absorptive state

decrease in plasma glucose/AA


Glucagon: Stimulus
increase SNS Activity

Glycogenolysis
What does Glucagon
Gluconeogenesis
Stimulate?
Ketone Synthesis

What is the net effect of increase in plasma glucose and ketones


Glucagon?

SNS/Epinephrine Responds to hypoglycemia

Cortisol effect on Glucagon permissive effect (increase its effectivness)

What hormones in high cortisol and GH


concentration inhibits insulin?

insulin deficiency from pancreatic beta-cells


destroyed by autoimmune response
Type 1 Diabetes

No insulin produced

How is type 1 diabetes insulin injected


treated?

What is type 1 diabetes young age


diagnosed?

Type 2 Diabetes Insulin not detected by cells

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high insulin and glucose and stiffening of plasma


What will the blood look like?
membrane

What is more common Type 1 Type 2


or Type 2 Diabetes?

glucose will interact with other molecules and


Chronic Hyperglycemia
change them in both type 1 and 2

1st law of thermodynamics Energy cannot be created or destroyed

mechanical work
What is energy converted into
heat
in the body for?
molecular sysnthesis

What are the three resting metabolic (60-70%)


components of total daily Thermic Effect of Food (10%)
energy expenditure? Physical Activity (20-30%)

What is the largest resting metabolic rate


component of energy
expenditure?

What affects rate of size, gender, age, stress (fat-free mass)


metabolism?

What hormones affect rest thyroid hormone (most important)


metabolic rate? SNS/Epinephrine

T3 = active
Thyroid Hormone
T4 = inactive

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SNS/Epinephrine works T3/T4 and independently

Brown Fat
What are the Receptors
White Fat

Brown Fat Function metabolic regulation

White Adipose Function storage

What are the effects of increase the metabolic rate of the body by
SNS/Epinephrine and Thyroid increasing ATP production
Hormones?

How does the body decrease consistently doing glycolysis and


ATP efficiency? gluconeogenesis

mitochondria allow ATP to easily to travel across


UCP1
the inner membrane

Diet-Induced Thermogenesis uses of energy to digest food

What molecules take more protein > carbohydrates > fats


eneryg to digest?

Exercise Thermogenesis energy uses

Non-Exercise Activity energy burned form standing


Thermogenesis (NEAT)

energy expenditure < energy intake = Weight


Positive Energy Balance
GAIN (anabolism)

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energy intake < energy expenditure = Weight LOSS


Negative Energy Balance
(catabolism)

Set Point ideal amount of energy stored in body

Appestat control by hypothalmus

Hunger trigger increase in ghrelin

Satiety Signal increase leptin

increase food taste, stress, conditioned to eat


What missed up appestat?
certain amount

Leptin peptide hormone release by fat cells

Leptin Effects negative feedback to prevent excessive fat

If fat cell is bigger more leptin released

Impact of Obesity early mortality (death) and morbidity (disease)

What cause Obesity? prolonged positive energy balance

ready availability of tasty, high calorie, poor


Obesogenic Environment
nutrient food

Where is fat stored? subcutaneous and visceral adipose tissue

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Subcutaneous Adipose Tissue fat under skin


(Location? Secretion? secrete leptin
Good/Bad?) best spot for fat

Visceral Adipose Tissue fat around organs


(Location? Secretion? secretes inflammatory response
Good/Bad?) bad spot for fat

Where does fat in females hips/thighs because of estrogen


go?

Where does fat in males go? belly area

Atherosclerosis hardening of arteries

alters protein structures and decreases biological


Glycation (glucose Toxicity)
activity

diet, exercise == weight loss


How to treat type 2 diabetes? decrease stress
quit smoking

endothelial damage + lipoprotein entering


Fatty Streak
subendothelial space causing inflammation

Foam Cell lipoprotein swalled by dendritic cell

Stable Plaque accumulation of smooth muscle/fibrin

Unstable Plaque cells die causing blockage up stream

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secreted by liver to transport triglycerides to the


VLDL
peripheral tissue

LDL transport mainly cholesterol

HDL Transport mainly cholesterol

it forms from the depletion of TG of VLDL after


How is LDL formed?
transporting the TG to the tissue

If TG levels high... more LDL produced

What is the different in HDl contain the apolipoprotein


structure between VLDL/LDL
and HDL?

High level of what protein ApoB lipoproteins (VLDL/LDL) on endothelial


cause damage to endothelial

} cells?

LDL Effect on endothelial can pernitrate membrane of damage cell and will
membrane become oxidized

Oxidization damage to endothelial cells

HDL Transport transfer cholesterol deleivery and return

HDL effect on atherosclerosis Protects its formation

If TG levels increase... HDL decreases

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Week 14 - Regulation of Metabolism and Diabetes Flashcards | Quizlet https://quizlet.com/651728905/week-14-regulation-of-metabolism-and-d...

Abnormally elevated cholesterol or fats (lipids) in


Dyslipidemia
the blood.

Dyslipidemia Treatment diet, exercise, smoking, stress, drugs

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