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Intro Bio II Exam 3 > Energy Balance > Flashcards

Energy Balance Flashcards

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1
Q

Two theories of appetite and satiety

A

Glucostatic theory

Lipostatic theory

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2
Q

Function of leptin

A

Leptin is secreted by adipose cells when fat stores increase. It inhibits the release of neuropeptide Y which signals to the hypothalamic feeding center.

Makes you feel FULL.

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3
Q

Ghrelin

A

A peptide hormone secreted by stomach during fasting. Makes you feel HUNGRY.

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4
Q

How do we measure energy expenditure?

A

Oxygen consumption is used as a proxy for energy expenditure
Metabolic rate = liters of oxygen consumed per day * kilocalories per liter of oxygen

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5
Q

Respiratory exchange ratio

A

Ratio between the volume of carbon dioxide produced per volume of oxygen used during metabolism

Each glucose molecule produced 6CO2 and 6O2, a 1:1 ratio

But fat molecules produce more O2 for every carbon… so LESS THAN 1

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6
Q

Glucostatic Theory

A

The theory that states that when blood glucose decreases, satiety center (in hypothalamus) is repressed and feeding center is dominant.

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7
Q

LIpostatic Theory

A

The theory states that fat stores help modulate body weight. Adipocytes secrete leptin, a hormone that signals satiety, so more fat equals more leptin.

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8
Q

Neuropeptide Y

A

Signals to hypothalamic feeding center to intake more food!! The signal that represses it is Leptin.

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9
Q

Peptides that increase food intake

A

Ghrelin (stomach)
NPY and Agouti-related protein (hypothalamus)
Orexins (hypothalamus)

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10
Q

Peptides that decrease food intake

A

CCK (small intestine, neurons)
GLP-1 (intestines)
PYY (intestines)
Leptin (adipose)
CRH (hypothalamus – this is a releasing hormone!)
alpha-MSH (hypothalamus)
CART and POMC (hypothalamus - ‘cocaine-and-ampehtamine-regulated transcript’… presumably activated by cocaine / speed, which is why people on cocaine / speed are so skinny!)

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11
Q

Sources of energy input

A

DIET

Hunter/appetite, satiety, social and psych factors

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12
Q

Forms of Energy output

A
  1. HEAT

2. WORK

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13
Q

components of heat as energy output

A

either unregulated (waste) or thermoregulation

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14
Q

components of work as energy output

A

transport across membranes
mechanical work e.g. movement
chemical work e.g. growth and energy storage via chemical bonds or high-energy phosphate bonds

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15
Q

RER for energy derived totally from fats?

A

0.7

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16
Q

RER for energy derived totally from carbs?

A

1.0

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17
Q

Biomolecules that we eat are either…

A
  1. Used to make energy (ATP, phosphocreatine, NADPH)
  2. Used to make stuff (like proteins, cytoskeleton)
  3. Stored (as glycogen or fat)
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18
Q

Difference between NADPH and NADH

A

NADH is used in the electron transport chain to make ATP

NADPH is a phosphorylated version of NADH that carries electrons, but to MAKE molecules, such as lipids, via “reductive biosynthesis”

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19
Q

Absorptive / Fed State

A

Nutrients enter blood from digestive tract, cells either USE what they need or STORE for later

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20
Q

Postabsorptive / Fasted state

A

Digestive tract is empty so nutrients enter blood from stored fat, glycogen, and gluconeogenesis

ALL CELLS mobilize resources: only liver and adipose supply nutrients to the rest of the body

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21
Q

What are the “generous” organs?

A

Liver, adipose

They will share their energy stores with other organs

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22
Q

What does heart typically use as a stored energy source?

A

Fats

Long term, sustainable source of energy

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23
Q

What does muscle typically use as a stored energy source?

A

Glycogen

Can immediately consume glucose for mechanical work

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24
Q

What does the brain typically use as a stored energy source?

A

Trick question, nothing! The brain uptakes free glucose from the blood. It gets first dibs on glucose, always.

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25
Q

Liver during absorptive state (feeding)

A

Receives GLUCOSE and AMINO ACIDS
(Glucose can be stored as glycogen or broken down to acetyl groups to make fatty acids)

Sends LIPIDS to adipose as VLDLs

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26
Q

VLDL

A

Very low density lipoprotein

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27
Q

Adipose during absorptive state (feeding)

A

Receives TRIGLYCERIDES packaged as chylomicrons in intestines, along with any excess GLUCOSE

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28
Q

Skeletal Muscle during absorptive state (feeding)

A

Receives GLUCOSE to store as glycogen

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29
Q

All tissues during absorptive state (feeding)

A

Use AMINO ACIDS to make proteins

Use GLUCOSE immediately according to needs

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30
Q

What can happen to an acetyl (or acetyl CoA) group?

A
  1. Enters TCA to make NADH/FADH2
  2. Used to make cholesterol
  3. Pasted together to make fatty acid chains (which is why fatty acids are always an even number of carbons)
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31
Q

What are the enzymes involved in fed-state metabolism

A

Glycogen synthase

Prompted by insulin

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32
Q

What enzymes are involved in fasted-state metabolism

A

Glycogen Phosphorylase

Prompted by glucagon: tells this enzyme to make free molecules of G6P

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33
Q

Fatty Liver Disease

A

When triglycerides are not properly transported from liver to adipose, so stay stuck in liver

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34
Q

Absorptive Fed State (General Synthesis of what everything is doing)

A
  1. Nutrients from gastrointestinal tract go into blood
  2. Muscle takes up glucose and amino acids
  3. Hepatocytes take AMINO ACIDS to make proteins, keto acids, fatty acids, and triglycerides
  4. Hepatocytes take GLUCOSE to make glycogen, GAP, and triglycerides
  5. Adipose takes up Triglycerides from liver
  6. Adipose takes up glucose, made into fatty acids or GAP
  7. ALL TISSUES use glucose as energy source
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35
Q

How is excess glucose stored in the liver?
How is excess glucose stored in adipose?
How is excess glucose stored in muscle?

A

LIVER: Glycogen
ADIPOSE: Triglycerides (sent from liver)
MUSCLE: Glycogen

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36
Q

What can an amino acid be used for during fed-state metabolism?

A
  1. Translation / make proteins

2. Oxidized into keto acids

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37
Q

Chylomicrons

A

The way triglycerides are packaged in the digestive tract and sent directly to adipose tissue for storage

Include cholesterol, lipoproteins, lipid complexes

HUGE - so big that cannot go via bloodstream

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38
Q

Transport and Fate of Dietary Fats (step by step)

A
  1. Bile salts help break down dietary fats
  2. Intestinal epithelial cells absorb cholesterol, lipoproteins, lipid complexes into chylomicrons
  3. Chylomicrons transported to blood via lymph system
  4. Lipoprotein lipase converts triglycerides into free fatty acids and glycerol
  5. Adipose cells reassemble free fatty acids and glycerol into triglycerides for storage. Other cells use free fatty acids for energy, EXCEPT THE BRAIN.
  6. Chylomicron remnants and HDL-C enter liver, creating LDL and VLDL. Some new cholesterol recycled in new bile salts.
  7. LDL-C transported via blod to most cells, where cholesterol is used for synthesis.
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39
Q

What can cholesterol be used for?

A
  1. Steroid hormones
  2. Phospholipid bilayer component
  3. Making new bile salts
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40
Q

What energy source does the liver prefer?

A

Fats!

It wants to spare glucose for the brain / NS; in general this organ DELIVERS glucose to the body… so it won’t use glucose if it can help it

Per the old adage: “Don’t get high on your own supply”

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41
Q

Limitations on glycogen and fat storage

A

Glycogen storage is LIMITED

Fat storage is UNLIMITED

This is why we as humans have a problem with obesity, not being super jacked / buff versions of ourselves

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42
Q

What enzyme turns acetyl CoA into fatty acids?

A

fatty acid synthatase

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43
Q

Triglyceride

A

One glycerol plus three fatty acids

Glycerol comes from glucose intermediate in glycolysis
Fatty acids come from acetyl CoA (this follow pyruvate oxidation)

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44
Q

Key role of the liver

A

To maintain blood glucose homeostasis

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45
Q

Postabsorptive/Fasted State Overview

A
  1. Glycogenolysis (glucose released by liver for other tissues)
  2. Lipolysis
  3. Gluconeogenesis from lactic acid / pyruvate (can take place liver, kidney, AND RBCs)
  4. amino acid breakdown in extra hepatic tissues
    * * in liver, amino acids used as substrates for gluconeogensis
  5. Oxidation of fatty acids to make ATP
  6. Oxidation of lactic acid by cardiac muscle
  7. Amino acid oxidation in liver
  8. Use of ketone bodies for ATP production
  9. Glycogenolysis in skeletal muscle for use in skeletal muscle
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46
Q

What happens to glucose in fasted state?

A
  1. Released by liver for other tissues
  2. Created from lactic acid / pyruvate in liver, kidney, and RBCs
  3. Created from amino acids in liver
  4. Released by muscle FOR ITSELF (selfish!)
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47
Q

What happens to amino acids in fasted state?

A
  1. Broken down in extra hepatic tissues for protein synthesis, energy, etc
  2. Used in liver to make glucose
  3. Oxidized in liver to make Keto acids, which can be used to make acetyl CoA and ATP
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48
Q

What happens to fats in fasted state?

A
  1. Generally broken down for energy

2. Oxidized to produce ATP

49
Q

What is the heart doing during fasted state that is unique?

A

Oxidizing lactic acid

50
Q

Cori Cycle

A

When lactic acid produced by muscles is moved to liver and turned into glucose
** This also takes place in kidneys, RBCs!!

51
Q

Where are ketone bodies made?

A

IN THE LIVER

Then transported to NS, other tissues, heart

Made from fatty acids

52
Q

Energy can come from which processes in the fasted state….?

A
  1. Glycogenolysis
  2. Amino acid oxidation
  3. Lipolysis
  4. Gluconeogensis
  5. Ketogenesis
53
Q

Glycogenolysis (General)

A

Glycogen breakdown, only in liver and skeletal muscle

Hepatic glucose comes in first, but after a few hours is ‘spared’ for the NS (so runs out)
Muscle glycogen ONLY USED in muscle cells

54
Q

Amino Acid Oxidation (General)

A

Come from breakdown of proteins, only occurs during a prolonged fast

55
Q

Lipolysis (General)

A

Breakdown of fats

Triglycerides broken down to fatty acids and glycerol

Glycerol can be converted to glucose in the liver

Fatty acids can be broken down into acetyl CoAs / oxidized as needed into ketone bodies

56
Q

Gluconeogenesis (General)

A

Make glucose from lactic acid or some amino acids

57
Q

Ketogenesis (General)

A

Another energy source for the brain

58
Q

Glycogenolysis (in depth)

A

Glycogen is a branched polymer of glucose: two different enzymes liberate glucose in the form of G6P from this branching.

The more important enzyme is Glycogen phosphorylase, which removes G1P from glycogen chain at UNBRANCHED points. An isomerase then converts to G6P and reenters glycolysis.

Monomers of unphosphorylated glucose are removed at branched points…we don’t need to know this.

59
Q

Does the liver have hexokinase? Why or why not?

A

NO! Hexokinase is less specific, high affinity glucose enzyme. Liver only has low affinity glucokinase (specific for glucose).

Liver is not a high priority glucose taker. It’s like the grandmother who takes the food last at the family dinner!

60
Q

What enzyme removes glucose from glycogen?

A

Glycogen phosphorylase! (takes out of glycogen to make G-1-P, which is converted to G-6-P)

61
Q

What enzyme pieces glucoses together to make glycogen?

A

Glycogen synthase!

62
Q

Amino Acid Oxidation (Biochemistry)

A

FIRST, amino acids must be deaminated to undergo oxidation. This produces ammonia and an organic acid.

The organic acid can go through glycolysis or TCA.

SECOND, the ammonia is caustic and must be converted to ammonium and then urea, excreted as waste.

63
Q

Deamination of amino acid produces…

A
  1. Ammonia
  2. Organic acid
  3. NADH! (and H+)
64
Q

Lipolysis (step-by-step)

A
  1. Lipases digest triglycerides into glycerol and 3 fatty acids.
  2. Glycerol becomes substrate in glycolysis.
  3. Beta-oxidation clips 2-carbon units from fatty acids.
  4. Acyl units become acetyl CoA and used in TCA.
65
Q

Beta Oxidation

A

The breakdown of fatty acids into acyl / acetyl groups

66
Q

What is the MAJOR source of energy in lipolysis?

A

Beta oxidation (produces acetyl CoA)

67
Q

What is a MINOR source of glucose in lipolysis?

A

Glycerol (enters glycolysis)

68
Q

Beta Oxidation produces…

A
  1. Acyl units / acetyl CoA

2. NADH and FADH2!

69
Q

Where does Beta oxidation take place?

A

In the mitochondria! (Since FADH2 is involved you know it’s near the membrane)

70
Q

Story of Fasting for Whole Body

A
  1. Liver glycogen becomes glucose. Free fatty acids become ketone bodies or glucose. All may take.
  2. Adipose lipids become free fatty acids and glycerol that enter blood. All may take.
  3. Muscle glycogen used for energy in muscle. Muscles also use fatty acids and break down their proteins to amino acids that enter the blood. ONLY FOR MUSCLE.
  4. Brain uses only glucose and ketones for energy.
71
Q

Glycolysis vs Gluconeogenesis

A

Glycolysis is ten steps to make glucose. It occurs in all cells.

Gluconeogenesis is a nine step REVERSE of glycolysis starting from pyruvate (amino acids, lactate) or glycolytic intermediates (amino acids, glycerol) to make G6P. It occurs in the LIVER and the KIDNEYS only.

72
Q

What steps are different between glycolysis and gluconeogenesis? Are these steps reversed?

A

Steps 1, 3, and 10 of glycolysis, aka the irreversible steps.

They are NOT reversed. They use entirely different enzymes. (The other steps are reversed.)

73
Q

Gluconeogenesis “Step 1” Variation

A

In glycolysis, hexokinase would phosphorylate glucose using ATP, a high-energy molecule.

But G-6-P is not high energy enough for a substrate-level phosphorylation. So cleave the Phosphate group with a phosphatase instead (glucose-6-phosphatase).

74
Q

Gluconeogenesis “Step 3” Variation

A

In glycolysis, PFK uses ATP to phosphorylate F-6-P, creating a bisphosphate.

But F-1,6-bisphosphate is not a high energy compound, so use a phosphatase to cleave the phosphate, making F-6-P (Fructose 1,6-bisphosphatase-1).

75
Q

Gluconeogenesis “Step 10” Variation

A

In glycolysis, PEP (a high-energy compound) phosphorylated ADP to make ATP and pyruvate.

However here the reaction must take TWO steps. ATP is used to convert pyruvate to oxaloacetate, then GTP is used to convert that into PEP.

So TWO molecules of ATP are used to reverse this step, when to make the compound one ATP was created.

76
Q

Why do Type II diabetes drugs block gluconeogenesis?

A

Because cells have become insensitive to glucose, the body does not realize that resources are plentiful so are expelling glucose - and going through a lot of gluconeogenesis unnecessarily!

77
Q

Where does lipolysis occur?

A

ALL CELLS except liver and brain

78
Q

Where does ketosis occur?

A

Just the liver!

79
Q

Ketosis

A

Fatty acids processed into ketones in the liver, these can be used as a second energy source by the brain

80
Q

What are the products of ketosis? And how many are acidic?

A

Acetoacetate
3-beta-hydroxybutyrate
Acetate

2/3 are acidic! All but acetate

81
Q

Ketoacidosis

A

Uncontrolled ketone production; a complication of Type I diabetes, lowers blood pH (high acid makes it difficult for cells to reach potential & fire)

Also causes dehydration and iron imbalances

82
Q

Glucose Sparing

A

Lipolysis occurs to allow for ATP production in cells when glucose is limited or being spared (so that brain gets dibs on glucose)

Triglycerides in adipose tissue catabolized to glycerol and fatty acids

83
Q

When is glycerol an important source of glucose?

A

Only during fasting!

84
Q

Fasted v Fed State Carbs

A

Fed:

  1. Used immediately glycolysis / TCA
  2. Lipoprotein synthesis in liver
  3. Stored as glycogen in liver & muscle
  4. Excess converted to fat & stored in adipose

Fasted:
1. Glycogenolysis in liver & kidney

85
Q

Fasted v Fed State Proteins

A

Fed:

  1. Protein synthesis most tissues
  2. Deaminated in liver and used for energy
  3. Excess converted to fat & stored in adipose

Fasted:

  1. Proteins broken down into amino acids
  2. Gluconeogenesis uses deaminated amino acids
86
Q

Fasted v Fed State Fats

A

Fed:

  1. Lipogenesis in liver and adipose
  2. Cholesterol used for steroids / bilayers
  3. Fatty acids used for lipoprotein and elcosanoid synthesis

Fasted:

  1. Lipolysis
  2. Beta oxidation
87
Q

What hormone(s) govern the homeostatic range of glucose?

A

Glucagon and insulin

88
Q

Endocrine Gland function of pancreas

A

Secrete glucagon and insulin into blood from Islets of Langerhans

Alpha cells - glucagon
Beta cells - insulin, amylin
D cells - somatostatin

89
Q

Exocrine function of pancreas

A

Secrete digestive enzymes via duct to small intestines

90
Q

What does insulin signal for?

A
  1. Glucose oxidation
  2. Glycogen synthesis
  3. Fat synthesis
  4. Protein synthesis
91
Q

What does glucagon signal for?

A
  1. Glycogenolysis
  2. Gluconeogenesis
  3. Ketogenesis

NOTE: Lipolysis is NOT HERE!

92
Q

Hormones when glucose above homeostatic range

A

High insulin

93
Q

Hormones when glucose in homeostatic range

A

Low to moderate insulin

94
Q

Hormones when glucose at low end of range

A

Low insulin plus presence of glucose

95
Q

Hormones in the fed state

A
  1. Eat a meal
  2. GI tract distends, stretch receptors fire, and PARAsympathetic NS stimulates insulin secretion
  3. Presence of carbs in GI lumen stimulates endocrine cells of small intestine, which release GLP-1 and GIP, stimulating insulin secretion
  4. nutrient digestion and absorption increase amino acids and plasma glucose, stimulating insulin secretion

** Increase in plasma glucose INHIBITS alpha cells

96
Q

Which autonomic NS inhibits insulin secretion?

A

Sympathetic

97
Q

Insulin Signaling (For adipose / skeletal muscle)

A
  1. Insulin binds to tyrosine kinase receptor
  2. Receptor phosphorylates insulin-receptor substrates
  3. Second messenger pathway alter protein synthesis and existing proteins.
  4. Glucose transport proteins are sent to cell surface via exocytosis, promoting glucose uptake.
98
Q

What membrane transporter protein is sent to cell surface in adipose / skeletal muscle?

A

GLUT-4

Facilitated diffusion, not as high affinity as transporters in the NS

ONLY FED STATE!

99
Q

What more complicated things does insulin signaling do within a cell?

A

Signals for changes in gene expression (MAP kinase, PTEN SHIP2, etc)
Effects activity of enzymes in glycogen synthesis
Hexokinase traps glucose to make G6P

100
Q

Insulin in the Liver (Fed & Fasted)

A
  1. In taste state, hepatocyte makes glucose and transports out using GLUT-2 transporters.
  2. In fed state, more glucose outside of cell than in, so glucose comes into cell via GLUT-2, where glucokinase phosphorylates to G-6-P.

GLUT-2 = facilitated diffusion

101
Q

Why are proteins only synthesized (aka translated) when there are lots of resources?

A

Because adding each amino acid to the peptide chain requires several molecules of GTP. This can only be done with lots of resources!

102
Q

Beta Cell Insulin Release (step by step)

A
  1. Glucose enters via GLUT2.
  2. Glucose becomes G6P by glucokinase.
  3. Some glucose is metabolized via cellular respiration, leading to ATP > ADP.
  4. Increased ATP binds to K+ leak channel.
  5. K+ leak channel closes, and K+ builds up in cell, depolarizing the cell.
  6. Voltage gated Ca2+ cells open, calcium enters.
  7. Calcium binds to SNARES in vesicles.
  8. Vesicles exocytose and insulin is secreted.
103
Q

What maintains the proportionality of the amount of insulin secreted relative to the amount of excess glucose in the blood?

A

The LOW AFFINITY of transporters / enzymes. The cell will equilibrate to blood glucose levels because the GLUT-2 transporters are passive and not high affinity. Glucokinase also has low affinity, so will never over signal for insulin release.

104
Q

When do you see zero insulin release?

A

Type 1 diabetics

105
Q

Low Blood Glucose Pathway (step by step)

A
  1. Blood glucose down
  2. Beta cells of pancreas are inhibited, decreasing insulin signal to muscle, adipose; these release lactate, pyruvate, amino acids, fatty acids, all of which head to the liver for processing
  3. Plasma glucose down and plasma amino acids up, signaling to alpha cells, which increase glucagon signaling to liver
  4. Liver takes materials and does glycogenolysis, gluconeogenesis, ketosis (for use by brain, other tissues)
  5. Blood glucose rises
106
Q

Glucagon Signaling Pathway (Liver) occurs during…

A

fasting

107
Q

Glucagon pathway (Liver)

A
  1. Glucagon binds to GCPR, heterotrimer talks to adenylate cyclase
  2. cAMP activated
  3. PKA activated
  4. phosphorylase kinase activates, glycogen synthase deactivated
  5. G1P created, made into G6P, gluconeogenesis
108
Q

what signaling pathway mimics the glucagon pathway in muscle and liver?

A

Epinephrine

Signal during exercise

109
Q

Four main hormonal controls

A
  1. Glucagon
    - glycogenolysis, gluconeogenesis
  2. Epinephrine
    - glycogenolysis, gluconeogenesis, AND lipolysis
  3. Cortisol
    - gluconeogenesis, lipolysis, inhibits glucose uptake (aka everything except glycogenolysis)
  4. Growth Hormone
    - same as cortisol
110
Q

Energy homeostasis during moderate exercise

A

Glucose gradually goes down
Insulin goes down same rate of glucose
Glucagon goes way up only when insulin levels low

  • Remember, epinephrine is involved, stimulating the liver
111
Q

Type I Diabetes

A

“Juvenile”

Caused by autoimmune destruction of beta cells; NO insulin is produced

Trigger is unknown, age of onset varies, may be genetic

112
Q

Type II Diabetes

A

“Adult onset”

Caused by chronic high blood glucose (genetic predisposition + lifestyle)

Downregulation of insulin receptors results in HIGH insulin levels; though in advanced cases, insulin impaired

113
Q

Diagnostic Criteria for Diabetes for “Normal” person

A

Fasting blood glucose less than 100 mg/dL

2 hour post test, glucose less than 140 mg/dL

114
Q

Diagnostic criteria for diabetes for pre-diabetes

A

Fasting blood glucose 100-125 mg/dL

2 hour post test, glucose 140-199 mg/dL

115
Q

Diagnostic criteria for diabetes for diabetic

A

Fasting blood glucose >125 mg/dL

2 hour post test, glucose >199 mg/dL

116
Q

When insulin release is impaired…

A

The body thinks that we are starving, but the only problem is lack of signal

Leads to tissue loss, hyperglycemia, polyphagia (ketosis)

117
Q

Hyperglycemia leads to…

A

Metabolic acidosis, dehydration

118
Q

Causes of metabolic acidosis, dehydration

A
  1. ACIDOSIS: Oveproduction of ketones, up ventilation and urine acidification + hyperkalemia
  2. DEHYDRATION: Increase glucose in urine leads to diuresis, dehydration, attempt to compensate leads to increased blood pressure, which leads to circulatory failure / death

Intro Bio II Exam 3 (8 decks)

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