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Human Physiology 2 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

metabolism is a process that supplied energy for ___________

A
  1. active transport
  2. DNA replication
  3. protein synthesis
  4. muscle contraction
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2
Q

food can be used in which two pathways

A
  1. food can be broken down into “building blocks”

2. food can be broken down into components for storage

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3
Q

what are the two types of metabolism

A

catabolism and anabolism

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4
Q

describe catabolism

A
  • > degradative reactions
  • > is the breakdown of complex molecules into simpler forms, resulting in the release of energy and the increase of body heat
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5
Q

exergonic vs endergonic

A

exergonic
- > release of energy (catabolism)
endergonic
- > use of energy (anabolism)

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6
Q

describe an example of catabolism

A
  • > glycogen that is broken down into glucose
  • > proteins which are broken down into amino acids/chains of amino acids
  • > triacylglycerides which are broken down into glucose/glycerol and fatty acids
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7
Q

describe anabolism

A
  • > when simple molecules combine to form body’s structural and functional components
  • > results in the use of energy
  • > can result in the storage of energy substrates
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8
Q

list an example of anabolism

A
  • > formation of peptide bonds between amino acids to form proteins
  • > the linkage of several molecules of glucose to form glycogen
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9
Q

Metabolic Rate (MR)

A
  • > the body’s rate of energy output
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10
Q

MR can be broken down into which subcategories

A

MR

  1. Basal Metabolic rate (BMR)
  2. Total Metabolic Rate (TMR)
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11
Q

how are MR and body temp linked

A

they rise and fall together

  • > an increased MR mean and increase in heat production through increased catabolic reactions to release energy
  • > and vice versa
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12
Q

stresses effects on MR

A

stress increases MR though sympathetic stimulation (fight or flight)

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13
Q

thyroxine

A
  • > the thyroid hormone
  • > the GREATEST determinant of MR
  • it does this by increasing oxygen consumption and heat production through increased ATP usage
    incr. thyroxine = incr. body heat = incr. MR
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14
Q

Basal Metabolic Rate (BMR)

A

basal means resting state, not sleeping but not active

- > BMR is the energy that the body needs to perform only essential activities (i.e. cardiac, respiratory)

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15
Q

Total Metabolic Rate (TMR)

A

the rate of kilocalorie consumption needed to fuel ALL body activities

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16
Q

the effects of skeletal muscle activity on TMR

A

skeletal muscle activity results in the greatest SHORT-term changes to TMR

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17
Q

food ingestion ______ TMR

A

increases

  • > food-induced thermogenesis
  • food induced thermogenesis is greatest when proteins (and alcohol) are ingested, mostly as a result of increased liver activity
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18
Q

hormonal determinants of MR

A
  1. Thyroid Hormones (TH)
  2. Catecholamines/Epinephrine and Norepinephrine
  3. Cortisol
  4. Glucagon
  5. Insulin
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19
Q

The release of thyroid hormones results in _______

A
  • > incr. use of glucose, fats and proteins due to increased tissue/cellular metabolism
  • > incr. GI absorption of glucose (from plasma into cells, for fuel)
  • > incr. catabolism of cholesterol in the liver
  • > incr. mobilization of lipids from the adipose(fat) tissue (to supply an energy substrate)
  • > inc. cardio-pulmonary activity, skeletal muscle activity and GI function
  • > the body’s oxygen consumption incr. as does the body’s heat production
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20
Q

functions of TH

A
  • > mental alertness and reflexes
  • > normal body growth
  • > facilitates activity of the sympathetic nervous system
  • > major determinant of the rate at which the body produces heat during basal metabolic state
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21
Q

summary of TH function

A

TH helps maintain plasma glucose levels for activity through the release of lipids from the adipose tissue and increasing absorption of glucose from the intestinal tract into the blood

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22
Q

How are Catecholamines/Epinephrine and Norepinephrine produced?

A
  • > Catecholamines/Epinephrine are secreted by the adrenal medulla
  • > Norepinephrine is secreted by sympathetic neurons
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23
Q

the release of Catecholamines/Epinephrine and Norepinephrine results in what?

A
  • > causes increased MR and increased catabolism of glycogen and triacylglycerol
  • > increased release of fatty acids and glycerol - increasing the formation of glucose
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24
Q

when is cortisol released

A
  • the stress hormone*
  • > released with stress and fasting and as a part of the normal circadian rhythm from the adrenal cortex
  • > it’s released early in the morning to get the system ready for activity
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25
Q

the release of cortisol results in ______

A
  • > incr. protein catabolism (not the key activity of cortisol)
  • > increased triglyceride breakdown from the adipocytes
  • > increased gluconeogenesis (formation of “new” glucose)
  • > decreased glucose intake (doesn’t take any more from the blood, maintains blood glucose concentration)
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26
Q

glucagon

A
  • > found primarily in the liver and plays a role in maintaining plasma glucose levels when GI tract is empty
  • > released in the post absorptive state
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27
Q

what happens after the release of glucagon

A
  • > increased glycogenolysis (breakdown of STORED glycogen, releasing glucose) in the liver
  • > increased gluconeogenesis (formation of new glucose) in the liver
  • > increased lipolysis and ketosis
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28
Q

insulin

A

the STORAGE hormone for glucose

  • > the key to maintaining plasma glucose
  • triggered/stimulated by an absorptive state
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29
Q

Insulin is released as a result of what?

A
  • > increased plasma glucose concentrations
  • > increased release of incretins (hormones secreted by endocrine cells in the GI tract)
  • > increased parasympathetic activity (rest and digest)
  • > increased release of osteocalcin from the osteoblasts (builders)
  • release of osteocalcin results in decreased plasma glucose and increased storage of glucose as glycerol and triglycerides
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30
Q

incretins

A

incretins amplify the insulins response to glucose, resulting in higher levels of insulin secretion than if plasma glucose concentration was the only controller

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31
Q

absorptive vs post-absorptive states

A

Absorptive
- > ingested nutrients result in a gull GI tract with associated reflexes, nutrients are absorbed into the bloodstream and either utilized for energy production or sent to storage
Post-Absorptive
- > the GI tract is relatively empty and nutrients must be released from stores for energy production. Stored energy (fats, glycogen) are released from stores, broken down into usable components and sent throughout the body via the bloodstream

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32
Q

How does your body stimulate the feeling of hunger?

A
  • > hypothalamic arcurate nucleus (first region)
  • > neuropeptide Y (NPY) and agouti-related peptide (AgRP) enhance appetite by stimulating LHA to release orexin
  • > orexin stimulates the feeling of hunger
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33
Q

How does your body stimulate the feeling of being full/suppressing appetite

A
  • > pro-opiomelanocortin (POMC) + cocain-amphetamine-regulated transcript (CART) released from ARC results in an appetite suppression by stimulating the ventromedial nucleus (VMN) to release CRH (corticotropin-releasing hormone)
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34
Q

how does the hypothalamus know which appetite pathway to activate

A
  • > the hypothalamus receives feedback signals from chemoreceptors, osmoreceptors, and mechanoreceptors that note the alterations to the contents of the GI tract lumen as well as the stretch of the GI tract walls
  • if stretch appetite suppression will occur
  • > neural signals from the GI tract to the hypothalamus travel through a 2-way vagal pathway
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35
Q

signals that can regulate appetite include

A
  1. increased plasma glucose - > depression of hunger
  2. increased plasma amino acids - > depression of hunger
  3. increased plasma fatty acids - > depression of hunger
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36
Q

signals/hormones that help regulate increased plasma glucose, amino acids and fatty acid levels

A
  • > insulin and cholecystokinin (CCK)
  • > glucagon and epinephrine
  • > ghrelin (Ghr)
  • > leptin
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37
Q

when are insulin and cholecystokinin (CCK) released

A

during food absorption

- > results in the depression of hunger (CCK specifically blocks NPY signals)

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38
Q

when is glucagon and epinephrine released

A

they’re released during a fasting/post-absorptive state to stimulate appetite

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39
Q

when is ghrelin (Ghr) produced?

A

produced by the stomach, peaks before meals, signalling the brain that it is time to eat

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40
Q

when is leptin secreted

A

it’s secreted by the adipose tissue in response to increased body fat mass, suppresses appetite (weak signal, we can ignore it easily)

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41
Q

classification of food

A
  1. carbohydrates
    - > breakdown results in monosaccharides (simple sugars; glucose)
  2. proteins
    - > breakdown results in amino acids
  3. fats
  4. vitamins and minerals
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42
Q

how are the products from carb and protein breakdowns transported for processing

A

monosaccharies (carb breakdown) and amino acids (protein breakdown) are sent through the hepatic portal system for processing via the bloodstream

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43
Q

how are fats transported during the absorptive state

A

digested fats are absorbed into the lymphatic system through the lacteals in the GI tract, from there, they enter the systemic blood system

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44
Q

which organs/structures carry absorbed nutrients from food ingestion to the liver? How do they do this

A
  1. small intestinal villi
  2. large intestin
  3. pancreas
  4. portions of the stomach
    - > they all have venous drainage that enters the liver through the hepatic portal vein
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45
Q

what happens to the blood-borne nutrient molecules once they passed through the liver after being processed/repackaged

A

blood borne nutrient molecules drain into the hepatic vein which carries they blood into the vena cava and eventually into the heart for whole body distribution

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46
Q

explain the livers blood supply

A

Arterial blood
- > the hepatic artery supplies the liver with oxygen and carries blood-borne metabolites to the liver for hepatic processing
Venous blood
- > the portal vein drains the digestive tract and carries newly absorbed nutrients in to the liver for processing
- > the hepatic vein leaves the liver and drains (out) into the vena cava

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47
Q

where does blood go once drain into the liver

A
  • > blood enters the liver via the hepatic portal vein and drains into the sinusoids (right and left), which are connected to the hepatic artery and hepatic vein
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48
Q

sinusoids

A

structures in the liver (type of capillary) connected to the hepatic artery and vein

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49
Q

Kupffer cells

A

cells that line the sinusoids and play a role in destruction of old red blood cells and bacteria (some immune defence activity

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50
Q

hepatocytes form _____?

A

“plates”, 2 cell layer thick with an edge facing the sinusoidal blood pool

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51
Q

bile canaliculus

A

thin, bile carrying channels that run between the “plates”
- > hepatocytes secrete bile components into these channels which carry bile/bile components into a bile duct at the liver periphery and then eventually the gallbladder

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52
Q

bile

A

removes metabolic waste/toxins and plays a role in dejestion of fats as the gallbladder secretes bile into the sm.intestine during absorptive state

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53
Q

digestive functions of the liver

A
  • > production of bile salts for digestion

- > processing and storage of dietary fats, carbs, proteins and vitamins and minerals

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54
Q

endocrine functions of the liver

A
  • > metabolism of glucorticoids, mineralcorticoids and sex hormones
  • > regulation of carb, fat and protein metabolism
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55
Q

hematologic functions of the liver

A
  • > temp storage of blood
  • > synthesis of bilirubin (orange-yellow pigment)
  • > production of clotting factors
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56
Q

excretory functions of the liver

A
  • > cholesterol production and secretion
  • > formation of bile pigment
  • > urea synthesis
  • > detoxification of drugs and other substances
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57
Q

1 glucose molecule is how may ATP molecules

A

38, though this number is dependant on whether the system is producing ATP via aerobic or anaerobic methods

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58
Q

what is carbohydrate catabolism

A

when the dietary carbohydrates (excluding fiber) are broken down and absorbed as monosaccharides, such as glucose, galactose and fructose

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59
Q

how does glucose and galactose gain entry into the epithelial cells of the GI tract (renal tubules)

A

through secondary active transport coupled to Na+ via sodium-glucose co-transport(SGLT1)
- > Na must first bind to the transporter to make the glucose/galactose binding site available and ATP is also a requirement to power the transport

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60
Q

how does fructose enter the epithelial cells of the GI tract (renal tubules)

A

enters the epithelial cells by facilitated diffusion via specialized integral protein carriers known as glucose transport, GLUT
- > absorption is slower for fructose than for glucose or galactose

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61
Q

How do fructose, glucose and galactose leave the epithelial cells, what does this mean

A
  • > they exit the cells into the interstitial fluid using facilitated diffusion and basolateral membrane GLUT.
  • > once in the interstitial fluid, the monosaccharides enter the blood through the capillary pores
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62
Q

What happens when intestinal lumen glucose conc. is too high

A

glucose can be transported into the enterocytes using GLUT2 transporters, which also transport galactose and fructose

63
Q

what happens when plasma concentration of glucose rise and levels of plasma insulin also increases

A

glucose transporters move to intracellular vesicles, storing monosaccharides intracellularly, decreasing the absorption of glucose into the blood

64
Q

what influences the location of the GLUT2 transporter

A

the signal from insulin and “sweetness receptors”

65
Q

enterocytes

A

intestinal epithelial cells

66
Q

GLUT5

A

fructose transporter into the enterocytes while GLUT2 moves enterocyte fructose into the portal vein for delivery to the liver

67
Q

what percentage of energy formed from carb metabolism goes to produce ATP

A

40%

68
Q

What happens if we increase the level of fructose intake

A

can result in intestinal distress
- > high dietary intake of fructose can occur with high intake of carbonated beverages sweetened with high fructose corn syrup

69
Q

levels of glycogen that the liver and muscle can store

A

the liver can store around 7% of your body weigh in glucose and the muscles are capable of storing around 1% of your body weight

70
Q

starch

A

majority of ingested carbs

71
Q

digestion of starches

A

digestion by salivary amylase begins in the mouth, but most starch digestion occurs in the small intestine with the presence of pancreatic amylase

72
Q

what does starch break down into

A

starch is broken down by pancreatic amylase and forms [glucose+galactose] and fructose
- > both are then transported into the intestinal epithelial cells, via their own transport methods and then into interstitial fluid

73
Q

what occurs when glucose enters most cells

A

energy production (immediate path ATP)

74
Q

what occurs when glucose enters adipocytes

A

alpha-glycerol phosphate is produced

75
Q

what occurs when glucose enters the liver

A

glycogen or alpha-glycerol phosphate+fatty acids are produced
- > fatty acids are then packaged into lipoproteins and sent into the blood

76
Q

what happens when fatty acids that were packaged into lipoproteins are sent into the blood

A

the lipoproteins are broken down by lipoprotein lipase in the capillary endothelial cells and monoglycerides are formed
- > these monoglycerides are then either diffused into adipocytes to form tryglycerides or they continue in the blood towards the liver

77
Q

Fatty acid formation

A

Glucose - > glycolysis - > pyruvate - > acetyl CoA - > acetyl group of 1 Acetyl CoA transferred to second acetyl CoA - > forms 4 carbon chain - > entire process is repeated until fatty acid is formed (12-14 carbon chain)

78
Q

Triglyceride formation

A

Glucose - > alpha-glycerol phosphate - > alpha-glycerol phosphate + 3 fatty acids - > triglyceride

79
Q

glycogen formation

A

glucose + ATP - > glucose-6-phosphate - > glycogen and pyruvate

80
Q

Final absorptive state summary for plasma glucose

A

SEE PAGE 16

81
Q

proteases

A

a class of enzymes which result in the release on amino acids

82
Q

the breakdown of amino acids includes _____

A

it includes the removal of nitrogen groups from amino acids using 2 reaction

83
Q

list both amino acid breakdown reactions that occur in the body

A
  1. Oxidative deamination

2. Transamination

84
Q

describe oxidative deamination

A

when an amino acid + a co-enzyme interact to form…
ammonia (NH3) + a keto acid + transformed co-enzyme
- > keto acid is then used for transamination

85
Q

describe transamination

A

involves the interaction between an amino acid and a keto acid (from oxidative deamination) to form a DIFFERENT amino acid and keto acid

86
Q

what happens if we have an accumulation of keto acids

A

this can result in a decrease in blood pH

87
Q

explain how we process NH3 from oxidative deamination

A

through the liver in the following pathway
NH3 + NH3 +CO2 = urea
- > we then send the urea into the blood where it travels to the kidneys

88
Q

what happens to urea once it travels to the kidneys

A

40% of the urea is excreted in urine while the other 60% is used as a solute by the renal system for increasing water reabsorption

89
Q

extensive protein breakdown can cause what?

A

it can overwhelm the liver due to the massive release of amino acids due to this breakdown
- > if there’s not enough liver enzymes to convert NH3 into urea, then NH3 can accumulate in the blood, which can damage the liver and CNS (neurotoxin)

90
Q

what if we end up having enough liver enzymes to keep up with an extensive protein breakdown

A

the amount of urea produced by liver enzymes can be too much for the kidneys to handle and can trigger kidney failure

91
Q

results of increased tubular fluid urea concentrations

A

inc, tubular fluid urea conc. can increase water reabsorption resulting in increased blood volume and blood pressure

92
Q

how many of the essential amino acids can be formed via transamination

A

11
- > the amino acids formed through transamination supply some of the amino acids used for building blocks for protein formation

93
Q

aminotransferase

A

the enzyme responsible for the transamination pathway
- > primary purpose is to remove the amino group from various alpha-amino acids and collect them in a single type of molecule, glutamate

94
Q

glutamate

A

acts as a single source of amino acids groups for continuous nitrogen breakdown

95
Q

where do we find most aminotransferases

A

in the cytoplasm of most cells and all have a group that is derived from the B6 vitamin

96
Q

how many amino acids cannot be synthesized sufficiently (or at all by the liver), what must we do to combat this issue

A

8 AA in adults, 10 in children

  • > we must get them from dietary sources
  • > they cannot be stored so if not used immediatly after absorption, they’ll be oxidized for energy and converted to carbs or fats
97
Q

essential amino acids

A
  1. isoleucine
  2. leucine
  3. methionine
  4. phenylalanine
  5. threonine
  6. lysine
  7. tryptophan
  8. valine
    (arginine and histidine in children)
    - > most plant proteins don’t provide enough of 1 or more essential AA but combining the appropriate one can get you all 8
98
Q

describe the AA pathways in the body

A

a) majority of AAs will enter the body cells and be used to form cell proteins (primary path of ingested proteins and AA)
b) some of the circulating AAs will be absorbed into the liver and used in several pathways

99
Q

list some of the pathways that AAs will take if they’re absorbed into the liver

A

see page 20

100
Q

triacylglycerol

A

fat

101
Q

what percentage of energy storage is stored as fat

A

80

- > stored mainly in the adipose tissue as triglycerides

102
Q

1x 18-carbon saturated fatty acid is how many ATP molecules

A

146, fats contain more than twice as much chemical energy as carbs or proteins

103
Q

when does triglyceride(fat) digestion start

A

starts in the mouth and stomach BUT the majority of digestion occurs in the small intestine with the digestive enzyme, pancreatic amylase
triglycerides —(lipase)—-> monoglycerides +2 fatty acids

104
Q

explain the emulsification of fats

A

2 processes

  1. Mechanical emulsification
    - > parts of GI tract (lower portions of the stomach and small intestine) churn the food as you digest
  2. Addition of an emulsification agent
    - > bile (provided by the liver) provides the emuls. agent
    - > bile salts result in the release of micelles
105
Q

micelles

A

tiny spheres of fatty acids that release fatty acids and monoglycerides in small quantities into the GI tract lumen for diffusion into the intestinal epithelial cells
- > the endoplasmic reticulum in the intes. epi. cells reform tryglycerides from the absorbed monoglycerides and fatty acids

106
Q

describe the process how we store fat in our cells using micelles

A

see page 22

107
Q

vitamins are used as _____

A

co-enzymes

- > helps the body use nutrients for energy production

108
Q

vitamins are derived from _____

A

food sources during the absorbative state

109
Q

What is B1 and what happens when we are deficient

A

Thiamine

  • > beriberi (nerve disorder),
  • > tingling,
  • > poor coordination,
  • > reduced cardiac function
110
Q

What is B2 and what happens when we are deficient

A

Riboflavin

- > skin lesion

111
Q

What is B3 and what happens when we are deficient

A

Niacin

- > skin and GI lesions; nerve disorders

112
Q

What is B6 and what happens when we are deficient

A

pyridoxine

  • > irritability
  • > convulsions
  • > muscular twitching
  • > anemia
113
Q

What is B5 and what happens when we are deficient

A

panthothenic acid

  • > fatigue
  • > numbness
  • > tingling of the hands and feet
114
Q

What is B9 and what happens when we are deficient

A

folacin

  • > anemia
  • > birth defects
115
Q

what happens when we are deficient in B12

A
  • > anemia

- > nervous system disorders

116
Q

What is vitamin C and what happens when we are deficient

A

ascorbic acid

- > scurvy (degradation of blood, teeth, skin)

117
Q

What is vitamin A and what happens when we are deficient

A

retinol

- > blindness and increased death rate

118
Q

what happens when we are deficient in vitamin D

A

rickets (children) and osteomalacia (adults)

119
Q

what happens when we are deficient in vitamin E, whats it called

A

alpha-tocopherol

- > degeneration of the nervous system

120
Q

what happens when we are deficient in vitamin K, whats the vitamin called

A

phylloquinone

- > defective blood clotting

121
Q

what happens when we are deficient in biotin

A
  • > scaly skin
  • > inflammation
  • > neuromuscular disorders
122
Q

what are the fat soluble vitamins

A

A D E K

- > all stored in the body (except for K) and over ingestion can lead to toxicity (especially A)

123
Q

water soluble vitamins

A

All B vitamins and C

  • > easily absorbed through simple diffusion in the GI tract (B12 does require a specific molecular complex formation for absorption)
  • > only retained in the body for a short time, excreted if not used
124
Q

post-absorptive state

A
  • > plasma glucose concentrations must be maintained

- > sources of blood glucose during the PA state are from stores outside of the GI tract

125
Q

what are the different systems we use for glucose production during the POST-absorptive state

A
  1. Liver processes
  2. Skeletal muscles
  3. Adipose tissue
  4. Protein breakdown
126
Q

glycogenolysis

A

hydrolosis(formation) of glucogen, first line of plasma maintenance in the PA state
Glycogen hydrolysis < - > Glucose-6-phosphate < - > Glucose

127
Q

what does the liver do during PA state to maintain plasma glucose

A

liver performs glycogenolysis; first line of plasma glucose maintenance
- > only effective for a few hours or until glycogen stores are depleted

128
Q

what do the skeletal muscles do to maintain plasma glucose during the PA state

A

glycogenolysis is also performed to produce glucose

  • > we then take that glucose to be used in ther energy pathways, creating either pyruvate or lactate as a waste product
  • > pyruvate/lactate is released into the bloodstream where it is sent to the liver and transformed into glucose
129
Q

what does the adipose tissue do to maintain plasma glucose during the PA state

A

lypolysis breaks down the stored fats (triglycerides) and releases the products into the blood

130
Q

what happens to the products of triglyceride breakdown

A

Triglycerides - > glycerol + free fatty acids

SEE PAGE 26

131
Q

does the brain like using ketones as fuel

A

the brain doesn’t like to use ketones
- > the brain continues to use glucose during the PA state but will also start using ketones as they build in the blood with prolonged fasting and increased energy needs

132
Q

how does protein breakdown help maintain plasma glucose during the PA state

A

protein in muscle and other tissues can be broken down, releasing amino acids into the blood
- > the AA go to the liver via the blood then go through the alpha-keto acid pathway to produce glucose

133
Q

what happens during fasting or with untreated diabetes mellitus

A
  • > with fasting, glycogen stores are depleted (pretty quickly) and cells require another fuel source: fat
  • > with Diabetes mellitus, the cellular inability to utilize plasma glucose triggers fat breakdown
  • both processes can result in increased plasma levels of ketone bodies
    inc fat breakdown - > inc. plasma beta-hydroxybutyrate, acetone and acetoacetate - > hyperketonemia
134
Q

glyconeogenesis

A

formation of glucose from STORED components

- > occurs primarily in the liver and secondarily in the kidneys

135
Q

what are the 2 pathways for the formation of glucose through gluconeogenesis

A
  1. glycerol from the breakdown of stored tryglycerides = glucose
  2. AA from protein breakdown/metabolism can be converted to glucose through the pyruvate/glycolytic pathway
136
Q

explain the process of gluconeogenesis

A
  • > gluconeogenesis utilizing the glycolytic pathway starts with the conversion of lactate and AA intermediates to PYRUVATE
  • > once pyruvate enters the path, the glycolytic process is reversed, producing fructose-6-phosphate
  • > once fuctose-6-phosphate is formed, the reversed glycolytic pathway can continue until glucose is formed
137
Q

how do we control the direction of the glycolytic pathway

A

through the release of hormone: glucagon reverses the pathway and produces glucose, while insulin causes the pathway to move in the forward direction producing pyruvate and lactate

138
Q

cori cycle

A

SEE PAGE 29

liver takes waste from muscle movements/ contractions and converts them into glucose

139
Q

Steps involved in maintaining plasma glucose during fasting/PA state

A
  1. Adipose tissue: increased lipolysis of triglycerides, releasing glycerol and free fatty acids
  2. blood delivers fatty acids to liver to form Acetyl CoA through beta-oxidation of the fatty acids
  3. Liver converts Acetyl CoA to ketones (Ketone bodies: acetone, acetoacetate, beta hydroxybutyrate) and released into the blood for use by most cells as an energy source
  4. As ketone bodies build in the blood, hyperketonemia may occur which causes ketacidosis (lungs play a role in eliminating this)
  5. With extreme fasting/diabetes, protein breakdown occurs, resulting AA are sent to liver to be converted into alpha-keto acids, producing urea that goes into the blood, alpha keto acids then go to produce glucose
    SEE PAGE 30 FOR EXTRA DETAILS
140
Q

explain how blood glucose change with exercise

A
  • > blood glucose levels change very little in short term, mild to moderate exercise
  • > BGL may increase slightly with strenuous short term activity
  • > with prolonged (more than 90min) activity, BGL tend to decrease, sometimes as much as 25% of baseline
  • > the changes during prolonged activity is similar to what happens during fasting
141
Q

what is the exception to the similarity between prolonged exercise and fasting

A

during exercise, glucose uptake into muscle cells increased while in fasting, it is very much reduced

142
Q

What activities happen during exercise to help maintain BGL

A
  1. increased liver glucose production (gluconeogenesis, glycogenolysis)
  2. increased triacylglyceride breakdown
  3. fatty acid utilization + ketone formation and utilization
  4. potential breakdown of stored protein, releasing products for gluconeogenesis and for repair of damaged tissues, if damage occurs
143
Q

hyperketonemia

A

Hyperketonemia is a condition with elevated blood levels of acetoacetate, 3-β-hydroxybutyrate, and acetone

144
Q

cellular requirements for energy (ATP)

A
  1. Na - K Pump: used for action potentials for muscle contractions
  2. Ca pump: used for Ca storage, which is used for skeletal and smooth muscle activity, action potentials, cardiac muscle contractions
  3. Phosphorylation of effector proteins: results in hundreds of cell functions
  4. Co-Transport of organic molecules: such as epithelial transport for maintenance of organic molecule concentrations in blood (nutrients and waste) mainly in GI tract and kidneys
145
Q

explain ATP and energy transfer

A
  • > they energy from the breakdown of fuels is transferred to the molecule, adenosine triphosphate
  • > the release of energy (ATP hydrolysis) is accomplished through the removal of a phosphate group from ATP resulting in the formation of ADP + P
146
Q

production of ATP

A

cellular energy production is through complex chemical reactions (metabolic pathways) that usually result in the movement of electron from one compound to another

147
Q

explain cellular energy and how it related to ATP production

A

since energy cannot be created or destroyed (1st law of thermodynamics) it must be transformed using biochemical reactions

148
Q

examples of how we classify compounds by their energy levels

A

high energy: phosphocreatine (stored in skeletal muscles)
Intermediate: ATP
Low energy, glucose-6-phosphate, ADP, glucose

149
Q

oxidation

A

gain 1 oxygen or lose a H

- > oxidized: loses energy

150
Q

reduction

A

gains an electron

- > reduces space on the atom, reduced substances gain energy

151
Q

redox reaction are catalyzed by what?

A

enzymes

  1. dehydrogenases = removal of H
  2. oxidases = transfer of oxygen
152
Q

2 molecules that serve important roles in redox reactions

A
  1. NAD (nicotinamide adrenine dinucleotide)
    - > derived from niacin (B3)
  2. FAD (flavin adenine dinucleotide)
    - > derived from riboflavin (B2)
153
Q

glucose sparing

A

the increased use of non-carb fuel molecules (especially triglycerides) to conserve glucose during prolonged periods without food

  • > we must have a glucose baseline/spare remaining glucose for the brain, NS and other systems as they especially require glucose, the remaining body systems switch to fatty acids as its fuel source
  • > body systems oxidize fat for energy and the liver converts fatty acids to ketones for cellular energy in the kreb cycle

Human Physiology 2 (3 decks)

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