Metabolism Flashcards
(153 cards)
1
Q
metabolism is a process that supplied energy for ___________
A
- active transport
- DNA replication
- protein synthesis
- muscle contraction
2
Q
food can be used in which two pathways
A
- food can be broken down into “building blocks”
2. food can be broken down into components for storage
3
Q
what are the two types of metabolism
A
catabolism and anabolism
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
5
Q
exergonic vs endergonic
A
exergonic
- > release of energy (catabolism)
endergonic
- > use of energy (anabolism)
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
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
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
9
Q
Metabolic Rate (MR)
A
- > the body’s rate of energy output
10
Q
MR can be broken down into which subcategories
A
MR
- Basal Metabolic rate (BMR)
- Total Metabolic Rate (TMR)
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
12
Q
stresses effects on MR
A
stress increases MR though sympathetic stimulation (fight or flight)
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
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)
15
Q
Total Metabolic Rate (TMR)
A
the rate of kilocalorie consumption needed to fuel ALL body activities
16
Q
the effects of skeletal muscle activity on TMR
A
skeletal muscle activity results in the greatest SHORT-term changes to TMR
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
18
Q
hormonal determinants of MR
A
- Thyroid Hormones (TH)
- Catecholamines/Epinephrine and Norepinephrine
- Cortisol
- Glucagon
- Insulin
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
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
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
22
Q
How are Catecholamines/Epinephrine and Norepinephrine produced?
A
- > Catecholamines/Epinephrine are secreted by the adrenal medulla
- > Norepinephrine is secreted by sympathetic neurons
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
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
25
the release of cortisol results in ______
- > 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)
26
glucagon
- > 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
27
what happens after the release of glucagon
- > increased glycogenolysis (breakdown of STORED glycogen, releasing glucose) in the liver
- > increased gluconeogenesis (formation of new glucose) in the liver
- > increased lipolysis and ketosis
28
insulin
the STORAGE hormone for glucose
- > the key to maintaining plasma glucose
* triggered/stimulated by an absorptive state
29
Insulin is released as a result of what?
- > 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
30
incretins
incretins amplify the insulins response to glucose, resulting in higher levels of insulin secretion than if plasma glucose concentration was the only controller
31
absorptive vs post-absorptive states
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
32
How does your body stimulate the feeling of hunger?
- > 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
33
How does your body stimulate the feeling of being full/suppressing appetite
- > 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)
34
how does the hypothalamus know which appetite pathway to activate
- > 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
35
signals that can regulate appetite include
1. increased plasma glucose - > depression of hunger
2. increased plasma amino acids - > depression of hunger
3. increased plasma fatty acids - > depression of hunger
36
signals/hormones that help regulate increased plasma glucose, amino acids and fatty acid levels
- > insulin and cholecystokinin (CCK)
- > glucagon and epinephrine
- > ghrelin (Ghr)
- > leptin
37
when are insulin and cholecystokinin (CCK) released
during food absorption
| - > results in the depression of hunger (CCK specifically blocks NPY signals)
38
when is glucagon and epinephrine released
they're released during a fasting/post-absorptive state to stimulate appetite
39
when is ghrelin (Ghr) produced?
produced by the stomach, peaks before meals, signalling the brain that it is time to eat
40
when is leptin secreted
it's secreted by the adipose tissue in response to increased body fat mass, suppresses appetite (weak signal, we can ignore it easily)
41
classification of food
1. carbohydrates
- > breakdown results in monosaccharides (simple sugars; glucose)
2. proteins
- > breakdown results in amino acids
3. fats
4. vitamins and minerals
42
how are the products from carb and protein breakdowns transported for processing
monosaccharies (carb breakdown) and amino acids (protein breakdown) are sent through the hepatic portal system for processing via the bloodstream
43
how are fats transported during the absorptive state
digested fats are absorbed into the lymphatic system through the lacteals in the GI tract, from there, they enter the systemic blood system
44
which organs/structures carry absorbed nutrients from food ingestion to the liver? How do they do this
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
45
what happens to the blood-borne nutrient molecules once they passed through the liver after being processed/repackaged
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
46
explain the livers blood supply
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
47
where does blood go once drain into the liver
- > 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
48
sinusoids
structures in the liver (type of capillary) connected to the hepatic artery and vein
49
Kupffer cells
cells that line the sinusoids and play a role in destruction of old red blood cells and bacteria (some immune defence activity
50
hepatocytes form _____?
"plates", 2 cell layer thick with an edge facing the sinusoidal blood pool
51
bile canaliculus
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
52
bile
removes metabolic waste/toxins and plays a role in dejestion of fats as the gallbladder secretes bile into the sm.intestine during absorptive state
53
digestive functions of the liver
- > production of bile salts for digestion
| - > processing and storage of dietary fats, carbs, proteins and vitamins and minerals
54
endocrine functions of the liver
- > metabolism of glucorticoids, mineralcorticoids and sex hormones
- > regulation of carb, fat and protein metabolism
55
hematologic functions of the liver
- > temp storage of blood
- > synthesis of bilirubin (orange-yellow pigment)
- > production of clotting factors
56
excretory functions of the liver
- > cholesterol production and secretion
- > formation of bile pigment
- > urea synthesis
- > detoxification of drugs and other substances
57
1 glucose molecule is how may ATP molecules
38, though this number is dependant on whether the system is producing ATP via aerobic or anaerobic methods
58
what is carbohydrate catabolism
when the dietary carbohydrates (excluding fiber) are broken down and absorbed as monosaccharides, such as glucose, galactose and fructose
59
how does glucose and galactose gain entry into the epithelial cells of the GI tract (renal tubules)
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
60
how does fructose enter the epithelial cells of the GI tract (renal tubules)
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
61
How do fructose, glucose and galactose leave the epithelial cells, what does this mean
- > 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
62
What happens when intestinal lumen glucose conc. is too high
glucose can be transported into the enterocytes using GLUT2 transporters, which also transport galactose and fructose
63
what happens when plasma concentration of glucose rise and levels of plasma insulin also increases
glucose transporters move to intracellular vesicles, storing monosaccharides intracellularly, decreasing the absorption of glucose into the blood
64
what influences the location of the GLUT2 transporter
the signal from insulin and "sweetness receptors"
65
enterocytes
intestinal epithelial cells
66
GLUT5
fructose transporter into the enterocytes while GLUT2 moves enterocyte fructose into the portal vein for delivery to the liver
67
what percentage of energy formed from carb metabolism goes to produce ATP
40%
68
What happens if we increase the level of fructose intake
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
levels of glycogen that the liver and muscle can store
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
starch
majority of ingested carbs
71
digestion of starches
digestion by salivary amylase begins in the mouth, but most starch digestion occurs in the small intestine with the presence of pancreatic amylase
72
what does starch break down into
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
what occurs when glucose enters most cells
energy production (immediate path ATP)
74
what occurs when glucose enters adipocytes
alpha-glycerol phosphate is produced
75
what occurs when glucose enters the liver
glycogen or alpha-glycerol phosphate+fatty acids are produced
- > fatty acids are then packaged into lipoproteins and sent into the blood
76
what happens when fatty acids that were packaged into lipoproteins are sent into the blood
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
Fatty acid formation
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
Triglyceride formation
Glucose - > alpha-glycerol phosphate - > alpha-glycerol phosphate + 3 fatty acids - > triglyceride
79
glycogen formation
glucose + ATP - > glucose-6-phosphate - > glycogen and pyruvate
80
Final absorptive state summary for plasma glucose
SEE PAGE 16
81
proteases
a class of enzymes which result in the release on amino acids
82
the breakdown of amino acids includes _____
it includes the removal of nitrogen groups from amino acids using 2 reaction
83
list both amino acid breakdown reactions that occur in the body
1. Oxidative deamination
| 2. Transamination
84
describe oxidative deamination
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
describe transamination
involves the interaction between an amino acid and a keto acid (from oxidative deamination) to form a DIFFERENT amino acid and keto acid
86
what happens if we have an accumulation of keto acids
this can result in a decrease in blood pH
87
explain how we process NH3 from oxidative deamination
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
what happens to urea once it travels to the kidneys
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
extensive protein breakdown can cause what?
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
what if we end up having enough liver enzymes to keep up with an extensive protein breakdown
the amount of urea produced by liver enzymes can be too much for the kidneys to handle and can trigger kidney failure
91
results of increased tubular fluid urea concentrations
inc, tubular fluid urea conc. can increase water reabsorption resulting in increased blood volume and blood pressure
92
how many of the essential amino acids can be formed via transamination
11
- > the amino acids formed through transamination supply some of the amino acids used for building blocks for protein formation
93
aminotransferase
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
glutamate
acts as a single source of amino acids groups for continuous nitrogen breakdown
95
where do we find most aminotransferases
in the cytoplasm of most cells and all have a group that is derived from the B6 vitamin
96
how many amino acids cannot be synthesized sufficiently (or at all by the liver), what must we do to combat this issue
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
essential amino acids
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
describe the AA pathways in the body
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
list some of the pathways that AAs will take if they're absorbed into the liver
see page 20
100
triacylglycerol
fat
101
what percentage of energy storage is stored as fat
80
| - > stored mainly in the adipose tissue as triglycerides
102
1x 18-carbon saturated fatty acid is how many ATP molecules
146, fats contain more than twice as much chemical energy as carbs or proteins
103
when does triglyceride(fat) digestion start
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
explain the emulsification of fats
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
micelles
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
describe the process how we store fat in our cells using micelles
see page 22
107
vitamins are used as _____
co-enzymes
| - > helps the body use nutrients for energy production
108
vitamins are derived from _____
food sources during the absorbative state
109
What is B1 and what happens when we are deficient
Thiamine
- > beriberi (nerve disorder),
- > tingling,
- > poor coordination,
- > reduced cardiac function
110
What is B2 and what happens when we are deficient
Riboflavin
| - > skin lesion
111
What is B3 and what happens when we are deficient
Niacin
| - > skin and GI lesions; nerve disorders
112
What is B6 and what happens when we are deficient
pyridoxine
- > irritability
- > convulsions
- > muscular twitching
- > anemia
113
What is B5 and what happens when we are deficient
panthothenic acid
- > fatigue
- > numbness
- > tingling of the hands and feet
114
What is B9 and what happens when we are deficient
folacin
- > anemia
- > birth defects
115
what happens when we are deficient in B12
- > anemia
| - > nervous system disorders
116
What is vitamin C and what happens when we are deficient
ascorbic acid
| - > scurvy (degradation of blood, teeth, skin)
117
What is vitamin A and what happens when we are deficient
retinol
| - > blindness and increased death rate
118
what happens when we are deficient in vitamin D
rickets (children) and osteomalacia (adults)
119
what happens when we are deficient in vitamin E, whats it called
alpha-tocopherol
| - > degeneration of the nervous system
120
what happens when we are deficient in vitamin K, whats the vitamin called
phylloquinone
| - > defective blood clotting
121
what happens when we are deficient in biotin
- > scaly skin
- > inflammation
- > neuromuscular disorders
122
what are the fat soluble vitamins
A D E K
| - > all stored in the body (except for K) and over ingestion can lead to toxicity (especially A)
123
water soluble vitamins
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
post-absorptive state
- > plasma glucose concentrations must be maintained
| - > sources of blood glucose during the PA state are from stores outside of the GI tract
125
what are the different systems we use for glucose production during the POST-absorptive state
1. Liver processes
2. Skeletal muscles
3. Adipose tissue
4. Protein breakdown
126
glycogenolysis
hydrolosis(formation) of glucogen, first line of plasma maintenance in the PA state
Glycogen hydrolysis < - > Glucose-6-phosphate < - > Glucose
127
what does the liver do during PA state to maintain plasma glucose
liver performs glycogenolysis; first line of plasma glucose maintenance
- > only effective for a few hours or until glycogen stores are depleted
128
what do the skeletal muscles do to maintain plasma glucose during the PA state
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
what does the adipose tissue do to maintain plasma glucose during the PA state
lypolysis breaks down the stored fats (triglycerides) and releases the products into the blood
130
what happens to the products of triglyceride breakdown
Triglycerides - > glycerol + free fatty acids
| SEE PAGE 26
131
does the brain like using ketones as fuel
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
how does protein breakdown help maintain plasma glucose during the PA state
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
what happens during fasting or with untreated diabetes mellitus
- > 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
glyconeogenesis
formation of glucose from STORED components
| - > occurs primarily in the liver and secondarily in the kidneys
135
what are the 2 pathways for the formation of glucose through gluconeogenesis
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
explain the process of gluconeogenesis
- > 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
how do we control the direction of the glycolytic pathway
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
cori cycle
SEE PAGE 29
| liver takes waste from muscle movements/ contractions and converts them into glucose
139
Steps involved in maintaining plasma glucose during fasting/PA state
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
explain how blood glucose change with exercise
- > 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
what is the exception to the similarity between prolonged exercise and fasting
during exercise, glucose uptake into muscle cells increased while in fasting, it is very much reduced
142
What activities happen during exercise to help maintain BGL
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
hyperketonemia
Hyperketonemia is a condition with elevated blood levels of acetoacetate, 3-β-hydroxybutyrate, and acetone
144
cellular requirements for energy (ATP)
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
explain ATP and energy transfer
- > 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
production of ATP
cellular energy production is through complex chemical reactions (metabolic pathways) that usually result in the movement of electron from one compound to another
147
explain cellular energy and how it related to ATP production
since energy cannot be created or destroyed (1st law of thermodynamics) it must be transformed using biochemical reactions
148
examples of how we classify compounds by their energy levels
high energy: phosphocreatine (stored in skeletal muscles)
Intermediate: ATP
Low energy, glucose-6-phosphate, ADP, glucose
149
oxidation
gain 1 oxygen or lose a H
| - > oxidized: loses energy
150
reduction
gains an electron
| - > reduces space on the atom, reduced substances gain energy
151
redox reaction are catalyzed by what?
enzymes
1. dehydrogenases = removal of H
2. oxidases = transfer of oxygen
152
2 molecules that serve important roles in redox reactions
1. NAD (nicotinamide adrenine dinucleotide)
- > derived from niacin (B3)
2. FAD (flavin adenine dinucleotide)
- > derived from riboflavin (B2)
153
glucose sparing
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
