Midterm 1 cards Flashcards

1
Q

Monosaccharide absorption

A

is by enterocytes (intestinal epithelial cells)
very efficient
nearly all monosaccharides are taken up by this process
includes transporters

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2
Q

enterocytes

A
  • are intestinal epithelial cells
  • they are polarized - meaning they have an up and a down
  • up is the APICAL
  • down is BASOLATERAL
  • where monosaccharides are taken up
  • have transporters
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3
Q

GLUT 2

A
  • basolateral transporter that absorbs monosaccharadiws
  • majority of monosaccarides are transported into blood by this
  • glucose, galactose and fructose enter blood via this guy
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4
Q

SGLT1

A

sodium glucose transporter 1
- vast majority of sugar is passed through (except fructose)
- in apical membrane

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5
Q

Na-K ATPase

A

transport of glucose and galactose from lumen into blood is dependant on this basolateral transport which regulates the concentration of Na and K which is essential for the function of the apical NaKGlt1 transporter

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6
Q

GLUT5

A

how fructose is taken up
- on apical surfact of enterocyte

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7
Q

Glucose function in the body

A

primary source of energy for cells
essential for proper functioning of cells in the CNS and RBCs

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8
Q

CHOs function in the body

A
  • spare proteins/prevent breakdown of protein for energy
  • allows protein to concentrate on building, repairing and maintaining body tissue
  • prevent ketosis - the breakdown of fat for energy and production of ketone bodies
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9
Q

Glycogenolysis

A
  • breaking down of glycogen reserves
  • catabolism
  • releasing glucose mlc from glycogen
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10
Q

Glycogenesis

A
  • making of glycogen reserves for a time of need
  • anabolic process
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11
Q

Glycolysis

A
  • breaking down of glucose to be used for energy
  • where most of energy from carbs comes from
  • does not require oxygen
  • happens in the cytoplasm
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12
Q

Gluconeogenesis

A

-generating glucose from other stuff
- ex. amino acids can by used to generate pyruvate which can be used to generate glucose

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13
Q

Krebs cycle

A

TCA cycle
- where bulk of energy is gonna be created
- happens in mitochondria
- acetyl Co-A from all macromlc is broken down to useable energy

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14
Q

Hexose-monophosphate shunt

A

produces precursors for nucleic acid using glucose

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15
Q

What are the 3 fates of glucose in a cell?

A

1) enters glycogenesis for energy storage
2)enters glycolysis for energy production
3) enters hexose monophosphate shunt to generate precursors for biogenesis

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16
Q

What are the enzymes involved in glycogenesis

A

glycogen synthase and glucokinase/hexokinase

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17
Q

glycogen synthase

A

enzyme used to store glucose in glycogen - removes a phosphate
- insulin positively regulates this
- promotes storage
- involved in glycogenesis

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18
Q

glucokinase and hexokinase

A

glucokinase (liver)
and hexokinase (muscle)
- both add a phosphate to glucose to make glucose-6-phosphate
- insulin positively regulates this
- promotes storage
- involved in glycogenesis

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19
Q

What enzymes are used in glycogenolysis

A

glycogen phosphorylase and glucose-6-phospohatase

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20
Q

glucose-6-phosphatase

A

ONLY IN LIVER
- converts glucose 6 phosphate into glucose
- (removes phosphate)
- during low blood sugar
- glucose will go from liver to blood
- part of glycogenolysis

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21
Q

glycogen phosphorylase

A
  • part of glycogenolysis
  • starts process of breaking down glycogen
  • targets alpha(1-4) glycosidic bonds
    -glycogen debranching enzyme
  • adds Pi to glucose from glycogen
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22
Q

What is Glycogenin??

A
  • an enzyme
    that serves as a scaffold on
    which to attach glucose
    molecules to build glycogen.
    – Think of this enzyme as a
    “primer”. It initially attaches
    glucose molecules to itself
    before glycogen synthase
    takes over and adds glucose
    to the growing glycogen store
    – 30,000+ glucose molecules
    can be contained in a single
    glycogen structure
    – This process requires energy
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23
Q

What is so special about the liver?

A

It’s the only tissue that can release glucose back into the blood!

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24
Q

Where/How is energy producesd in the cell?

A
  1. Substrate level phosphorylation
  2. Oxidative Phosphorylation
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25
Substrate level phosphorylation
One of two ways energy is produced in the cell - important for cells that don't have mitochondria - getting energy from removing a phosphate from high energy molecules
26
Oxidative phosphorylation
ETC In mitochondria (electron transport chain) - getting energy from the transfer of electrons across a proton gradient to produce the bulk of our energy
27
Where does glycolysis occur?
in cytoplasm - all glycolytic ensymes are in cytoplasm
28
Why is glycolysis so important?
- It's the only way red blood cells can generate ATP since they don't have any mitochondria - all life on earth performs glycolysis - doesn't require oxygen
29
What are the products of glycolysis
- 2 net ATP - 2 NADH - 2 Pyruvates
30
What are the steps of glycolysis that you need to know for this course?
Glucose to G6P - by glucokinase/hexokinase - uses ATP to phosphorylate G6P to F6P - where fructose can just jump in here F6P to fructose 1,6-bisphosphate - by enzyme phosphofructokinase = first committed step - uses ATP to phosphorylate that to 2 x G3P (glyceraldehyde 3 phosphate) and then that to pyruvate to geterate 4 ATP
31
What is the first committed step of glycolysis
Phosphofructokinase it is irreversible
32
under what conditions does phosphofructokinase step NOT occur
Phosphofructokinase is first importatn step in glycolysis 1. High levels of ATP or 2. high levels of glucagon in the liver will prevent this step and block glycolysis from proceeding
33
What is the metabolic fate of pyruvate
- Depends on oxygen status Aerobic --> Krebs cycle Anaerobic --> lactate
34
Lactic acid (lactate) production
- Anaerobic metabolism of glucose - Occurs in muscle during prolonged exercise and in red blood cells – Pyruvate is converted into lactate in the cell’s cytosol – Regenerates NAD+, which allows glycolysis to continue – A net of 2 ATP is produced when glucose is converted to lactate (from glycolysis) - uses LACTATE DEHYDROGENASE enzyme
35
Anaerobic metabolism of glucose
Lactic acid (lactate) production (in humans) Ethanol / fermentation (in bacteria)
36
Making ethanol
anaerobic metabolism of glucose in bacteria - Doesn’t happen in the body – This is the basis of fermentation when you make wine and beer – Yeast breaks down pyruvate into CO2 and ethanol – Regenerates NAD+ - uses enzyme ALCOHOL DECARBOXYLASE to form acetaldehyde intermediate and enzyme ALCOHOL DEHYDROGENASE to form ethanol from it
37
Cori Cycle
- occurs in times where oxygen is unavailable (anaerobic state) in the muscle, leading to the production of lactate. - Lactate is transported back to the liver, - where gluconeogenesis allows for the conversion of pyruvate back to glucose. - For 2 molecules of lactate to form glucose the cell consumes 6 ATP molecules.
38
How many ATPs does the cell use to convert 2 mlc of lactate to glucose
6
39
Hexose Monophosphate shunt
- Important for NADPH (nicotinamide adenine dinucleotide phosphate) production and ribose synthesis * Occurs in the cytoplasm of a cell
40
Why is the hexose monophosphate shunt so important?
- Produces NADPH which is really important for the biosynthesis of fatty acids and they also play an important role in dealing with ROS ALSO nucleotide synthesis is super important cause every cell has DNA and RNA
41
Pyruvate dehydrogenase
The Gatekeeper to the Krebs Cycle - in mitochondria - where pyruvate is converted to acetyl-CoA - generates 1 NADH requires several enzymes and cofactors
42
What are the 4 vitamins required for pyruvate dehydrogenase complex
1. thiamine 2. niacin 3. riboflavin 4. pantothenic acid
43
what all is required for pyruvate dehydrogenase??
- pyruvate - pyruvate dehydrogenase enzyme 1. thiamine 2. niacin 3. riboflavin 4. pantothenic acid - Co-ASH - NAD+
44
Where does Krebs cycle take place
In mitochondrial matrix
45
Why is Krebs cycle so important?
over 90% of energy in food is released in this biochemical process its a common and final catabolic pathway for products of proteins, lipids and carbohydrates!
46
WHat are the products from the Krebs cycle
3 NADH 1 FADH 2 CO2 1 GTP = 12 ATP
47
What are the intermediates in the krebs cycle
Citrate Isocitrate a-ketoglutarate succinyl-CoA Succinate fumarate malate oxaloacetate (needs acetyl-CoA input)
48
The 3 irreversiple steps of glycolysis and the enzymes that can bypass each in gluconeogenesis
1) Glucokinase / Hexokinase 2) Phosphofructokinase 3) Pyruvate kinase ENZYMES that can bypass 1)Glucose-6- phosphatase 2) Fructose-1,6- bisphosphatase 3) Pyruvate carboxylase & PEP carboxykinase
49
Where does gluconeogenesis occur?
 Very active in liver, but can also happen in the kidney during starvation
50
Can gluconeogenesis happen in the muscle?
NO since Muscle & adipose tissue lack enzymes for gluconeogenesis
51
What is the first step of gluconeogenesis?
- happens in mitochondria Pyruvate carboxylase enzyme - only expressed in mitochondria - pyruvate is converted to oxaloacetate with this enzyme (uses an ATP), then - oxaloacetate is converted to malate (NADH --> NAD+) - malate can exit mitochondria - once exited, malate is converted to oxaloacetate (NAD+ --> NADH)
52
Starch
amylose and amylopectin (branched) both forms are polymers of D-glucose
53
Dietary fibre
Non-digestible complex CHO - structural part of plants - has water holding and absoptive ability includes insoluble and soluble
54
Insoluble fibre
(does not dissolve in water) cellulose, lignin, some hemicelluloses * Remain intact throughout the digestive system * Reduce transit time (i.e., things move quickly through the gut) * Increases fecal bulk
55
Soluble fibre
(pectins, gums, β-glucans, some hemicelluloses) * Forms a gel * Delays gastric emptying, increases transit time * Slows down the rate of nutrient absorption
56
Cellulose
Both a dietary fibre (naturally occurring in a food) and functional fibre (naturally occurring fibre that is added to a food that normally doesn’t have any cellulose) – Homopolysaccharide of β-1,4 glucose units in a linear chain – Poorly fermented by human gut bacteria * Because humans generally lack cellulose-fermenting microbes in their gut microbiome (known as metanogens) – Rich in bran, legumes, nuts, peas, etc.
57
Hemicellulose
Heteropolysaccharide that varies between plants – A mixture of α and β glycosidic linkages – Can contain both pentoses and hexoses * Xylose is the most common monosaccharide in hemicellulose – Exists as both branched and linear structures – The solubility and fermentability of hemicellulose depends on the sugar composition – Found in bran, whole grains, nuts, and some vegetables/fruits
58
Pectin
– Both a dietary and functional fibre – Part of the primary cell wall of plants – Backbone of unbranched α-1,4-linked-D galacturonic acid – Stable at low pH – Highly fermented by gut bacteria * Considered to be a good bulking agent in animal feeds – Rich in fruits, such as apples, oranges, lemons, and grapefruit
59
resistant starch
– Four main types, termed RS1 – 4 (found in different foods) – Typically found in plant cells walls – Resistant to amylase activity – Conveys some advantages of both soluble and insoluble fibres * Fun Fact: Allowing a banana to ripen will cause resistant starches to break down and become simple sugar
60
Health benefits of fibre
aintains function & health of the gut ↓ constipation (insoluble fibre) * Stimulates muscle contraction to break down waste * Decreases risk of bacterial infections ↑ satiety (soluble fibre) * Delays gastric emptying * Slows down nutrient uptake Decrease cardiovascular disease risk by lowering blood cholesterol ***Can also lower the risk of type II diabetes by binding some glucose in the digestive tract
61
carb digestion in mouth
α-amylase (salivary) breaks down α-1,4-glycosidic bonds – Produces only a few monosaccharides – Cellulose and lactose are resistant, as are α-1,6-bonds
62
carb digestion in stomach
α-amylase digestion continues until pH drops, then enzyme is inactivated – At this point, the pool of dietary CHO consists of small polysaccharides and maltose
63
carb digestion in small intestine
α-amylase (pancreas) – Active at a neutral pH – α-1,6 bonds are resistant and eventually produce isomaltose
64
brush border enzymes
ALPHA DEXTRINASE Also called isomaltase (breaks α-1,6 glycosidic bonds). MALTASE breaks maltose to  2 glucose INVERTASE - Also called sucrase breaks sucrose  glucose + fructose LACTASE - breaks lactose  glucose + galactose
65
Lipid functions
1. Concentrated source of energy  9 kcal/g 2. Palatability of foods & increase satiety 3. Source of essential fatty acids  α-linolenic acid (omega-3), linoleic acid (omega-6) 4. Source of fat-soluble vitamins  (A, D, E, and K) 5. Necessary for growth and development 6. Important precursors for production of hormones 7. Affect inflammation and blood clotting 8. Key roles in disease development  Atherosclerosis, diabetes, obesity, etc...
66
Examples of saturated, monounsaturated and poly unsaturated fatty acids...
saturated: butyric acid, palmitic acid monounsaturated: oleic acid (cis) elaidic acid (trans) poly unsaturated fatty acids: arachidonic acid
67
Essential Fatty Acid Discovery
In 1929, George and Mildred Barr fed rats diets that were completely fat free – Stunted growth, lost fur, inflamed & scaly tails What about humans? * In 1963, infants were fed diets that differed in fat content. Diets with <0.1% linoleic acid had poor growth and thickened dry skin
68
What are the essential Fatty Acids? and why are they essential?
Linoleic Acid (18:2 n-6) and Alpha Linolenic Acid (18:3 n-3) Humans lack the enzymes necessary to insert double bonds beyond the delta-9 position of a fatty acid The delta-12 and delta-15 fatty acids are produced in plants They are important cause they're precursors for other important fatty acids
69
What are signs of an omega 6 deficiency?
(linoleic acid) dermatitis decreased growth low reproductive maturity
70
What are signs of an omega 3 deficiency?
less CNS development (lower IQ) and less retinal development (visual acuity)
71
What are the proposed changes in dietary fatty acid intake over time?
- that for a long time, fat consumption was balanced - there was a change during the industrial revolution - due primarily to increased intake of high fructose corn syrup - omega 6 increase - total fat increase - saturated fat increase - trans fat increase - omega 3 decrease
72
EFA Desaturation and Elongation steps
Linoleic Acid 1. Desaturation by delta-6 desaturase (New double bond added at 6th position of carbon backbone from the carboxyl end) produces Gamma Linolenic Acid (GLA) 2. Elongation by elongase 5, (Two carbons added (from malonyl CoA) at carboxyl end) produces Dihomo Gamma Linolenic Acid (DGLA) 3. Desaturation by delta 5 desaturase (New double bond added at 5th position of carbon backbone from the carboxyl end) produces arachidonic acid (AA) alpha linolenic acid (ALA) undergoes exact same steps but process/intermediates is 1. SDA 2. ETA 3. ETA
73
omega 3 deficiency in pets symptoms
Impaired reproductive efficiency, impaired wound healing, dry coat, scaly skin. Rare in companion animals unless they eat low-fat dry foods
74
Why are dogs and cats susceptible to an omega 3 deficiency?
DOGS  can convert ALA to EPA, but not DHA (require DHA in their diet) CATS  lack enzymes to make any long chain fatty acids (required in their diet)
75
What are Eicosanoids??
Metabolites of 20-carbon fatty acids (mostly derived from AA and EPA)  Produced by most cells in the body  Hormone-like, but function locally  Role in inflammation, platelet aggregation, blood pressure, etc.  Implications for diseases characterized by inflammation include: PGD2 prostglandins TXA2 thromboxanes LTE4 leukotrienes
76
What is the first step of eicosanoid production beginning from a phospholipid?
Phospholipid w an arachidonic fatty acid arachidonic acid gets cleaved off by PLA2 (phospholipase A2) enzyme then there are 3 pathways this arachidonic acid can go
77
Three pathways arachidonic acid can go
1. cyclogenase pathways by COX enzymes - results in prosaglandins and thromboxanes 2. Epoxidase pathways results in diff. types of eicosanoids 3. lipoxygenase pathways by LOX enzymes resultes in HPETES and then other leukotrienes or HETES and then orhwe lipoxins
78
TAG
Main dietary lipid * Major storage lipid * Critical in several processes: * De novo lipogenesis * Lipolysis * Transported in lipoproteins 3 fatty acids attatched to glycerol by ester linkages Structures * Monoacylglycerol (MG, MAG) * Diacylglycerol (DG, DAG) * Triglyceride / Triacylglycerol (TG, TAG) * Fatty acid composition determines physicochemical properties
79
Phospholipids
PL Structural features * More polar than TAGs * Hydrophilic phosphate head group
80
Primary functions of phospholipids
- Components of membranes * Source of physiologically active fatty acids for eicosanoid synthesis * Anchors membrane proteins * Intracellular signaling
81
Sterols
Steroid alcohols – Monohydroxy alcohols * Structural features – Free or esterified with a fatty acid * Cholesterol ester (CE) basically a cholesterol
82
Sources of cholesterol
Diet: meat & eggs (~40%) – Endogenous production (~60%)
83
Primary functions of sterol:
Essential components of membranes – Precursor for : * Bile acid production * Steroid sex hormone production (e.g., testosterone, estrogen, etc) * Vitamin D synthesis
84
Bile salts
are bile acids that are conjugated (with taurine, glycine, etc) in the liver to improve solubility in the intestinal lumen. Digested lipids are emulsified by conjugated bile acids Bile salts are deconjugated by gut bacteria, and bile acids are reabsorbed and recycled through enterohepatic circulation.
85
Mixed Micelles
are small, spherical complexes containing lipid digestion products plus bile salts (like they have cholesterol, phospholipid, fatty acid)  Can access the spaces between microvilli in the intestine  Originally thought that digested lipids were delivered into intestinal enterocyte cells by passive diffusion, but carrier-mediated transporters have now been identified  Bile salts are deconjugated by gut bacteria, and bile acids are reabsorbed and recycled through enterohepatic circulation
86
Enterohepatic circulation
IN THE LIVER: cholesterol combines with bile acids to form bile salts bile salts are stored in the gallbladder released through bile duct to the small intestine 95% bile acids reabsorbed and recycled back to the liver 5% bile acids lost in feces
87
How do soluble fibres reduce cholesterol?
reduce the efficiency of enterohepatic circulation by holding on to bile acids, which are then secreted in feces
88
How are lipoproteins classified?
Lipoprotein classification determined by: 1. Ratio of Lipid-to- Protein (which affects density) 2. Specific apolipoprotein (Apo) content (which affects receptor interactions)
89
Chylomicron
Biggest lipoprotein in circulation High Lipid, Low Protein ApoB-48 ApoC and ApoE Chylomicrons increase in circulation after a meal * Enter circulation at a slow rate * Peaks between 30min-3hr after eating
90
Why are dietary lipids available to adipose and muscle before arriving at the liver??
Since chylomicrons enter the lymphatic system before entering the blood
91
LPL
Lipoprotein lipase an enzyme NOT expressed in liver, but IS expressed by adipose and muscle activated by ApoC in chylomicrons and VLDL hydrolyzes the TAG in chylomicrons (and VLDL) into 2-MAG + 2 fatty acids
92
Chylomicron remnants
When chylomicrons become TAG-depleted, they are referred to as a “chylomicron remnant” Chylomicron remnants are removed from circulation through ApoE- mediated interactions with a receptor in the liver
93
VLDL
the main transporter of newly synthesized hepatic TAG High Lipid, Low Protein - has ApoB-100 and ApoC, ApoE gets converted to IDL and LDL as it looses TAGs
94
HDL
ApoA family "Good cholesterol" collects cholesterol from around body and brings it back to liver (cholesterol is esterified directly on HDL)
95
LCAT
Lecithin-Cholesteol Acyltransferase - esterifies a fatty acid to cholesterol Like, when HDL is going around and picking up its fatty acids from around the body, it is the thing that sticks the fatty acid to the HDL so that it can be brought back to the liver
96
SR-B1
(scavenger receptor class B1) transports cholesterol from HDL into the liver
97
CETP
(cholesterol ester transfer protein) transfers cholesterol from HDL to VLDL and/or LDL
98
 REVERSE CHOLESTEROL TRANSPORT
 when HDL picks up cholesterol around the body and brings it to the liver
99
Three fates of cholesterol in the liver
1. Converted into bile acids to replenish the bile acid pool 2. Secreted “as is” directly with bile, to be eliminated in feces 3. Packaged into VLDL and sent around the body
100
How do plant sterols lower cholesterol uptake?
Plant sterols are not absorbed. they compete with cholesterol for uptake by NPC1L1, but plant sterols are then pumped back into the lumen by ABCG5 / G8 apical transporters
101
Hexose monophosphate shunt Oxidative phase
ONLY cells that perform biosynthesis will use the oxidative phase! in the oxidative phase, glucose-6-phosphate goes to 6-PG (by producing NADPH) then 6-PG goes to 6-PG lactone, which goes to ribulose-5-phosphate (by producing NADPH and CO2). ribulose-5 phosphate then goes to nonoxidative phase to produce ribose-5-phosphare which is used for nucleotide synthesis!
102
Nonoxidative phase of hexose monophosphate shunt
G6P to F6P then F6P to intermediates then to ribose-5-phosphate ribose 5 phosphate gets used for nucleotide synthesis all cells use the non oxidative phase
103
Reticulum
Honeycomb appearance; can capture nutrients and trap foreign materials (wire, nails, etc.) that are accidently swallowed – Can cause “hardware disease” * Rich in bacteria (fermentation vat)
104
Rumen
- The largest section of the stomach * Rich in bacteria (fermentation vat) * Rumen papillae  increases surface area for absorption (like microvilli in the human intestine) * Food is mixed & partially broken down, and stored temporarily * 60-80% of total energy produced here as SCFA
105
Omasum
(3rd stomach) Resorption of water and some electrolytes * Filters large particles
106
Abomasum
Digestive enzymes secreted from gastric glands (HCl, mucin, pepsinogen, lipase, etc) - "True stomach" - region resembling our stomach the most, where enzymes are released - similar to monogastric system
107
Pros and cons of ruminant digestive system
Advantages * Vitamin synthesis (e.g., B Vitamins, Vitamin K) * Non-protein nitrogen used for making protein – Disadvantages * Carbohydrates degraded into gases and lost through eructation * Heat production
108
Distinct features of avian digestive system
- Beaks and claws are important for breaking up foods into smaller pieces that birds can swallow. * Rapid digestion – Birds can starve if deprived of food for even a short time (i.e., hours) - Crop - Two-chamber stomach * Glandular portion = Proventriculus * Muscular portion = Gizzard
109
Two chambers of an avian stomach and their functions
Two-chamber stomach * Glandular portion = Proventriculus  Gastric enzymes and HCl are secreted * Muscular portion = Gizzard  Grind and digest tough food
110
cloaca
Last part of avian system where the digestive, urinary and reproductive systems meet
111
Total collection method
Allow the animal to adapt to the diet over a 7-21 day period * Isolate animal for quantitative analyses * Measure intake over a 3-10 day period * Collect and weigh all feces * Analyze for nutrient of interest Apparent digestibility = Total Intake – Total Feces Total Intake
112
Limitations of total collection method
- Accuracy in measuring food intake * Metabolic cages create anxiety in animals, which may then behave abnormally * Labour intensive * Animals confined in costly equipment * Not feasible for captive wild animals
113
Indicator method
Also referred to as the “Marker Technique” * Requires a marker: – Internal (a natural component of the feed) – External (a component added to the feed)
114
Characteristics of a marker
1. Non-absorbable 2. Must not affect or be affected by the GIT 3. Must mix easily with the food 4. Easily & accurately measured in sam ured in samples * e.g., ferric oxide, chromic oxide, silica, lignin
115
Indicator method steps
1. Adapt animal to test diet (which contains a marker) 2. Collect a feed and fecal sample 3. Analyze each for marker and nutrient of interest relative to your indicator
116
indicator method calculation
Apparent Digestibility Coefficient = A – B A A = Ratio of Nutrient/ Marker in Feed; B = Ratio of Nutrient/ Marker in Feces
117
Apparent digestibility vs. True digestibility
Apparent digestibility under-estimates True digestibility The following are examples of things not considered when calculating Apparent digestibility: * Endogenous secretions * Epithelial cells E.g., fatty acids released from dying intestinal cells * Bacterial growth in gut * Nutrient synthesis E.g., biotin produced by gut bacteria * Digestive enzymes * Protein secretion
118
True digestibility steps!
1. Perform digestibility study using a TEST DIET. 2. Switch to diet containing none of the nutrient of interest (ZERO NUTRIENT DIET). 3. Analyze feces after TEST DIET is cleared. 4. Subtract level of nutrient in feces of animals fed the ZERO NUTRIENT DIET from the TEST DIET
119
True digestibility calculation/coefficient!
True Digestibility Coefficient = A – (B – C) A A = Ratio of Nutrient/Marker in TEST DIET B = Ratio of Nutrient/Marker in Feces C = Ratio of Nutrient/Marker in Feces after ZERO NUTRIENT DIET
120
Factors that affect digestibility
- Feed intake * Particle size * Chemical composition * Climate * Age
121
Positive energy imbalance
(energy in > energy out) *Weight gain / obesity *Infertility *Increased blood lipids *Insulin resistance
122
Negative energy imbalance
(energy in < energy out) *Weight loss *Infection *Loss of performance *Reduced bone mass Energy Balance
123
Antoine Lavoisier
- Compared heat produced by a guinea pig with the production of CO2 – Ice calorimeter (heat produced estimated by the amount of ice that melted) – CO2 formed from the reaction between oxygen and organic matter
124
Justin Liebig
recognized that protein, carbohydrates, and fats are oxidized by the body
125
Max Rubner
measured energy values of certain foods to determine Caloric content
126
Bomb calorimetry
Dry and weigh sample (~1g), and place in enclosed chamber (the ‘bomb’) with oxygen * Sample ignited * Heat released is absorbed by water and measured * Heat of combustion (gross energy) – Gross energy = maximum energy
127
Gross energy
maximum energy / heat of combustion from a bomb calorimeter reading
128
Why does fat provide more kcal per gram than CHO or protein?
The heat of combustion describes the total energy released during a chemical reaction between a hydrocarbon and oxygen to release CO2 and H2O and heat. * The chemical structure of CHO, fat, and protein influences the heat of combustion for macronutrients. CHO  ratio of hydrogen to oxygen = 2:1 Protein  has nitrogen, which affects gross energy measurement. However, in the body, nitrogen combines with hydrogen and is eliminated asurea. This loss of hydrogen affects the heat of combustion. Lipid  lipids are less oxidized than CHO and protein  ratio of hydrogen to oxygen much greater than 2:1  lipids have lots of hydrogen atoms available for cleavage and oxidation for energy
129
HIF
Heat Increment of Feeding - Also called the thermic effect of food  Energy used for the digestion, absorption, distribution & storage of nutrients  Comprises 5-30% of daily energy usage  Used to determine Net Energy  (Net Energy = Metabolizable Energy – HIF)
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Net energy
Net Energy = Metabolizable Energy – HIF
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What's that energy arrow diagram?
GROSS ENERGY Energy lost in feces (not100% digestible) DIGESTIBLE ENERGY Gases (ruminants) Energy lost in urine (birds) METABOLIZABLE ENERGY Heat Increment of Feeding NET ENERGY = Basal Metabolic Activity WHAT'S LEFT OVER = Excess Energy
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How is BMR measured?
- Shortly after waking * Post-absorptive state * Lying down * Completely relaxed * Comfortable room temperature
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BMR Calculation!
BMR = A×[M^0.75] kcal/day * Based on ‘metabolic weight’ A = Metabolically active tissue * i.e., fat free mass (muscle and bone) * Value for humans = 70; every species has its own value M= Body weight (M)  in kilograms 0.75 (Kleiber’s Law) – a constant used for all vertebrates, invertebrates and even unicellular organisms
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What is the BMR for a 74 kg (165 lb) person?
BMR = (70)×[(74 kg)0.75] = 1766 kcal
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What is the Harris Benedict Equation?
A more accurate method of calculating the BMR taking into consideration - biological sex - weight - height - age and - physical activity
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What factors can affect BMR?
Genetics – Inheritance of a fast or slow metabolic rate * Age – Young > old (because of greater muscle mass) * Biological Sex – Men > women (because of greater muscle mass) * Exercise changes body tissue proportions -Fat tissue (20% body weight, 5% metabolic activity) -Muscle (30-40% body weight, 25% metabolic activity
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Katch-Mcardle MBR equation
Taking body fat % into consideration to calculate BMR - same formula for men and women - use fat free mass= 100% -%body fat x mass
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What are the two ways to measure total energy expenditure?
- Direct calorimetry - Indirect calorimetry
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What is the general combustion equation?
Fuel + O2 ---> CO2 + H2O + HEAT
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Direct calorimetry
Measures the heat a person generates; total heat loss * Very expensive! * Impractical
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Indirect calorimetry
Energy-releasing reactions in the body depend on the use of oxygen * Indirect calorimetry estimates energy requirements by measuring: – Oxygen consumption (L) – Carbon dioxide production (L) – {Urinary nitrogen loss (g) note that this method cannot account for anaerobic processes (production of lactic acid)
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Pros and cons of indirect calorimetry
Disadvantages: Hyperventilation, hard to get an airtight seal, masks are impractical Advantages: Useful with animals, can determine the type of substrate being oxidized
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RQ
Respiratory Quotient Provides information about: * Energy expenditure * Biological substrate being oxidized * Ratio of metabolic gas exchange RQ = CO2 produced / O2 consumed
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Carbohydrate combustion equation and RQ value!
C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O + energy RQ = 6 CO2 / 6 O2 = 1
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Fat combustion equation (balanced) and RQ value!
C16H32O2 + 23 O2  16 CO2 + 16 H2O + energy RQ = 16 CO2 / 23 O2 = 0.7
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Three components of energy expenditure
1. Basal metabolic rate (BMR) 2. Thermic Effect of Food (same thing as “HIF”) 3. Physical Activity Energy Expenditure (PAEE) 4. (Thermoregulation)
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sucrose
- Found in sugar cane, fruits * glucose + fructose * Non-reducing! (both anomeric carbons used) - digested by sucrase/invertase
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lactose
* Found in milk * galactose + glucose * Reducing! Free anomeric carbon - digested by lactase
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maltose
* Found in beer & liquor * glucose + glucose * Reducing! Free anomeric carbon - digested by maltase
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polysaccharides
Long strings or branches of monosaccharides (min. of 6) attached by glycosidic bonds * Homopolysaccharides * Heteropolysaccharides – Both exist in nature, but homopolysaccharides are more abundant in food Polysaccharides
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lipase
hydrolyze ester linkages (lipolosis)
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HSL
Hormone Sensitive Lipase In adipose tissue, HSL (hormone sensitive lipase) cleaves a fatty acid from the glycerol backbone – HSL inhibited by insulin The complete breakdown of a TAG molecule releases 1 glycerol and 3 fatty acids
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What's insulins effect on HSL
Insulin inhibits HSL (hormone sensitive lipase) cause why would we want to break down fat if we have glucose! (why insulin was secreted in the first place)
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What happens to the glycerol from lipolysis
Glycerol can enter into glycolysis or gluconeogenesis (depends on the needs of the cell)
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steps of beta oxidation
Dehydrogenation (FAD+ to FADH2) Hydration Oxidation (NAD+ to NADH) Thiolysis an acetyl CoA is made - Each round of β-oxidation removes 2 carbons (acetyl CoA) and produces 1 NADH and 1 FADH2 *You don’t need to memorize all the steps
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partial hydrogenation
cis to trans
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as we increase the amount of hydrogenation, what happens to the degree of saturation
it increases
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CLA
conjugated linoleic acid trans fat in milk milk fat contains up to 4-8% trans fat - Natural trans fats are made in the rumen through bacterial fermentation. – Health affects linked with natural trans fats are equivocal.
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Trans fats and CVD risk
High intake of industrial trans fatty acids:  LDL - cholesterol  total - cholesterol  inflammation ↓ HDL - cholesterol * Linked to CVD * On a per-calorie basis, trans fats appear to increase the risk of CVD more than any other nutrient * The impact of natural trans fats on CVD risk is equivocal in the scientific literature
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determinants influencing bacterial number in various regions
Regional oxygen level, pH, bile acids, gut transit time, mucus, and immune factors are all important determinants
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purpose of functional caecum
- enormous hindgut (20-30L capacity) filled with bacteria * SCFA provide 70% of total energy needs for host * Site for the production of vitamins
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Eructation
belching
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DNL
de nova lipogenesis synthesis of triglycerides from carbs and proteins In the liver! glucose to G6P to trioseP then triose P can go to glycerol to make TAGs or triose P to pyruvate to acetyl CoA to fatty acid - this step is like de nova lipogenesis so is creation of fatty acids from amino acid - we remove the NH3 to make pyruvate and oxaloacetate and acetyl CoA to make fatty acids to contribute to fatty acid pool
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