Exam 4. Metabolism Flashcards
Chapter 26. Metabolism
Nutrient
Anything we consume that will help to grow, repair or maintain
Macronutrients
Large quantities
water, carbs, lipids, proteins
Micronutrients
Small quantities
minerals and vitamins
Calorie
Unit of energy
Short tern regulators
Work hourly giving us sensations of hunger or not
Ghrelin
Peptide
CCK
Ghrelin
From pariental cells in the stomach
Sensation of hunger
Peptide YY
Sensation of satisfaction
CCK
Slows down motility
From small intestine
Long term regulators
Suppress appetite
Leptin
Insulin
Leptin
Potent
From adipose tissue
The more adipose, the more leptin, the more we inhibit appetite in the long term
Insulin
Pancreas B-cells Decreases blood glucose After a meal we secrete insulin The more we eat the more we secrete Long term inhibitor or appetite
Leptin and obese individuals
The hormone is secreted but they lack the receptors for the hormone. This means the hormone doesn’t bind and has no effect causing overeating. The person is not getting the signal.
Hypothalamus stimulator and suppressant
NPY- stimulator. Influenced by ghrelin. Influences appetite
Melanocortin- Suppressor of hunger
The primary source of energy
Carbohydrates
Pathway of glucose catabolism
Glycolysis
Anaerobic Fermentation
Aerobic respiration
Gycolosys
In the cytosol, where the enzymes needed are.
We start with glucose and end with 2 pyruvic acid molecules. 2 ATP and 2 NADH
Glucose (6C) to pyruvic (3C)
Anaerobic fermentation
For example when the muscles have used up all the oxygen.
Pathway when no oxygen is available
The pyruvic acid molecules get converted to lactic acid
The lactic acid gets stored until oxygen is available.
It then gets converted to pyruvic acid again and moved to aerobic respiration pathway
Aerobic respiration
Oxygen is available
Continue to oxidize pyruvic molecules producing CO2 H2O and ATP.
From here we go to the acetyl coe, Krebb cycle, and electron transport chain.
Coenzymes of glucose catabolism
Electron carriers
NAD+
FAD
Undergo redox reactions
Glycolysis
Happens in cytosol
2 ATP required
Hexokinase
Initiates glycolysis
It phosphorylates glucose into glucose 6 phosphate to keep glucose gradient.
PGAL
Lipids can be turned into PGAL
Glycolysis
1st step: Glycolysis
Where is it happening: Cytosol
Products: 2 pyruvic acids, 2 ATP, 2 NADH
Aerobic respiration
Lactid acid was converted to pyruvic acid and continues to mitochondria.
Pyruvic decarboxylation
Where it’s happening? outside matrix of mitochondria in
the intermembrane space
What is the product? 2 Acetyl CoA
Pyruvic Cannot get into the matrix of mitochondria
It has to go through pyruvic decarboxylation
This produces CO2 which converts to Acetyl CoA
Acetyl groups are left which combine with coenzyme A to form acetyl CoA which can now move into mitochondria matrix
Matrix reactions
Krebb cycle
Enzymes are in the fluid of mitochondrial matrix
Where its happening? Matrix of mitochondria
Products? Electron carriers which go to the electron transport chain
Membrane reactions
Enzymes are bound to membranes of the mitochondrial cristae
Where? Mitochondria membrane
Purpose? Take electrons from electrons carriers to create ATP and recycle electron carriers (NAD+, FAD)
Members of the transport chain
FMN
CoQ
Cytochromes
FMN
Where NADH and H+ dumps its electrons
CoQ
Where FADH2 drops electrons
Cytochromes
a3 the last member of the electron chain
after this, the electron has to jump off and Oxygen needs to pick it up.
Chemiosmotic mechanism
Chemical osmosis
Diffusion of chemicals
H+
- Glycolysis
In cytosol
Produces 2 pyruvic acid, NADH, H+
- Pyruvic decarboxylation
Oxygen has to be present (if not, anaerobic fermentation)
- Happens in intermembrane space of mitochondria
-Decarboxylate pyruvic into an acetyl group
-Acetyl group combines with Coenzyme A making Acetyl-CoA
- Main product? 2 Acetyl-CoA
it goes into the Kreb cycle
- Kreb cycle
In the matrix of mitochondria
Products? Electron carriers
- Electron transport chain
happens in Inner mitochondria membrane
Produces ATP
Glycogen
Short term energy storage molecule
Can be broken down to make more glucose
Glycogenesis
Making of glycogen.
Starting with glucose
- Stimulated by insulin
- After a meal
Glycogenolysis
Breaking down glycogen into glucose
- Stimulated by glucagon and epinephrine
Gluconeogenesis
Not consuming carbs, the body will use other molecules to make glucose.
Hexokinase
Starts glycolosys
Triglycerides
3 carbon glycerol bound to 3 fatty acid tails
stored in body’s adipocytes
Gets converted into lipids
Lipogenesis
Synthesis of fat from other molecules
AA and sugars used to make fatty acids and glycerol
we make triglycerides
Lipolysis
Breaking down fat for fuel we break apart the triglycerides we end with glycerol and FFA that can be converted to PGAL and plugged in to glycolysis 1 triglyceride 1 PGAL
Beta oxidation
Cutting the fatty acid tails
2 carbons at a time
Produces 2 carbon molecule (Acetyl CoA)
This can not be plugged in to the Kreb cycle
16 carbons, so 8 times around Kreb cycle more electron carriers than glucose.
Gives more energy than glucose
protein metabolism
Deamination (into urea cycle)
What remains is 2 carbon molecule, which can be plugged into acetyl-coA step
NH3
By product of using protein as energy source
Toxic to us
in the liver it goes through urea cycle
Urea cycle
Liver takes two NH3 and combines them with CO2
This forms Urea
Urea is still toxic, but less than NH3 and we can tolerate higher levels
Then, urea gets dumped in the urine
Deaminate
Remove amino group
NH2 breaks off
It picks up another H, making NH3
What remains is 2 carbon molecule
Liver in metabolism
Urea cycle
Glucogenesis
Detoxify
Metabolic rate
How we use macromolecules as energy source
Amount of energy used and produced per unit time
Absorptive state
Nutrients are being absorbed
and that is what we are using for metabolic demands
Post absorptive state
Energy needs met from stored fuel
