BIOC 192 – Metabolism Module Study Guide
Metabolism is all about getting energy from what we eat and using that energy to do
cellular work. Overall, this allows us to carry out day-to-day functions. Catabolism is the
breakdown of complex molecules to release energy (captured as ATP) while anabolism is the
build-up of complex molecules to store energy away for when it’s needed.
Energy in the Body
We have three main sources of energy: carbohydrates, lipids, and proteins. The first law of
thermodynamics describes that total energy within a system is constant.
Einput = Eoutput + Estored
In the perfect energy balance, there is no stored energy. However, in general, we take in
more energy than we put out. We therefore get stored energy in the form of adipose tissue.
In theory, weight loss can be achieved by decreasing input, increasing activity, or increasing
basal metabolism. Leptin is a chemical that indicated when we are full. Obese people are
leptin-resistant, so there is no indicator as to when to stop eating. We measure energy in
joules or calories, where 1 Cal = 4.184 kJ.
Energy intake is measured using bomb calorimetry where food is oxidised and the released
heat is measured. Some molecules cannot be used for fuel, like cellulose, so the adjusted
energy values are called the Atwater factors.
Energy output is measured using direct and indirect calorimetry. Direct calorimetry
measures heat output from an individual using a whole-body calorimeter to determine basal
metabolic rate. Indirect calorimetry measures gas exchange using respirometers. We can
then calculate the respiration exchange ratio (CO2/O2) to determine what type of fuel is
being burned, given that carbohydrates have a 1 RER and fats have a 0.7 RER.
Basal metabolic rate is required for vital bodily functions. BMR differs between individuals
as a result of genetic factors, age, sex, drugs, body composition, hormonal status, stress
levels, and disease status. BMR can be increased with athletic training, fever, drugs,
caffeine, and hyperthyroidism. It can be decreased with malnutrition, sleep, drugs, and
hypothyroidism.
Digestion of Complex Molecules
Carbohydrates make up 40-50% of our energy intake. They
consist mainly of starches (amylose and amylopectin) and
glycogen. Some of the foods we eat contain simple sugars like glucose and fructose. The
goal of carbohydrate digestion is to break the complex molecules down into
monosaccharides. Salivary amylase begins the process of carb digestion in the mouth,
hydrolysing glycosidic down into dextrans, polysaccharides, and oligosaccharides. Salivary
amylase is denatured in the stomach by low pH, and mechanical digestion continues
breakdown into oligosaccharides and trisaccharides. Pancreatic amylase continues the
process of digestion in the small intestine, forming disaccharides. The Disaccharidases from
intestinal epithelial cells can then break these down into their monomer units:
Sucrose ---> Glucose + Fructose
Maltose ---> Glucose + Glucose
Lactose ---> Glucose + Galactose
, BIOC 192 – Metabolism Module Study Guide
Monosaccharides are absorbed across the epithelial cells by
active symport with sodium via the SGLT 1 transporter on the
epithelial lining. Na+/K+ ATPase is important for this process as
it generates a concentration gradient for sodium to travel
down. Glucose is travelling up its concentration gradient, so the
process is secondary active transport. On the basal membrane
GLUT 2 transports monosaccharides passively out of the cell.
Once in the circulation, GLUT 3 transports glucose into the brain and GLUT 4 transports
glucose into muscle and adipose tissue. GLUT 1 is ubiquitous.
Fats are hydrophobic, so they need to be solubilised before they can be digested.
Triacylglycerol, TAGs, and cholesterol are the main fats we ingest. Bile salts are derived from
cholesterol – they are hydroxylated to make them more soluble. The presence of fats in the
small intestine stimulate the release of cholecystokinen, which releases bile salts and
lecithin. These bind to the TAGs and cholesterol to form micelles, and co-lipase anchors
lipase to the surface of the micelles. Lipase hydrolyses the first and third ester bonds to gain
monoacylglycerols (MAGs) and free fatty acids. Smaller micelles are
formed and these are absorbed across the intestinal cell membrane.
Once inside the cell, the MAGs and free fatty acids are resynthesised
into TAGs and packaged into lipoproteins. These have a number of
membrane proteins referred to as Apolipoproteins. The lipoproteins are
exocytosed to give chylomicrons, which are absorbed into the lacteal
and give lymph a milky appearance.
In the exogenous pathway of lipid transport, chylomicrons come directly
from the small intestine. Apo CII is used as a cofactor to activate
lipoprotein lipase in the tissue where fats are needed. This hydrolyses
TAGs into MAGs and fFAs, which are moved across the membrane and
resynthesised into TAGs. The leftover chylomicron moves to the liver, where ApoE and
ApoB48 act as ligands for receptors on the liver.
In the endogenous pathway, VLDL from the liver uses ApoCII to activate lipoprotein lipase.
Half of the remaining VLDL goes to the liver, while the other half form LDLs and undergo
further catabolism by hepatic lipase. Familial hypercholesterolemia occurs when there is a
mutation in the LDL receptor gene and LDL cannot be taken up by the liver. As a result, LDL
remains in the blood stream, increasing risk of atherosclerosis.
Proteins are an important source of essential amino acids – amino acids that out bodies
cannot synthesis. This include Leu, Ile, Lys, Thr, Trp, Phe, Val, and Met. All proteases are
secreted as zymogens. Pepsinogen from the stomach is
activated by acid. The protons remove the inhibitory
domain from the active site of the enzyme. The domain is
then autolytically cleaved to gain pepsin, which breaks
proteins down into shorter chains. Trypsinogen,
chymotrypsinogen, and pro-carboxypeptidase are secreted
from the pancreas into the small intestine. Trypsinogen is
activated by enterokinase and goes on to activate the other peptidases. Each peptidase is
specialised for different amino acids. Endopeptidases like trypsin and chymotrypsin target
the middle of protein sequences. Exopeptidases such as carboxypeptidase target the end of
Metabolism is all about getting energy from what we eat and using that energy to do
cellular work. Overall, this allows us to carry out day-to-day functions. Catabolism is the
breakdown of complex molecules to release energy (captured as ATP) while anabolism is the
build-up of complex molecules to store energy away for when it’s needed.
Energy in the Body
We have three main sources of energy: carbohydrates, lipids, and proteins. The first law of
thermodynamics describes that total energy within a system is constant.
Einput = Eoutput + Estored
In the perfect energy balance, there is no stored energy. However, in general, we take in
more energy than we put out. We therefore get stored energy in the form of adipose tissue.
In theory, weight loss can be achieved by decreasing input, increasing activity, or increasing
basal metabolism. Leptin is a chemical that indicated when we are full. Obese people are
leptin-resistant, so there is no indicator as to when to stop eating. We measure energy in
joules or calories, where 1 Cal = 4.184 kJ.
Energy intake is measured using bomb calorimetry where food is oxidised and the released
heat is measured. Some molecules cannot be used for fuel, like cellulose, so the adjusted
energy values are called the Atwater factors.
Energy output is measured using direct and indirect calorimetry. Direct calorimetry
measures heat output from an individual using a whole-body calorimeter to determine basal
metabolic rate. Indirect calorimetry measures gas exchange using respirometers. We can
then calculate the respiration exchange ratio (CO2/O2) to determine what type of fuel is
being burned, given that carbohydrates have a 1 RER and fats have a 0.7 RER.
Basal metabolic rate is required for vital bodily functions. BMR differs between individuals
as a result of genetic factors, age, sex, drugs, body composition, hormonal status, stress
levels, and disease status. BMR can be increased with athletic training, fever, drugs,
caffeine, and hyperthyroidism. It can be decreased with malnutrition, sleep, drugs, and
hypothyroidism.
Digestion of Complex Molecules
Carbohydrates make up 40-50% of our energy intake. They
consist mainly of starches (amylose and amylopectin) and
glycogen. Some of the foods we eat contain simple sugars like glucose and fructose. The
goal of carbohydrate digestion is to break the complex molecules down into
monosaccharides. Salivary amylase begins the process of carb digestion in the mouth,
hydrolysing glycosidic down into dextrans, polysaccharides, and oligosaccharides. Salivary
amylase is denatured in the stomach by low pH, and mechanical digestion continues
breakdown into oligosaccharides and trisaccharides. Pancreatic amylase continues the
process of digestion in the small intestine, forming disaccharides. The Disaccharidases from
intestinal epithelial cells can then break these down into their monomer units:
Sucrose ---> Glucose + Fructose
Maltose ---> Glucose + Glucose
Lactose ---> Glucose + Galactose
, BIOC 192 – Metabolism Module Study Guide
Monosaccharides are absorbed across the epithelial cells by
active symport with sodium via the SGLT 1 transporter on the
epithelial lining. Na+/K+ ATPase is important for this process as
it generates a concentration gradient for sodium to travel
down. Glucose is travelling up its concentration gradient, so the
process is secondary active transport. On the basal membrane
GLUT 2 transports monosaccharides passively out of the cell.
Once in the circulation, GLUT 3 transports glucose into the brain and GLUT 4 transports
glucose into muscle and adipose tissue. GLUT 1 is ubiquitous.
Fats are hydrophobic, so they need to be solubilised before they can be digested.
Triacylglycerol, TAGs, and cholesterol are the main fats we ingest. Bile salts are derived from
cholesterol – they are hydroxylated to make them more soluble. The presence of fats in the
small intestine stimulate the release of cholecystokinen, which releases bile salts and
lecithin. These bind to the TAGs and cholesterol to form micelles, and co-lipase anchors
lipase to the surface of the micelles. Lipase hydrolyses the first and third ester bonds to gain
monoacylglycerols (MAGs) and free fatty acids. Smaller micelles are
formed and these are absorbed across the intestinal cell membrane.
Once inside the cell, the MAGs and free fatty acids are resynthesised
into TAGs and packaged into lipoproteins. These have a number of
membrane proteins referred to as Apolipoproteins. The lipoproteins are
exocytosed to give chylomicrons, which are absorbed into the lacteal
and give lymph a milky appearance.
In the exogenous pathway of lipid transport, chylomicrons come directly
from the small intestine. Apo CII is used as a cofactor to activate
lipoprotein lipase in the tissue where fats are needed. This hydrolyses
TAGs into MAGs and fFAs, which are moved across the membrane and
resynthesised into TAGs. The leftover chylomicron moves to the liver, where ApoE and
ApoB48 act as ligands for receptors on the liver.
In the endogenous pathway, VLDL from the liver uses ApoCII to activate lipoprotein lipase.
Half of the remaining VLDL goes to the liver, while the other half form LDLs and undergo
further catabolism by hepatic lipase. Familial hypercholesterolemia occurs when there is a
mutation in the LDL receptor gene and LDL cannot be taken up by the liver. As a result, LDL
remains in the blood stream, increasing risk of atherosclerosis.
Proteins are an important source of essential amino acids – amino acids that out bodies
cannot synthesis. This include Leu, Ile, Lys, Thr, Trp, Phe, Val, and Met. All proteases are
secreted as zymogens. Pepsinogen from the stomach is
activated by acid. The protons remove the inhibitory
domain from the active site of the enzyme. The domain is
then autolytically cleaved to gain pepsin, which breaks
proteins down into shorter chains. Trypsinogen,
chymotrypsinogen, and pro-carboxypeptidase are secreted
from the pancreas into the small intestine. Trypsinogen is
activated by enterokinase and goes on to activate the other peptidases. Each peptidase is
specialised for different amino acids. Endopeptidases like trypsin and chymotrypsin target
the middle of protein sequences. Exopeptidases such as carboxypeptidase target the end of
