BIOCHEMISTRY

INTRO TO METABOLISM
Dr. Lourdes Balcueva | 09/27/2017

OUTLINE  Most organisms derive both the raw materials and the energy
I. Metabolism for biosynthesis from organic fuel molecules such as glucose
A. Definition  Metabolic Pathways
II. Categories of Metabolism  Sequences of reactions that include the reactants,
A. Catabolic Pathway intermediates, products, and the enzymes involved
B. Anabolic Pathway  4 major groups of biomolecules whose metabolic pathways
C. Amphibolic Pathway are considered separately
III. Metabolic Process  Carbohydrates
IV. Metabolic Fuels  Fats
A. Fates of Glucose  Proteins
B. Fates of Lipids  Nucleotides
C. Fates of Amino Acids
V. Integration of Metabolism (Tissue and Organ
Level)
A. Dietary Lipids
B. VLDL
C. Intracellular Locations of Major Pathways
VI. Metabolic Location of Major Pathways
A. Fed State
B. Fasting State
C. Starved State
VII. Metabolic Regulation
A. Metabolic Regulation Concepts
B. Patterns of Metabolic Regulation
VIII. Clinical Correlation

OBJECTIVES

 General Objective
 To explain thoroughly how cells carry out and regulate
complex reaction sequences.
 Specific Objectives
 To be able to differentiate between anabolic and catabolic Figure 1. Outline of the pathways for the catabolism of carbohydrate,
protein, and fat. All these pathways lead to the production of acetyl-CoA,
pathways. which is oxidized in the citric acid cycle, ultimately yielding ATP by the
 To be able to explain briefly how carbohydrates, fats, and process of oxidative phosphorylation.
proteins are metabolized.
 To be able to correlate relationships between each pathway.
II. CATEGORIES OF METABOLISM
Metabolism can be divided into three categories:
I. METABOLISM  Catabolism
 The process related to degradation of complex substances to
A. DEFINITION liberate smaller molecules and energy
 Ex. glycogenolysis, glycolysis, proteolysis, TAG degradation
 An entire network of chemical reactions carried out by living  Anabolism
cells.  The process concerned primarily with synthesis of complex
 Living cells carry out thousands of reactions simultaneously. organic molecules needed for cell maintenance, growth, and
 Each reaction sequence is controlled so that unwanted reproduction
accumulations or deficiencies of intermediate products do not  glycogenesis,gluconeogenesis, uronic acid pathway, protein
occur synthesis, cholesterol synthesis, TAG synthesis, Fatty Acid
 Metabolism includes: Synthesis
 Interconversion of chemical compounds in the body  Amphibolic
 Pathways taken by molecules  Acts as links between anabolism and catabolism
 Interrelationships between the pathways  It is the crossroad between the two pathways
 Regulating mechanisms  Kreb’s Cycle
 Intermediary Metabolism
 Applied to reactions involving the low molecular weight
molecules that are metabolites of the degradation or Acetyl CoA and the Citric Acid Cycle
biosynthesis of biopolymers Acetyl-coA: Major common product of digestion from
 Energy Metabolism dietary carbohydrate, lipid and protein
Citric Acid Cycle: Oxidizes acetyl-coA into by products
 Part of intermediary metabolism consisting of pathways that
(Catabolic), Uses Intermediates as precursors of other
store or generate metabolic energy
compounds (anabolic)

Trans # 2 Group 1: Abalos, Abante, Abdul, Abilgos, Abuan M. 1 of 8

 Table 1. Difference bet.Catabolic and Anabolic Pathway (based on ppt)

III. METABOLIC PROCESS

 Depends on the nature of the diet

 Requirement for metabolic fuel is constant (PA increases
metabolic rate by 40-50% over the basal metabolism)
 Need to form glycogen and triacylglycerides to provide for
energy in between meals
 Obesity
 If intake of metabolic fuels greater than expenditure
 Emaciation
 If intake is consistently lower than expenditure Figure 2. Overview of carbohydrate metabolism showing the major
pathways and end products. Gluconeogenesis is not shown.

IV. METABOLIC FUELS

B. FATES OF LIPIDS
 Fed state – metabolic fuel is glucose
 Fasting state – glycogen, fatty acids, amino acids, ketone Acetyl-CoA formed by β-oxidation of fatty acids may undergo three
bodies fates (Figure 3):
 Major hormones that control utilization of fuel:
 Insulin 1. As with acetyl-CoA arising from glycolysis, it is oxidized to CO2
+ H2O via the citric acid cycle
 Glucose
2. It is the precursor for synthesis of cholesterol and other
steroids
A. FATES OF GLUCOSE 3. In the liver, it is used to form the ketone bodies, aceto-acetate
and 3-hydroxybutyrate, which are important fuels in prolonged
1. Converted to pyruvate  acetyl CoA  CO2 + H20 (linked to fasting and starvation.
formation of ATP in oxidative phosphoryltation
2. Glycogen – storage for glucose in the liver and skeletal muscle FATE OF TRIACYLGLYCERIDE (TAG)
3. Pentose phosphate pathway - provides NADPH and ribose  Triacylglyceride → cleaved via phospholipases → 1
sugar for nucleic acid synthesis glycerol + 3 fatty acids
4. Triose phosphates – glycerol moeity provides for synthesis of
triacylglycerides FATE OF FATTY ACIDS
5. Pyruvate, α-ketoglutarate and oxaloacetate – precursors of  Carried by Albumin in the blood
amino acids
 Taken up by adipocyte or muscle
6. Lactate (during anaerobic respiration)
 Even number chain: FA undergoes β-oxidation →
FATES OF PYRUVATE acetyl-CoAs (2-carbon compound)→ enters Kreb’s
Cycle, becomes cholesterol or kentone bodies
GLUCONEOGENESIS  Odd number chain: FA undergoes β-oxidation →
 Synthesis of glucose from non-carbohydrate acetyl-CoAs (enters Kreb’s. or can become
sources. cholesterol/ketone bodies) + 1 proprionyl-coA (3-C
 Lactate compound)→enters Kreb’s via Succinyl-CoA
 Amino Acids
 Glycerol FATE OF GLYCEROL
 Taken up by liver
 Converted to Glycerol-3-phosphate
 Glycerol-3-phosphate may:
 Enter glycolysis/gluconeogenesis via
Dihydroxy-acetone phosphate
 Synthesis of TAG or Phophoplipids

BIOCHEMISTRY INTRODUCTION TO METABOLISM 2 of 8

  During severe starvation, glucogenic amino acids will be
catabolized and the carbon skeleton will be used for energy.
The amino group will be converted to urea and eliminated in
the urine.
 Amino acids are used for protein synthesis and production of
non-protein nitrogen derivatives.

GLUCOGENIC VS KETOGENIC AMINO ACIDS

V. INTEGRATION OF METABOLISM (TISSUE AND

ORGAN LEVEL)

 Glucose and amino acids are absorbed by the liver via

hepatic portal vein
 Liver maintains blood level by:
1. Glycogenolysis
Figure 3. Overview of fatty acid metabolism showing the major 2. Gluconeogenesis
pathways and end products. The ketone bodies are acetoacetate, 3-
hydroxybutyrate, and acetone (which is formed nonenzymically by
decarboxylation of acetoacetate).

C. FATES OF AMINO ACIDS

AMINO ACIDS
 For protein synthesis and synthesis of non-protein nitrogen
derivatives

1. Oxidized to CO2 and H2O

2. Gluconeogenesis
3. Form ketone bodies

Figure 5. Transport and fate of major carbohydrate and amino acid

substrates and metabolites.

 Glucose can be converted to amino acids after going to the

liver via the portal hepatic vein.
 Excess glucose will be taken up and be used to synthesize
glycogen (glycogenesis) or fatty acids (lipogenesis)
 The liver is responsible for glycogenolysis (glycogen break
down) and gluconeogenesis (synthesis of glucose) in times
of starvation or in between meals.
 The amino acids that enter the portal hepatic vein are used
to synthesize protein molecules. In addition, amino acids can
also be converted to glucose to provide energy. In excess,
amino group is converted to urea and will then be excreted
into the urine.
 The skeletal muscles use glucose aerobically (product: CO2)
and anaerobically (product: lactate). It can also store
Figure 4. Overview of amino acid metabolism showing the major
pathways and end products
glycogen used for muscle contraction and produces muscle
proteins from amino acids.

BIOCHEMISTRY INTRODUCTION TO METABOLISM 3 of 8

 A. DIETARY LIPIDS

 TAGs are hydrolyzed to monoacylglycerols and fatty acids 

re-esterified in intestinal mucosa and packaged with protein
 lymphatic system as chylomicrons  metabolized by
muscle and adipose tissue via lipoprotein lipase (LPO)

B. VLDL (VERY LOW DENSITY LIPOPROTEIN)

 TAGs from liver lipogenesis are the main fuel reserve of the
body
 Ketone bodies – product of partial oxidation of FA in the liver;
used as fuel by extrahepatic tissues including the brain but
not by erythrocytes

Figure 7. Intracellular location and overview of major metabolic

pathways in a liver parenchymal cell

VI. METABOLIC LOCATIONS OF MAJOR PATHWAYS

A. FED STATE
 Metabolic reserves are laid down
 The organs participating in metabolism are active. This is the
period from start of absorption until absorption is complete.
 With the use of glucose for the major fuel for oxidation, there is
an increase in the respiratory quotient (Table 2).
 Respiratory Quotient
Figure 6. Transport and fate of major lipid substrate and metabolites  ratio of CO2 produced to oxygen consumed

Table 2. Energy Yields, Oxygen Consumption, and Carbon Dioxide

 In the small intestines, triacylglycerol from the diet is broken Production in the Oxidation of Metabolic Fuels
down into 2 fatty acids and monoacylglycerol
 In the intestinal wall, it is absorbed and converted again into
triacylglycerol and brought into the circulation by the
chylomicrons.
 In adipose tissues and skeletal muscles, it is taken up as
fatty acid in the presence of lipoporotein lipase (LPL).
 Fatty acid is again esterified to triacylglycerol for storage
(lipogenesis) or it can be used as energy (lipolysis)
 TAGs are broken down and are converted to VLDL (Very  Glucose uptake into the muscle and adipose tissue is
Low Density Lipoprotein) and go back to adipose and controlled by insulin (secreted by -islet cells of pancreas), in
muscles via the blood stream response to increased concentration of glucose in portal
 Fatty liver will occur if there is an excess in fatty acids blood.
entering the liver.  GLUT 4
 glucose transporter in muscles and adipose tissues
C. INTRACELLULAR LOCATIONS OF MAJOR
PATHWAYS B. FASTING STATE
 Metabolic fuel reserves are mobilized
 Cytosol:  There is small change in plasma glucose
 Glycolysis  As the fasting is prolonged, the plasma concentration of
 Pentose phosphate pathway ketone bodies increases (Table 3; Figure 8).
 Lipid synthesis
 Protein synthesis
 Gluconeogenesis
Table 3. Plasma Concentrations of Metabolic Fuels (mmol/L) in the Fed and
 Glycogenesis and Glycogenolysis Fasting States

 Mitochondria:
 Citric acid cycle
 Electron Transport Chain
 ATP synthesis
 Synthesis of ketone bodies
 Beta oxidation of fatty acids

BIOCHEMISTRY INTRODUCTION TO METABOLISM 4 of 8


Figure 8. Relative changes in plasma hormones and metabolic fuels during
the onset of starvation
Blood Glucose and the Role of Liver During Fasting
 The liver maintains blood glucose levels during fasting, and its
role is thus critical.
 Glucose is the major fuel for tissues such as the brain and
neural tissue and the sole fuel for red blood cells.
 Most neurons lack enzymes required for oxidation of fatty acids,
but they can use ketone bodies to a limited extent.
 Red blood cells lack mitochondria, which contain the enzymes
of fatty acid and ketone body oxidation, and can use only
glucose as a fuel.
 Therefore, it is imperative that blood glucose not decrease too
rapidly nor fall too low. Initially, liver glycogen stores are
degraded to supply glucose to the blood, but these stores are
limited.
 This pathway is known as glycogenolysis (the lysis, or splitting
of glycogen to form glucose subunits). Although liver glycogen
levels may increase to 200-300 g after a meal, only
approximately 80 g remain after an overnight fast. Fortunately,
the liver has another mechanism for producing blood glucose,
known as gluconeogenesis.
 Gluconeogenesis means formation (genesis) of new (neo)
glucose, and, by definition, converts new (noncarbohydrate)
precursors to glucose.
 In gluconeogenesis, lactate, glycerol, and amino acids are used
as carbon sources to synthesize glucose.
 As fasting continues, gluconeogenesis progressively adds to the
glucose produced by glycogenolysis in the liver.
 Lactate is a product of glycolysis in red blood cells and
exercising muscle; glycerol is obtained from lipolysis of adipose
triacylglycerols; and amino acids are generated by the
breakdown of protein.
 Because our muscle mass is so large, most of the amino acid is
supplied from degradation of muscle protein.
 These compounds travel in the blood to the liver, where they
are converted to glucose by gluconeogenesis.
 Because the nitrogen of the amino acids can form ammonia,
which is toxic to the body, the liver converts this nitrogen to
urea. Urea has two amino groups for just one carbon.
BIOCHEMISTRY INTRODUCTION TO METABOLISM
 It is a very soluble, nontoxic compound that can be readily
excreted by the kidneys and thus is an efficient means for
disposing of excess ammonia.
Role of Adipose During Fasting
 Adipose triacylglycerols are the major source of energy during
fasting.
 They supply fatty acids, which are quantitatively the major fuel
for the human body.
 Fatty acids are oxidized not only directly by various tissues of
the body; they are also partially oxidized in the liver to four-
carbon products called ketone bodies.
 Ketone bodies are subsequently oxidized as a fuel by other
tissues. As blood insulin levels decrease and blood glucagon
levels rise, adipose triacylglycerols are mobilized by a process
known as lipolysis (lysis of triacylglycerol).
 They are converted to fatty acids and glycerol, which enter the
blood. It is important to realize that most fatty acids cannot
provide carbon for gluconeogenesis.
 Thus, of the vast store of food energy in adipose tissue
triacylglycerols, only the small glycerol portion travels to the liver
to enter the gluconeogenic pathway.
 Fatty acids serve as a fuel for muscle, kidney, and most other
tissues.
 They are oxidized to acetyl coenzyme A (acetyl-CoA), and
subsequently to CO2 and H2O in the tricarboxylic acid (TCA)
cycle, producing energy in the form of adenosine triphosphate
(ATP).
 In addition to the ATP required to maintain cellular integrity,
muscle uses ATP for contraction, and the kidney uses it for
urinary transport processes. Most of the fatty acids that enter
the liver are converted to ketone bodies rather than being
completely oxidized to CO2.
 The process of conversion of fatty acids to acetyl-CoA produces
a considerable amount of energy (ATP), which drives the
reactions of the liver under these conditions.
 The acetyl-CoA is converted to the ketone bodies, acetoacetate
and α-hydroxybutyrate, which are released into the blood (Fig.
3.3). The liver lacks an enzyme required for ketone body
oxidation.
 Nevertheless, ketone bodies can be further oxidized by most
other cells with mitochondria, such as muscle and kidney. In
these tissues, acetoacetate and α-hydroxybutyrate are
converted to acetyl-CoA and then oxidized in the TCA cycle,
with subsequent generation of ATP.
In Summary
 In the initial stages of fasting, stored fuels are used for energy
 The liver plays a key role by maintaining blood glucose levels in
the range of 80 to 100 mg/dL, first by glycogenolysis and
subsequently by gluconeogenesis.
 Lactate, glycerol, and amino acids serve as carbon sources for
gluconeogenesis.
 Amino acids are supplied by muscle. Their nitrogen is converted
in the liver to urea, which is excreted by the kidneys.
 Fatty acids are released from adipose tissue by the process of
lipolysis. It serve as the body’s major fuel during fasting.
 The liver oxidizes most of its fatty acids only partially, converting
them to ketone bodies, which are released into the blood. Thus,
during the initial stages of fasting, blood levels of fatty acids and
ketone bodies begin to increase.
5 of 8
 Muscle uses fatty acids, ketone bodies, and (when exercising Role of Adipose During Fasting
and while supplies last) glucose from muscle glycogen.  During prolonged fasting, adipose tissue continues to break
 Red blood cells, the brain, and other neural tissues use mainly down its triacylglycerol stores, providing fatty acids and glycerol
glucose to the blood.
 These fatty acids serve as the major source of fuel for the body.
C. STARVED STATE (PROLONGED FASTING)
 The glycerol is converted to glucose, whereas the fatty acids
are oxidized to CO2 and H2O by tissues such as muscle.
Metabolic Changes During Prolonged Fasting
 In the liver, fatty acids are converted to ketone bodies that are
 If the pattern of fuel utilization that occurs during a brief fast
oxidized by many tissues including the brain.
were to persist for an extended period, the body’s protein would
 Several factors determine how long we can fast and still survive.
be quite rapidly consumed to the point at which critical functions
would be compromised.  The amount of adipose tissue is one factor, because adipose
tissue supplies the body with its major source of fuel.
 Fortunately, metabolic changes occur during prolonged fasting
that conserve (spare) muscle protein by causing muscle protein  However, body protein levels can also determine the length of
turnover to decrease time we can fast. Glucose is still used during prolonged fasting
(starvation), but in significantly reduced amounts.
Role of Liver During Prolonged Fasting  Although we degrade protein to supply amino acids for
 After 3 to 5 days of fasting, when the body enters the starved gluconeogenesis at a slower rate during starvation than during
state, muscle decreases its use of ketone bodies and depends the first days of a fast, we are still losing protein that serves vital
mainly on fatty acids for its fuel. functions for our tissues.
 The liver, however, continues to convert fatty acids to ketone  Protein can become so depleted that the heart, kidney, and
bodies. The result is that the concentration of ketone bodies other vital tissues stop functioning, or we can develop an
rises in the blood. infection and not have adequate reserves to mount an immune
 The brain begins to take up these ketone bodies from the blood response. In addition to fuel problems, we are also deprived of
and oxidizes them for energy. Therefore, the brain needs less the vitamin and mineral precursors of coenzymes and other
glucose than it did after an overnight fast. compounds necessary for tissue function.
 Glucose is still required, however, as an energy source for red  Because of either a lack of ATP or a decreased intake of
blood cells, and the brain continues to use a limited amount of electrolytes, the electrolyte composition of the blood or cells
glucose, which it oxidizes for energy and uses as a source of could become incompatible with life.
carbon for the synthesis of neurotransmitters.  Ultimately, we die of starvation.
 Overall, however, glucose is “spared” (conserved). Less
glucose is used by the body and, therefore, the liver needs to Table 4. Summary of Metabolic Locations of Major Pathways
produce less glucose per hour during prolonged fasting than
during shorter periods of fasting.
 Because the stores of glycogen in the liver are depleted in
approximately 30 hours of fasting, gluconeogenesis is the only
process by which the liver can supply glucose to the blood if
fasting continues.
 The amino acid pool, produced by the breakdown of protein,
continues to serve as a major source of carbon for
gluconeogenesis.
 A fraction of this amino acid pool is also used for biosynthetic
functions (e.g., synthesis of heme and neurotransmitters) and
new protein synthesis, processes that must continue during
fasting.
 However, as a result of the decreased rate of gluconeogenesis
during prolonged fasting, protein is “spared”; less protein is
degraded to supply amino acids for gluconeogenesis.
 While converting amino acid carbon to glucose in
gluconeogenesis, the liver also converts the nitrogen of these
amino acids to urea.
 Consequently, because glucose production decreases during
prolonged fasting compared with early fasting, urea production
also decreases.

BIOCHEMISTRY INTRODUCTION TO METABOLISM 6 of 8


Figure 9. Metabolic interrelationships among adipose tissue, liver, and
extra hepatic tissues
Reasons for Multistep Pathway
 Limited reaction- specificity of enzymes; each active site
catalyzes only a single step of the pathway
 To control energy input and output – energy flow is
mediated by energy donors and acceptors
Figure 10. Carbon Cycle (Dr. Balcueva’s ppt)
 Catabolism of metabolic fuels yield 3 types of
compounds that mediate the release of energy:
 acetyl CoA
 nucleoside triphosphate (ATP)
 reduced coenzymes (NADH & FADH)
 Some compounds can be substrates or products of more
than 1 enzyme so they can have 2 or more metabolic
functions.
 To establish control points:
BIOCHEMISTRY INTRODUCTION TO METABOLISM
 balance of energy supply and demand in living cells
 ability to respond to internal signals or change in the
environment
VII. METABOLIC REGULATION
 Most pathways are irreversible under physiologic conditions
 When a metabolite enters the pathway each step occurs in
sequence without backing up or wasting cellular material or
energy (avoids futile cycles)
 Futile cycle- occurs when tow metabolic pathways run
simultaneously in opposite directions (ex. Glycolysis and
gluconeogenesis) and have no overall effect other than
to dissipate energy in the form of heat.
 Reactions are regulated so as to proceed in only one direction
 Regulation depends largely on two concepts:
 Enzymatic control - regulation of enzyme activity helps
control metabolism.
 Substrate availability - utilization of metabolic fuels by
different organs in the human body is controlled at the
cellular level as a function of nutrient availability.
A. METABOLIC REGULATION CONCEPTS
 Enzymatic Activity Control via Compartmentalization
 Differentiation of enzymes between organelles
 In this stage of metabolic regulation, specific enzymes
are bound within the domains of specific organelles to
prevent reactions from going on unhindered.
 The cytosol exclusively contains enzymes for
glycolysis, pentose phosphate pathway, and fatty
acid synthesis
 The mitochondrion has enzymes and proteins that
largely revolve around redox reactions within the
Citric Acid Cycle (TCA cycle) and the Electron
Transport Chain.
 However, some metabolic pathways in a single metabolic
pathway can be found in multiple areas, such as the urea
cycle.
 Concentration of Substrate
 Glucose concentration is the key metabolic regulator of
in terms of substrate concentration, acting as a sensor of
how much energy is present, since both protein and lipid
energy pathways lead into the use of glucose.
Figure 11. Blood glucose concentration against time during meals
7 of 8
 B. PATTERNS OF METABOLIC REGULATION synthesis.
 Allosteric Modification - allosteric effectors bring about
catalytic modification by binding to the enzyme at distinct
Thyroxine Promotes glycogenolysis,
allosteric sites; Reversible gluconeogenesis and lipolysis.
 Negative Feedback Inhibition and Positive Forward
Activation Growth Hormone Promotes amino acid uptake
 Feedback inhibition - when the end product of a pathway into cells, protein synthesis,
controls its own rate of synthesis. glycogenolysis and lipolysis.
 Feedforward activation - when a metabolite produced
Cortisol Promotes gluconeogenesis,
early in the pathway activates an enzyme that catalyzes
lipolysis and breakdown of
a reaction further down the pathway. proteins.
 Covalent Modification - addition or removal of a phosphate
or adenylate protein kinase group using ATP; Reversible Testosterone Promotes protein synthesis.
 Alters catalytic rate by attachment to some group by a
covalent bond (usually a phosphate group)
 Phosphorylation
- Catalyzed by protein kinase VIII. CLINICAL CORRELATION
- Activates enzymes regulating catabolic
pathways (hence, uses ATP).  Cachexia
- Inhibits enzymes regulating anabolic pathways.  In prolonged starvation, adipose tissue reserves are
 Dephosphorylation depleted, muscle tissues are catabolized and used as
- Catalyzed by protein phosphatase fuel
- Activates enzymes regulating anabolic  Diabetes Mellitus
pathways.  Glucose is not utilized by the cells because of receptor
- Inhibits enzymes regulating catabolic pathways. resistance to insulin (Type II) or lack of insulin due to
 Supply of substrate membrane permeability destruction of -cells of the pancreas (Type I)
 Ribosomal synthesis of enzyme
 RNA synthesis REFERENCES
 Hormonal influence
 Hormones play a vital role in maintaining whole body 1. 2020A Biochemistry Trans
energy homeostasis. 2. 2020C Biochemistry Trans
 Insulin 3. Dr. Balcueva’s lecture/ppt
 A polypeptide hormone that regulates carbohydrate 4. Harpers Illustrated Biochemistry 28th Edition
metabolism. 5. Boundless. “Hormonal Regulation of Metabolism.”
 When blood glucose levels rise, insulin will be Boundless Biology. Boundless, 26 May. 2016. Retrieved
secreted by the pancreas, lowering blood glucose by 30 Sept. 2017 from
increasing its uptake in cells and stimulating the liver https://www.boundless.com/biology/textbooks/bo
to convert glucose to glycogen, in which form it can undless-biology-textbook/the-endocrine-
be stored. system37/regulation-of-body-processes-
 Stimulation of key glycolytic enzymes.
212/hormonalregulation-of-metabolism-799-12035/
 Glucagon
6. Marks’ Basic Medical Biochemistry A Clinical Approach
 Opposes the action of insulin by stimulating the
production of sugar.
 When blood glucose levels fall, glucagon is secreted
by the pancreas, which increases blood glucose
levels by stimulating the breakdown of glycogen into
glucose and the creation of glucose from amino
acids.
 Acts as an inhibitor for glycolytic key enzymes
(glukokinase, PFK-1 and pyruvate kinase).

Table 5. Hormones and their Metabolic Effects. Adapted from Boundless.

Hormone Metabolic Effects

Insulin Promotes glucose uptake into

cells, glycogenesis, lipogenesis,
amino acid uptake into cells
and protein synthesis. Inhibits
lipolysis.

Glucagon and Epinephrine Promotes glycogenolysis,

gluconeogenesis and protein

BIOCHEMISTRY INTRODUCTION TO METABOLISM 8 of 8