NUTR Exam 4

Ch. 9, 11, 14, 15

Energy metabolism

Deriving energy from macronutrients

• Synthesis of new substances (ATP)

• Excretion of waste

• Is slow when resting

• Is fast when physically active

Metabolic pathway

Series of chemical reactions (A → B → C)

Intermediate

Compoinds formed at steps along a metabolic pathway (A → B → C)

Anabolism

Building large molecules from small molecules, uses energy

(A + B → C); ANts like to build

Catabolism

Breaking large molecules into small molecules, produces energy

(A → B + C); CATs like to break

Metabolic pathways (4)

• Carbohydrates

• Fats

• Proteins

• Alcohol

Primary product made from catabolism

Adenosine triphosphate (ATP)

Secondary products made from catabolism (3)

Heat, carbon dioxide, water

ATP

Adenosine triphosphate = Adenosine + 3 (high energy) phosphate groups

• Making phosphate bonds → stores energy

• Breaking phosphate bonds → releases energy

Needs for ATP in the body (3)

• Mechanical work (muscle contraction)

• Transport work (pumping ions across membranes)

• Chemical work (condensation reactions, anabolism)

ADP

Adenosine diphosphate = adenosine + 2 pi (inorganic phosphate)

AMP

Adenosine monophosphate = adenosine + 1 pi (inorganic phosphate)

Redoc (reduction-oxidation) reactions

Exchange of electrons in the form of hydrogen ions: (OIL RIG), controlled by enzymes (dehydrogenases)

Oxidation

• Losing electrons/H ions (OIL)

• Gaining oxygen

Reduction

• Gaining electrons/H ions (RIG)

• Losing oxygen

Niacin coenzyme + redox forms

Coenzyme: nicotinamide adenine dinucleotide (NAD)

Oxidized form: NAD⁺ (the plus shows that it lost an electron!)

Reduced form: NADH (the H present shows that it gained an electron… in the form of a H ion!)

Reducing pyruvate

Creates lactate; 2 electrons are gained from NADH + H⁺

Oxidizing lactate

Creates pyruvate; 2 electrons are lost from lactate

Riboflavin coenzyme + redox forms

Coenzyme: flavin adenine dinucleotide (FAD)

Oxidized form: FAD

Reduced form: FADH₂

Cellular respiration

Carbohydrate food molecules are oxidized to form ATP

• Oxygen is the final electron acceptor

• May be aerobic or anaerobic

Aerobic cellular respiration

• Occurs with oxygen

• More efficient

• Creates 30-32 ATP

• Slow

Anaerobic cellular respiration

• Occurs without oxygen

• Less efficient

• Creates 2 ATP

• Fast

Stages of aerobic respiration

Glycolysis → transition reaction → citric acid/TCA cycle/Kreb’s cycle → electron transport chain

Glycolysis

Glucose → 2 pyruvate

• Does not need oxygen

• Requires 2 ATP

• Occurs in the cytosol

Products of glycolysis

• 2 pyruvate

• NADH + H⁺

• 2 net ATP (4 were created throughout, but 2 were used in the process)

Transition reaction

Pyruvate → Acetyl-CoA

• Requires oxygen and 4 B vitamins (thiamin, riboflavin, niacin, pantothenic acid)

• Irreversible

• Occurs from the cytosol to the mitochondria

Products of transition reaction

• Acetyl-CoA (2-carbon compound)

• CO₂ waste (exhaled)

• NADH + H⁺

Citric acid cycle/TCA cycle/Krebs cycle

Acetyl-CoA → Oxaloacetate

• Does not need oxygen

• Does 2 cycles for each glucose molecule

• Occurs in the mitochondria

Products of the citric acid cycle/TCA cycle/Krebs cycle

• NADH + H⁺

• FADH₂

• 2 Guanosine triphosphate (GTP = a potential/small ATP)

• CO₂

Electron transport chain/oxidative phosphorylation

• Requires oxygen (O), copper (Cu), iron (Fe)

• Electrons move through electron carriers (protein complexes)

• Occurs in the mitochondria

Products of the electron transport chain

• 28 ATP (90%)

• Water

• Heat

Events in the ETC

• Protein complexes I, III, IV in the inner membrane directly pump H⁺ from the inner → outer compartment (this creates a pressure gradient)

• Protein complex II in the inner membrane facilitates electron transfer from the inner → outer compartment (this promotes H⁺ transfer in protein complexes III, IV)

• Enzyme ATP synthase pumps H⁺ from the outer → inner compartment (where it joins oxygen as the final electron acceptor and becomes water as a byproduct)

• Phosphate and ADP cross channels in the inner membrane from the outer → inner compartment and join to form ATP

• Uncoupling proteins in the inner membrane send H⁺ overflow from the outer → inner compartment (these H ions produce heat)

Anaerobic glycolysis

Pyruvate → lactate

• In cells that do not have mitochondria (RBCs)

• Occurs with little/no oxygen

• Not very efficient

Products of anaerobic glycolysis

• Lactate

• NAD⁺

Cori cycle

Lactate → glucose

• Occurs during intense physical activity for quick ATP

• H+/lactate accumulates in muscle → more acidity in the muscles → burning sensation → reduced physical output

• Lactate is sent to the liver and converted to glucose, and then returned to the muscles

• A 1 enzyme reaction

Lipid metabolism steps

Lipolysis → Beta-Oxidation → Ketogenesis

Lipolysis

Breakdown of lipids during fasting/low-calorie intake

• Hormone-sensitive lipase becomes activated in adipose tissue

• Triglycerides breakdown → free fatty acids and glycerol

• Increased by glucagon, growth hormone, epinephrine

• Free fatty acids enter cells and are shuttled into mitochondria by carnitine carrier

Beta-oxidation

2 carbons at a time are cleaved off the Beta-carbon

• Acetyl-CoA enters the citric acid cycle/Krebs cycle/TCA cycle

• NADH + FADH₂ become chemical energy storage

• 106 ATP are made from 16 carbon free fatty acid

Carbohydrate aids fat metabolism

• Citric acid cycle/krebs cycle/TCA cycle metabolites enter other pathways → reducing oxaloacetate

• Pyruvate → oxaloacetate (by cells)

• Carbs generate pyruvate

**oxidation of fatty acids is more efficient with carbs!!!

Ketogenesis process

Decline in oxaloacetate → slowing down of citric acid/krebs/TCA cycle → continuation of beta-oxidation → accumulation of Acetyl-CoA → ketogenesis → ketosis

Ketogenesis

Formation of ketone bodies

Causes of ketosis

• Low insulin levels/type 1 diabetes

• Low carb diet/semi starvation or fasting

Ketosis from type 1 diabetes

• Insufficient insulin production by pancreas

• Low insulin → glucose inability to enter cells

• Rapid lipolysis creates excessive ketone body buildup

• Ketone bodies contain acid groups → lower blood pH (becomes acidic) → diabetic ketoacidosis (DKA)

Ketosis from semistarvation/fasting

• Glucose and insulin levels decline

• Liver creates ketone bodies → used for fuel by heart, muscles, kidneys, brain

• Protein sparing/fat is used instead → fat loss

Protein metabolism steps

Gluconeogenesis → urea cycle

Deamination

Loss of an amino group (eg. Glutamic acid → alpha-ketoglutaric acid)

Gluconeogenic amino acids

Carbon skeletons that form glucose or enter citric acid/krebs/TCA cycle directly

Ketogenic amino acids

Carbon skeletons that form acetyl-CoA or ketones

Gluconeogenesis

Creation of glucose from a new substrate; amino acids, glycerol, lactate (pyruvate → glucose)

• Occurs in the liver and kidneys

• Begins with oxaloacetate

• Reverse glycolysis to form glucose

• Requires ATP, biotin, riboflavin, niacin, B-6

• Glycerol can be used, but little glucose will be produced

Urea cycle

Amino groups (NH₂) converted to ammonia (NH₃)

• Ammonia is toxic to the brain

• Liver converts ammonia → urea → kidneys → excreted as urine

Alcohol dehydrogenase

Ethanol → acetaldehyde and NADH + H⁺

Acetaldehyde dehydrogenase

Acetaldehyde → acetyl-CoA and NADH + H+

• Requires coenzyme A (CoA)

• Can enter the krebs/citric acid/TCA cycle

  • Too much, krebs/citric acid/TCA cycle slows → acetyl-CoA can’t enter

  • Acetyl-CoA becomes triglycerides and free fatty acids

  • Results in steatosis (fat in liver) → cirrhosis

Regulation of energy metabolism

• Liver!!!

• ATP concentrations

• Enzymes

• Hormones

• Vitamins

• Minerals

Key functions of the liver

• Conversions between forms of simple sugars

• Fat synthesis

• Nutrient storage

• Amino acid metabolism

• Urea production

• Ketone body production

• Alcohol metabolism

Result of high ATP concentrations

• Promote anabolic reactions (building)

• Decrease energy-yielding reactions (breaking)

Result of high ADP concentrations

Stimulate energy-yielding pathways

Consequences of low levels of insulin

• Gluconeogenesis

• Protein breakdown; proteolysis

• Lipolysis

Consequences of high levels of insulin

• Glycogenesis

• Fat synthesis

• Protein synthesis

Post prandial fasting

0-6 hours, primary energy source from carbs

Short term fasting

3-5 days, primary energy source from proteins

Long term fasting

5-7 days, primary energy source from fats

Adaptations to fasting

Slowed metabolism (reduced energy requirements, slower loss of lean body mass), nervous system uses less glucose (more reliance on ketone bodies, protein catabolism continues to provide glucose)

**after 50% of lean body mass is lost, death occurs (7-10 weeks)

Effects of feasting

• Fat (stored as adipose tissue)

• Protein (amino acid pool → proteins, excess amino acids → fatty acids)

• Carbs (fuel for body, increase glycogen stores, excess stored as body fat)