The document summarizes carbohydrate and lipid metabolism. It discusses the key pathways of carbohydrate metabolism including glycolysis, the citric acid cycle, glycogenesis, glycogenolysis, and gluconeogenesis. It also discusses lipid metabolism, covering lipid digestion and absorption, transportation, catabolism including beta-oxidation, and biosynthesis of triglycerides, fatty acids, and cholesterol. The pathways are regulated by hormones like insulin and glucagon and enzymes like HMG-CoA reductase.

1. CARBOHYDRATE
AND
LIPID METABOLISM
Submitted by : Meet H. Padhiyar
Submitted to : Mr. J S Patel (asst. Professor)
College of basic science and Humanities
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2. • Content
CARBOHYDRATE METABOLISM
1. Introduction
2. Glycolysis
3. Oxidation of pyruvate
4. Citric acid cycle
5. Glycogenesis
6. Glycogenolysis
7. Gluconeogenesis
8. HMP shunt
LIPID METABOLISM
1. Introduction
2. Lipid Digestion & Absorption
3. Lipid Transportation
4. Lipid Catabolism
5. Lipid Metabolism (Membrane
lipid,Triglycerides,fatty acids, cholesterol)
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3. • Metabolism : The entire spectrum of chemical reactions, ocuuring in
living organisms, are collectively referred to as metabolism.
• There are two categories of metabolism.
1. Catabolism : The degradative processes concerned with the
breakdown of complex molecules to simpler ones, with release of
energy
2. Anabolism : The biosynthetic reactions involving the formation of
complex molecules from simple precursors, with utilization the energy.
• Introduction
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4. • Carbohydrate metabolism
• Carbohydrates are most abundant organic molecules on earth and major source of energy
for living cells.
• Carbohydrate metabolism is the whole of the biochemical processes responsible for the
metabolic formation, breakdown, and interconversion of carbohydrates in living organisms.
• Plants synthesize carbohydrates from carbon dioxide and water through photosynthesis,
allowing them to store energy absorbed from the sunlight.
• Animal and fungi consume plants, they use cellular respiration to break down these stored
carbohydrates to make energy available to ccells.
• Human consume a variety of carbohydrates, digestion breaks down complex carbohydrates
into a few simple monomer (monosaccharides) for metabolism: glucose, fructose,
and galactose.
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5. • GLYCOLYSIS
• Glycolysis : is defined as the sequence of reactions converting
glucose pyruvate /lactate with the production of ATP.
• This pathway is often referred to as Embden-Meyerhof pathway
(E.M, pathway)
• Salient Features :
1. Substrate - Glucose
2. Products - Pyruvate (in aerobic condition)
. Lactate (in anaerobic condition
3. Site - All cells and tissues cytoplasm
4. Nature - Catabolic
5. Specialty - can occur aerobically and anaerobically.
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6. Aerobic pathway
Anaerobic pathway
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7. • Regulation :
1. HEXOKINASE - INHIBITED BY HIGH LEVELS OF GLUCOSE-6-PHOSPHATE,
WHICH PREVENTS THE PHOSPHORYLATION OF GLUCOSE.
2. PHOSPHOFRUCTOKINASE - INHIBITED BY HIGH LEVELS OF ATP AND
ACTIVATED BY HIGH LEVELS OF ADP AND AMP.
3. PYRUVATE KINASE - INHIBITED BY HIGH LEVELS OF ATP OR ACETYL COA.
• Inhibitors :
1. Iodoacetate : inhibit the glyceraldehyde-3-phosphate dehydrogenase enzyme.
2. Arsenite : inhibits ATP synthesis by stoping oxidative phosphorylation.
3. Fluride : inhibits enolase enzyme .
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8. • Oxidation of pyruvate
• Pyruvate oxidized into acetyl
coa with the help of : enzyme
pyruvatedehydrogenase(PDH)
and
Thyaminpyrophosphate(TPP).
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9. • The citric acid cycle (CAC) – also known as the TCA cycle (tricarboxylic acid
cycle) or the Krebs cycle.
• Is a series of chemical reaction used by all aerobic respiration to release stored
energy through the oxidation of acetyl-coa derived from carbohydrates, fats,
and proteins.
• Salient features:
1. Substrate : Acetyl CoA
2. Products : Reduced Coenzymes,Co2 & GTP/ATP
3. Sites : In eukaryotes-inner membrane of mitochondria .
• Citric Acid Cycle
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11. • Regulation
• Regulation-1 : Formation of acetyl Coa from pyruvate.
Activate by Ca++.
Inhibits by products NADH & acetyl Coa amount.
• Regulation-2 : Formation of citrate from a acetyl Coa & Oxaloacetate.
Inhibits by product citrate amount and also by succinyl Coa.
• Regulation-3 : Enzyme isocitrate dehydrogenase & alpha ketoglutrate-
dehydrogenase.
Activates by Ca++
Inhibit by NADH product amount.
• Inhibitors:
1. Fluroacetate : Inhibits the Aconitase enzyme.
2. Malonate : Inhibits the succinate dehydrogenase enzyme.
3. Arsenite : Inhibits the alpha ketoglutrate dehydrogenase.
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12. • Glycogen metabolism
• Glycogenesis :
• Definition : Synthesis of glycogen from glucose.
• Salient Features:
1. Substrate : Glucose
2. Product : Glycogen
3. Site : 1. Liver & 2. Skeletal Muscles
4. ATP requirements: 3 ATP for each Glucose added in chain.
5. Also activated by insulin in response to high Glucose levels. And
inhibited by cAMP.
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13. 13

14. • Glycogenolysis:
• Break down of Glycogen and synthesis of Glucose.
• Salient Features:
1. Substrate: Glycogen
2. Product : Glucose
3. Site : Liver and Skeletal Muscles (cell cytoplasm)
4. ATP : No ATP used or produced.
5. Break down of Glycogen stimulates by Glucagon.
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16. • Gluconeogenesis
• Definition: A metabolic pathway that results in the generation of glucose
from certain non-carbohydrate carbon substrates.
• This pathway consisting of a series of eleven enzyme-catalyzed reactions
• Salient Features:
1. Substrate : Glucogenic amino acids, Glycerol, Pyruvate, Lactate, lipids
2. Product : Glucose
3. Site : Liver and Kidney (cytoplasm or mitochondria of those cell)
4. ATP requirement : 6 ATP is needed.
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17. PATHWAY : 17

18. • Gluconeogenesis from Glycerol :
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19. Gluconeogenesis from TCA intermediates
/pyruvate /lactate :
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20. • Regulation :
• Global control of gluconeogenesis is mediated by Glucagon (released when
blood glucose is low).
• Glucagon triggers phosphorylation of enzymes and regulatory proteins
by Protein kinase A resulting in inhibition of glycolysis and stimulation of
gluconeogenesis.
• Insulin react on glucagon by inhibiting gluconeogenesis.
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21. • Hexose Monophosphate Shunt :
• Definition: The HMP shunt (Pentose Phosphate Pathway, 6-
Phosphogluconate) is a metabolic pathway alternative to glycolysis. It
generates NADPH and pentoses as well as ribose 5-phosphate, a
precursor for the synthesis of nucleotides.
• Salient Features :
1. Substrate : Glucose-6-Phosphate
2. Product : Ribose sugar,NADPH
3. Site : Liver, adipose tissue, RBC, adrenal glands, lactating glands
4. Nature : catabolic, No ATP consumed or produced.
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23. • Lipid Metabolism
• Lipids are molecules that contain hydrocarbons and make up the building blocks of
the structure and function of living cells.
• Examples of lipids include fats, oils, waxes, certain vitamins (such as A, D, E and K),
hormones and most of the cell membrane that is not made up of protein.
• Lipid metabolism is the synthesis and degradation of lipids in cells, involving
the breakdown or storage of fats for energy and the synthesis of structural and
functional lipids.
• There are two sources of fats that organisms can use to obtain energy: from
consumed dietary fats and from stored fat.
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24. • Lipid Digestion & Absorption
• Digestion is the first step to lipid metabolism, and it is the process of breaking
the triglycerides down into smaller monoglycerides units with the help
of lipase enzymes.
• Digestion of fats begin in the mouth through chemical digestion .
• The majority of lipid digestion and absorption, however, occurs once the fats
reach the small intestines.
• Chemicals from the pancreas are secreted into the small intestines to help
breakdown the triglycerides.
• pancreatic lipase that is responsible for signaling for the hydrolysis of the
triglycerides into separate free fatty acids and glycerol units.
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25. • Absorption :
• The second step in lipid metabolism is absorption of fats.
• Once the triglycerides are broken down into individual fatty acids
and glycerol, along with cholesterol, they diffuses to the epithelial cells.
• In the cytosol of epithelial cells, triglycerides and cholesterol are packaged
into bigger particles called chylomicrones .
• which are amphipathic structures that transport digested lipids.
• Chylomicrons will travel through the bloodstream to enter adipose and other
tissues in the body.
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26. • Lipid Catabolism:
• Once the chylomicrons (or other lipoproteins) travel through the tissues, these
particles will be broken down by lipoprotein lipase and to relaease triglycerides.
• Triglycerides will get broken down into fatty acids and glycerol before entering cells
and remaining cholesterol will again travel through the blood to the liver.
• The main steps of fatty acids Catabolism occur in the mitochondria.
• Fatty acid firstly converted to acyl CoA in cytoplasm and then cross the mitochondria
membrane and enter the process of beta oxidation.
• Beta Oxidation: Catabolic process by which fatty acid molecules are broken
down in cytosol in prokaryotes and in mitochondria in eukaryotes to
generate acetyl coA, which enters the TCA cycle.
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27. • Beta Oxidation
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28. • Alpha Oxidation :
• This oxidation occure in peroxisomes.
• The process in which fatty acids are
shortened by one carbon atom.
• Substrate: phytanic acid present in
the milk or derived from phytol which
is present in chlorophyll and fat.
• Alpha oxidation occurs in those fatty
acids that have a methyl group(CH3)
at the beta-carbon, which blocks beta
oxidation.
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29. • Omega Oxidation
• Cellular site: Endoplasmic reticulum
• oxidation occurs at (w-omega) carbon-the carbon most distant
from the carboxyl group.
• Substrates : Medium and long chain fatty acid
• It is a minor pathway but becomes active when beta oxidation is
defective.
• The product formed are di-carboxylic.
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30. • Triglycerides Biosynthesis:
• The biosynthesis of triacylglycerides occurs in the endoplasmic
reticulum (ER)
• The overall process
of triglyceride (triacylglycerol) biosynthesis consists of four
biochemical pathways:
1. fatty acyl-CoA biosynthesis, (Glycerol kinase).
2. conversion of fatty acyl-CoA to phosphatidic acid,(glycerol phosphate
acyl transferase).
3. conversion of phosphatidic acid to diacylglycerol,
4. and conversion of diacylglycerol to triacylglycerol.(diacylglycerol acyl
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32. • De Novo synthesis of fatty acids:
• Site : Liver , kidney, Lung, Lactating memory gland, Adipose tissue. (cell
cytoplasm)
• Acetyl-CoA is the immediate substrate, and free palmitate is the end product.
• lts cofactor requirements include NADPH, ATP, biotin and HCO, (as a source of
Co).
1. Transport of acetyl coA mitochondria to cytosol.
2. Activation of acetyl coA by carboxylation.
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33. • Transportation • Activation
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34. • Synthesis of fatty acids 34

35. • Regulation:
1. Allosteric Regulation: Acetyl-CoA carboxylase, the rate-
limiting enzyme in fatty acid biosynthesis. Citrate
allosteric activator of fatty acid biosynthesis.
• And feedback inhibition by palmitoyl coA .
• 2. Hormonal Regulation: Activate by insulin and Inhibits
by glucagon.
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36. • Ketogenesis :
• Ketones are formed when there is
not enough sugar or glucose to
supply the body's fuel needs. This
occurs overnight, and during dieting
or fasting.
• Ketone bodies are produced mainly in
the mitochondria of liver cells.
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37. • Cholesterol Biosynthesis:
• Biosynthesis of cholesterol generally takes place in the liver, intestine, adrenal
cortex of endoplasmic reticulum.
• Cholesterol also serves as a Precursor for the biosynthesis of steroid hormone, bile
acids and vitamin D.
• 5 Important step in biosynthesis:
1. Synthesis of HMG coA
2. Formation of Mevalonate
3. Conversion of mevalonate to IPP(isopentenyl pyrophosphate)
4. Formation of Squalene
5. Conversion of squalene to Cholesterol.
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39. • Regulation:
• HMG-CoA reductase is the rate-controlling enzyme of the cholesterol
biosynthesis
1. Competitive Inhibition : Inhibit by Statins (Lovastatin, Mevastatin, Atorva
Statin etc.) are the reversible competitive inhibitors of HMG CoA
reductase.
2. Feedback inhibition: HMG CoA reductase is inhibited by Mevalonate and
Cholesterol.
3. Covalent modification : Glucagon favors formation of the inactive (phosphorylated
form) decreases the rate of cholesterol synthesis.
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40. Thank you
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