Explore the fascinating world of carbohydrates, the body’s primary source of energy. This presentation covers: Definition & Classification of carbohydrates Monosaccharides, Disaccharides, and Polysaccharides with examples Functions in human health and nutrition Digestion, Absorption & Metabolism pathways (including glycolysis & glycogen storage) Clinical importance and related disorders Perfect for students, educators, and health enthusiasts who want a clear and concise understanding of carbs, their biological roles, and their impact on health.

1. Unit 1:- Carbohydrates
Akanksha N. Kotangale
B.Sc. Nursing

2. • Introduction:-
- Carbohydrates are organic compounds made of carbon (C), hydrogen
(H), and oxygen (O), usually in the ratio C:H:O= 1:2:1
- They are also called saccharides or Sugar, sweet in taste.
- General formula is Cn(H2O)n
• Definition:-
Carbohydrates is one of the most important macronutrient required in
our body and main source of energy made up of compound C,H, & O.

3. • Classification of carbohydrates:-
A) On the basis of sugar residues :- 4 types of carbohydrates
1. Monosaccharides:-
Saccharides means sugars that cannot be hydrolysed into simpler
carbohydrate.
Ex.- Glucose, Fructose, Galactose.
Structure of glucose:- C6H12O6

4. 2. Disaccharides:-
Condensation products of two monosaccharides.
Ex.- i) Maltose= Glucose + Glucose
ii) Lactose= Glucose + Galactose
iii) Sucrose= Glucose + Fructose
3. Oligosaccharides:-
Condensation products of three to ten monosaccharides.
Ex.- Raffinose (glucose + galactose + fructose)

5. 4. Polysaccharides:-
Condensation products of more than ten monosaccharide units.
Polysaccharides further divided into two types on the basis of
monomeric unit:
i) Homosaccharide:- Made up of same sugar molecule.
Ex.- starch, glycogen, and cellulose made from glucose molecule.
ii) Heteropolysaccharide:- Made up of Different sugar molecules.
Ex.- Hyaluronic acid made from Glucuronic acid + N-acetylglucosamine,
Heparin made from Glucuronic acid + Glucosamine sulphate

6. B) On the basis of Functional group:- 2 Types of functional group
present in the monosaccharide unit.
1. Aldoses:-
• Contain an aldehyde group (–CHO) at carbon 1.
• The first carbon is part of the aldehyde functional group.
• These are called aldose sugars.
Ex.-Glucose, Galactose, etc.,
2. Ketoses:-
• Contain a ketone group (C=O) usually at carbon 2.
• These are called ketose sugars.
Ex.- Fructose, ribulose, etc.,

7. C) Based on the number of carbon atom:- Carbohydrates (specifically
monosaccharides) are classified according to the number of carbon atoms
they contain.
Name No. of Carbon Atoms Examples
Biose
Triose
2
3
Glycolic Aldehyde
Glyceraldehyde, Dihydroxyacetone
Tetrose 4 Erythrose, Erythrulose
Pentose 5 Ribose, Ribulose, Xylose
Hexose 6 Glucose, Fructose, Galactose
Heptose 7 Sedoheptulose
Octose 8 2-keto-3-deoxy-manno-octonate
Nonose 9 Neuraminic acid (sialic acid)

8. Digestion of Carbohydrates:-
Carbohydrate digestion is the process by which
large, complex carbohydrates (like Polysaccharide
and oligosaccharide) are broken down into simple
sugars (Monosaccharide) that can easily absorbed
and unitized in the body (in the form of energy).

9. Mechanism:- Starch – sugar polysaccharide
Mouth(5% digest)
(Salivary amylase enzyme)
Stomach(Hcl)
(digestion paused due to acidic environment)
Small Intestine
(Pancreatic amylase enzyme)
Breakdown of starches
Disaccharides
Maltose
Sucrose
Lactose
Maltase enzyme
Sucrase
enzyme
Lactase enzyme
G+G
G+F
G+Gala

10. Process:-
1. Mouth:- Salivary glands secrete saliva , containing an enzyme called salivary
amylase or ptyalin which start breaking down complex carbohydrates in simpler
sugar like maltose.
2. Stomach:- digestion process paused in the stomach due to acidic environment.
Temporarily inactivates salivary amylase due to acidic environment.
3. Small Intestine:-
• Pancreatic amylase:- Pancreas release amylase into small intestine, continuing
the breakdown of starches & other disaccharide.
• Brush Border Enzymes:- Enzymes like maltase, sucrase and lactase(located on
the lining of small intestine. It help in breakdown disaccharide in
monosaccharide(simple sugar).
Maltose=Glucose + Glucose
Sucrose=Glucose + Fructose
Lactose=Glucose + Galactose

11. Absorption of Carbohydrates
• Process of absorbing assimilating substances into the cell or across
the tissue & organ through the process of diffusion or osmosis.
• Diffusion:- Movement of particles from area of high concentration to
low concentration, no energy needed(passive).
• Osmosis:- Movement of water from area of more water to less water
through a semi-permeable membrane, no energy needed(passive).
• Facilitated diffusion:- It is a type of passive transport where
molecules move across a cell membrane with the help of special
proteins, without using energy (ATP).

12. Process:-
• GLUT-5 = Glucose transporter 5 (facilitate diffusion)
• SGLT-1 = Sodium-Glucose Linked Transporter (uses
energy- Active transport)
• GLUT-2 = Glucose transporter 2.
1. Monosaccharides( Glucose, Fructose, Galactose)
are absorbed through small intestine wall into the
bloodstream via GLUT-2.
2. Glucose and galactose are absorbed by active
transport using sodium glucose, transport
protein( SGLT-1)

13. 3. Fructose is absorbed by facilitated diffusion using GLUT-5 transporter.
4. Transported to liver : portal vein carries absorbed monosaccharides to
liver .
5. Liver Processing:- convert fructose and galactose into glucose with the
help of enzymes called fructokinase and galactokinase.
6. Cellular utilization:- glucose can be used by the cells for energy
production through cellular respiration.
7. Excess glucose can be stored as glycogen in liver and muscle cells for
further energy use.

14. Metabolism of Carbohydrates:-
• Metabolism is the set of chemical reactions in living organisms that converts
food in to energy and for growth, and eliminate waste products.
• This ensures that cells have a constant supply of energy and necessary
components for growth and repair.
• It is the process of catabolism and anabolism.
• Catabolism:- process of breaking down larger molecules into smaller one to
produce energy.
EX.- glycolysis.
• Anabolism:- process of building up complex molecules from simpler one,
which require energy.
Ex.- Gluconeogenesis.

15. Glycolysis:-
• Also called Embden-Meyerhof Pathway (EMP).
• Glycolysis is a ten step long reaction.
• Occurs It occurs in the cytoplasm.
• Definition:- Glycolysis is the partial oxidation of molecule of glucose
forming two pyruvic acid (Pyruvate) or lactate, producing ATP.
• Glycolysis is the metabolic pathway that breaks down glucose (a 6-
carbon sugar) into pyruvate (a 3-carbon compound), releasing energy
that is used to form ATP and NADH. It is the first step in cellular
respiration and occurs in the cytoplasm of the cell.

16. • Anaerobic Glycolysis occurs in the absence of oxygen Lactate(end
product)
• Aerobic glycolysis occurs in the presence of oxygen Pyruvate
(end product)
• Pyruvate:- Pyruvate is a small 3-carbon molecule that your body
makes when it breaks down glucose (sugar) during glycolysis — the
first step of getting energy from food.
Oxygen What Happens to Pyruvate Product
✅ Yes
Goes into mitochondria → used for
energy
Acetyl-CoA → ATP
❌ No Stays in cytoplasm → fermentation Lactic acid (in humans)

17. Glycolysis pathway:-

18. Process :-
Step 1:- glucose is converted into glucose-6-phosphate in the presence of
enzyme Hexokinase using energy (ATP ADP)
Step 2:- Glucose-6-phosphate is converted into Fructose-6-phosphate in
the presence of enzyme phosphoGlucose isomerase.
Step 3:- Fructose-6phosphate is converted into fructose-1,6-biphosphate
in the presence of enzyme phosphoFructose kinase using energy(ATP
ADP)
Step 4:-fructose-1,6-biphosphate splited and converted into
Glyceraldehyde-3-phosphate(GLAP) and Dihydroxyacetone
phosphate(DHAP) .
Step 5:- GLAP and DHAP can be interchanged.

19. Step 6:- Glyceraldehyde-3-phosphate converted into 1,3-
biphosphoglycerate in the presence of GLAP hydrogenase enzyme and
produce 2 NADH(high-energy electrons for later use in ATP production).
Step 7:- 1,3-biphosphoglycerate converted into 3-phosphoglycerate in
the presence of enzyme Phosphoglycerate kinase and produce 2 ATP.
Step 8:- 3-phosphoglycerate is converted into 2-phosphoglycerate in
the presence of enzyme Phosphoglycerate mutase.
Step 9:- 2-phosphoglycerate converted into phosphoenolpyruvate in
the presence of enzyme Enolase.
Step 10:- Phosphoenolpyruvate is converted into Pyruvate in the
presence of enzyme pyruvate kinase and produces 2 ATP.

20.  Glycolysis is dived into 3 phase:-
• Step 1,2 & 3= Energy Investment phase or Primary stage.
• Step 4 &5 = splitting phase.
• Step 6,7,8,9 & 10 = Energy Generation Phase.
• Net Reaction:-
Glucose+2ATP+2NAD 2 Pyruvate+2ATP+ 2NADH

21. Kreb Cycle:-
• Kreb cycle is named after its discover sir Hans Kreb (1937).
• Also known as citric acid cycle or Tricarboxylic acid cycle(TCA cycle).
• Definition:- Kreb cycle is a series of chemical reactions that occur in
the mitochondria of cell to generate the energy.
• Site:- Mitochondria.

22. • Steps of Kreb cycle:-
Step 0 – Entry into the cycle
• Pyruvate (from glycolysis) is converted into Acetyl-CoA by the enzyme
pyruvate dehydrogenase.
• This step also produces NADH and releases CO₂.
Step 1 – Formation of Citrate
• Acetyl-CoA (2C) combines with Oxaloacetate (4C) → Citrate (6C).
• Enzyme: Citrate synthase.
Step 2 – Isomerization of Citrate
• Citrate is rearranged to Isocitrate.
• Enzyme: Aconitase.

23. Step 3 – Oxidative decarboxylation #1
• Isocitrate → α-Ketoglutarate (5C) + CO₂.
• NAD⁺ is reduced to NADH.
• Enzyme: Isocitrate dehydrogenase.
Step 4 – Oxidative decarboxylation #2
• α-Ketoglutarate → Succinyl-CoA (4C) + CO₂.
• NAD⁺ → NADH.
• Enzyme: α-Ketoglutarate dehydrogenase.
Step 5 – Substrate-level phosphorylation
• Succinyl-CoA → Succinate.
• GDP + Pi → GTP (can be converted to ATP).
• Enzyme: Succinyl-CoA synthetase.

24. Step 6 – Oxidation of Succinate
• Succinate → Fumarate.
• FAD → FADH₂.
• Enzyme: Succinate dehydrogenase
Step 7 – Hydration
• Fumarate → Malate.
• Enzyme: Fumarase.
Step 8 – Oxidation of Malate
• Malate → Oxaloacetate.
• NAD⁺ → NADH.
• Enzyme: Malate dehydrogenase.
• Oxaloacetate is regenerated to start the cycle again.

25.  Total ATP generation in Kreb cycle:-
• 3NADH 7.5 ATP
• FADH 1.5 ATP
• GTP 1 ATP
• Total 10 ATP
• Purpose of krebs cycle:-
1. Energy Production
• Generates ATP (or GTP) directly in one step.
• Produces NADH and FADH₂, which carry high-energy electrons to the electron transport chain
for further ATP production.
• Regulation of kreb cycle:-
1. Enzyme regulator:- Citrate Synthase, Isocitrate Dehydrogenase, α-Ketoglutarate
Dehydrogenase.

26. Gluconeogenesis:-
• Gluconeogenesis is the process of synthesizing glucose from non-
carbohydrate precursors.
It is basically the reverse of glycolysis, but with some bypass steps
because certain glycolysis reactions are irreversible.
• Purpose:- Maintain blood glucose levels during fasting, starvation, or
intense exercise.
• Site:-
Organs: Liver (major), kidney cortex (minor)
Cell location: Cytoplasm (most steps), mitochondria (some steps), and
ER (final step).

28. Importance of gluconeogenesis:-
1. Maintains Blood Glucose Levels
• Keeps blood glucose constant when dietary glucose is unavailable.
• Essential for tissues dependent on glucose, like:
Brain , Red blood cells and Renal medulla.
2. Prevents Hypoglycaemia
• During fasting or starvation, gluconeogenesis ensures enough glucose for
survival.
• Protects the body from low blood sugar symptoms such as confusion,
seizures, and coma.
3. Utilizes Non-Carbohydrate Precursors
• Converts lactate (from anaerobic glycolysis), glycerol (from fat breakdown),
and glucogenic amino acids (from muscle proteins) into glucose.

29. Carbohydrate metabolic disorder:-
1. Lactose Intolerance:- Deficiency of lactase enzyme in the intestine.
c/m :- diarrhea, gas after dairy intake.
2. Fructose Intolerance :- Deficiency of Aldolase B (enzyme that breaks
fructose-1-phosphate into DHAP + glyceraldehyde).
hereditary d/o.
After fructose ingestion:
• Vomiting
• Hypoglycaemia (sweating, irritability, seizures)
• Jaundice
• Hepatomegaly(enlargement of the liver ).

30. 3. Galactosemia:-
• It is a rare inherited metabolic disorder that prevents the body from breaking down
galactose.
• Galactose is a sugar found in dairy products and breast milk.
• Buildup of galactose can reach toxic level.
• Due to this liver and kidney damage chances occurs called galactosemia.
4. Glycosuria:-
• Glycosuria means presence of glucose in the urine in amounts higher than normal.
• Seen in diabetic mellitus.
• There are two types of glycosuria :-
a) Renal Glycosuria:- glucose in urine.
b) Alimentary Glycosuria:- glucose in stool.
5. Diabetes mellitus:-
• Increase blood glucose level(hyperglycaemia) due to insufficient insulin.

31. Regulation of blood sugar level:-
• Blood glucose level is an important indicators of person well being.
• Normal blood glucose levels:-
Fasting:-
normal- 70 to 99 mg/dl
Prediabetic:- 100 to 125 mg/dl
Diabetic:- 126 mg/dl or higher.
Random (Non-Fasting):-
Normal- below 140 mg/dl
Prediabetic:- 141 to 199 mg/dl
Diabetic:- 200mg/dl or higher.

32. Mechanism:-

33. Low blood glucose High blood glucose
Pancreas Pancreas
Glucagon (Released by pancreas) Insulin
Glucagon convert glucose in liver
and releases into blood
Glucose convert glycogen in liver and
body cell absorbed glucose from blood

34. • Importance of normal blood glucose level:-
1. Preventing Hypoglycaemia
2. Preventing Hyperglycaemia
3. Prevent diabetes
4. Organ functions.

35. Diabetes mellitus
• Introduction:- It is a chronic health condition that affects how the
body processes blood sugar (glucose).
• Definition:- Diabetes mellitus is a chronic metabolic disorder
characterized by high blood glucose levels (hyperglycemia) due
to either insulin deficiency or insulin resistance leading to various
health complication

36. Types of Diabetic Mellitus:-
1. Type 1 Diabetes Mellitus (Insulin-dependent ):-
• Autoimmune destruction of pancreatic beta cells → no insulin production.
• Usually occurs in childhood or adolescence.
• Requires lifelong insulin therapy.
2. Type 2 Diabètes Mellitus (Non-insulin dependent)
• Insulin resistance + relative insulin deficiency.
• Strongly associated with obesity, sedentary lifestyle, and genetics.
• More common in adult specially after age 45.

37. Symptoms:-
Classic “3 P’s”:
Polyuria – Excessive urination
Polydipsia – Excessive thirst
Polyphagia – Excessive hunger.
Other common symptoms:
•Unexplained weight loss (more in Type 1)
•Fatigue and weakness
•Blurred vision
•Slow healing of wounds
•Frequent infections (skin, urinary tract, yeast infections)
•Tingling or numbness in hands/feet (neuropathy)
•Dry, itchy skin

38. Complication of D.M:-
1. Acute Complications (sudden, emergency conditions):-
• Diabetic ketoacidosis (DKA) – common in Type 1 DM.
A serious, acute, life-threatening complication of diabetes mellitus,
mostly Type 1, caused by severe insulin deficiency → high blood
glucose + breakdown of fat → ketone production → metabolic
acidosis.
• Hyperosmolar hyperglycemic state (HHS) – common in Type 2 DM

39. 2. Chronic complications (long term)
• Microvascular complications (small blood vessels):-
Diabetic retinopathy → blindness
Diabetic nephropathy → kidney failure
Diabetic neuropathy → numbness, pain, tingling in limbs
• Macrovascular complications (large blood vessels):-
Coronary artery disease → heart attack
Cerebrovascular disease → stroke
Peripheral artery disease → poor circulation
• Others:-
Foot ulcers and infections (“Diabetic foot”)
Increased risk of skin infections and dental problems
Sexual dysfunction

40. Management of D.M.
A. Management of Type 1 Diabetes Mellitus (Insulin-dependent):-
• Insulin therapy – Lifelong requirement
• Dietary management-balanced diet
• Regular physical activity – improves insulin sensitivity
• Self-monitoring of blood glucose (SMBG) – frequent checks
• Patient education – insulin injection technique.
B. Management of Type 2 Diabetes Mellitus (Initially non-insulin dependent):-
• Lifestyle modification (first step)
Diet: calorie restriction if overweight, low sugar/simple carbs
Exercise: at least 150 min/week of moderate activity
Weight management
• Insulin therapy
• Self-monitoring of blood glucose
• Patient education – foot care, diet planning, medication adherence

41. Investigation of Diabetes mellitus
1. OGTT Oral Glucose Tolerance Test
• Definition:- The Oral Glucose Tolerance Test is a laboratory test used to
diagnose diabetes mellitus, prediabetes, and gestational diabetes by
measuring the body’s ability to metabolize glucose after a fixed oral
dose.
• Purpose / Uses:-
Diagnosis of Type 2 Diabetes Mellitus
gestational diabetes
Prediabetes

42. • Procedure for OGTT:-
1. Fasting – 8 to 12 hours (only water allowed).
2. Take fasting blood sample for plasma glucose.
3. Patient drinks 75 g of anhydrous glucose dissolved in water (adults).
4. Blood samples are taken 2 hours after glucose intake.
5. No food, drink (except water), smoking, or physical activity during
the test.

43. Interpretation:-
Status Fasting (mg/dL) 2-hr after OGTT (mg/dL)
Normal <100 <140
Prediabetes (IGT) 100–125 140–199
Diabetes Mellitus ≥126 ≥200

44. GTT curve:-
• A graphical representation of blood glucose levels measured at set
intervals during the Glucose Tolerance Test (GTT / OGTT).
• X-axis → Time (minutes or hours after glucose intake)
• Y-axis → Blood glucose level (mg/dL or mmol/L)

45. Mini Glucose Tolerance Test( Mini GTT):-
• The Mini GTT is a simplified version of the Oral Glucose Tolerance Test used mainly for screening (not
full diagnosis) of diabetes mellitus or impaired glucose tolerance, especially in large-scale community
programs or for quick assessment.
• Procedure (General):-
1. Patient fasts overnight (8–12 hours).
2. Fasting blood glucose sample is taken.
3. Patient drinks 50 g of glucose (instead of 75 g in standard OGTT).
4. Blood sample is taken 1 hour after glucose load.
• Interpretation (varies slightly by protocol)
<140 mg/dL → Normal
140–199 mg/dL → Impaired glucose tolerance (needs full OGTT for confirmation)
≥200 mg/dL → Suggestive of diabetes (needs repeat or confirmatory test)

46. Extended Glucose Tolerance Test (Extended GTT):-
• The Extended GTT is a prolonged version of the standard OGTT where
blood glucose is measured for a longer duration (up to 3–5 hours) after
a glucose load.
It is used in special cases to study detailed glucose and insulin
response.
• Procedure:-
1.Fasting – 8–12 hours
2.Fasting blood sample collected
3.Patient drinks 75 g glucose (adults)
4.Blood samples taken at:
•0, 30, 60, 90, 120, 180, and 240 minutes (sometimes up to 300 min)
5.Glucose, insulin, and sometimes C-peptide levels are measured

47. Glucose Challenge Test (GCT):-
• The Glucose Challenge Test is a screening test mainly used in
pregnancy to detect gestational diabetes mellitus (GDM).
It does not require fasting and involves giving a fixed glucose load
followed by a single blood glucose measurement.
• Purpose / Uses:-
Routine screening for GDM between 24–28 weeks of pregnancy
• Procedure:-
1.No fasting required – test can be done at any time of the day.
2.Patient drinks 50 g glucose solution.
3.Blood sample taken 1 hour later for plasma glucose measurement.

48. HbA1C:-
• It’s a form of hemoglobin that has glucose molecules attached to it, and
it reflects the average blood glucose level over the past 2–3 months.
• Why 2–3 months?
Red blood cells (RBCs) live about 120 days.
The amount of glucose attached to hemoglobin depends on the average
blood sugar during their lifespan.
• Clinical Uses:-
Diagnosis of diabetes mellitus.
Monitoring long-term glucose control in diabetic patients.
Monitoring long-term glucose control in diabetic patients.

49. Hypoglycaemia:-
• Hypoglycaemia means a condition where blood glucose levels fall
below normal.
• Blood glucose level < 70 mg/dL is called hypoglycaemia.
• Causes :-
1. Excess insulin or hypoglycaemic drugs (commonly in diabetic
patients)
2. Prolonged fasting or skipping meals
3. Excessive exercise without adequate food intake
4. Alcohol consumption (alcohol-induced hypoglycaemia)
5. Liver, kidney, or hormonal disorders

50. • Symptoms:-
1. Sweating
2. Palpitations (fast heartbeat)
3. Hunger
4. Dizziness
5. Confusion
6. Blurred vision
7. Seizures
8. Loss of consciousness
• Complications
• Coma
• Brain damage
• Death (if untreated)

51. Thank You