BBCCT 113 key facts: June 2026
- Course code: BBCCT 113 (printed BBCCT-113)
- Course title: Metabolism of Amino Acids and Nucleotides
- Programme: B.Sc. (Hons.) Biochemistry (BSCBCH)
- Credits: 4 (theory); lab course BBCCL 114 carries 2 credits
- Blocks and units: 4 blocks, 13 units
- Maximum marks: 70 (term-end examination)
- Duration: 3 hours
- Questions in the paper: 8 of 14 marks each; attempt any 5; printed code A-1417
- Paper language: printed in English and Hindi
- Solved answers shown on this page: 2 (Q1 and Q2); all 8 in the paid file
BBCCT 113 Solved Question Paper June 2026 is the complete answer set for Metabolism of Amino Acids and Nucleotides, the 4-credit core theory course of the IGNOU B.Sc. (Hons.) Biochemistry (BSCBCH) programme.
1. What the June 2026 Solved Paper Covers
The course follows nitrogen from the air into amino acids, then through their breakdown, their role as precursors of hormones and haem, and finally into purine and pyrimidine nucleotides and their disorders. IGNOU splits it into 4 blocks and 13 units.
The June 2026 paper tested nitrogen cycle and Krebs cycle notes, inborn errors, kwashiorkor and marasmus, serine and pyruvate family biosynthesis, pyrimidine and purine degradation, white versus brown adipose tissue, the liver as metabolic hub, protoporphyrias, haem biosynthesis, ribonucleotide reductase, nucleotide coenzymes, SCID, gout, and de novo versus salvage synthesis.
Two printing slips are worth knowing. Question 3(b) says "serene", which means serine, and Question 5(a) says "the liver in called", which means "is called". Our file answers the questions as IGNOU intended them, so you are not confused by the typing errors in the exam hall.
2. Two Answers Solved in Full, Six Held Back
Question 1 and Question 2 of the June 2026 paper are answered in full below, worth 28 of the 70 marks, and the remaining six questions are listed exactly as printed without answers.
Both answers use the terms and pathways of the IGNOU study material. Read them as proof of how every answer in the full file is built.
Nitrogen cycle, biological nitrogen fixation and the Krebs cycle
Question 1: Write notes on the following. (5 + 3 + 6)
(a) Nitrogen cycle
(b) Biological nitrogen fixation
(c) Krebs cycle
(a) Nitrogen cycle (5 marks)
Nitrogen forms about 78 per cent of the atmosphere as dinitrogen (N≡N), yet most organisms cannot use it because the triple bond is very stable. The nitrogen cycle is the sequence of biological and physical conversions that moves nitrogen between air, soil, water and living organisms, so that it can enter amino acids and nucleotides and finally return to the atmosphere.
- Nitrogen fixation: N2 is reduced to ammonia (NH3). Most of it is biological fixation by the enzyme nitrogenase in bacteria; smaller amounts come from lightning, which forms nitrogen oxides, and from the industrial Haber-Bosch process.
- Ammonification: when plants, animals and microbes die or excrete wastes such as urea and uric acid, decomposer bacteria and fungi break down proteins and nucleic acids and release ammonium (NH4+) into the soil.
- Nitrification: an aerobic, two-step oxidation by chemoautotrophic bacteria. Nitrosomonas oxidises NH4+ to nitrite (NO2−), and Nitrobacter oxidises nitrite to nitrate (NO3−), the main form taken up by plants.
- Assimilation: roots absorb nitrate. Nitrate reductase reduces it to nitrite and nitrite reductase reduces nitrite to NH4+, which glutamine synthetase and glutamate synthase (the GS-GOGAT pathway) fix into glutamine and glutamate. Animals obtain this organic nitrogen through food.
- Denitrification: in waterlogged, oxygen-poor soils, bacteria such as Pseudomonas and Paracoccus denitrificans use nitrate in place of oxygen and reduce it through NO2−, NO and N2O back to N2, which returns to the air.
Flow to draw in the exam: N2 → NH3/NH4+ → NO2− → NO3− → plant amino acids → animal proteins → NH4+, with a side arrow NO3− → N2 for denitrification. Every amino acid, purine and pyrimidine in the body carries nitrogen that first entered the biosphere through fixation.
(b) Biological nitrogen fixation (3 marks)
Biological nitrogen fixation is the enzymatic reduction of atmospheric N2 to ammonia by certain prokaryotes called diazotrophs. Symbiotic fixers include Rhizobium in legume root nodules and Frankia in alder; non-symbiotic fixers include Azotobacter, Clostridium and cyanobacteria such as Anabaena, which fix nitrogen in heterocysts.
The reaction is catalysed by the nitrogenase complex, made of dinitrogenase reductase (the Fe protein) and dinitrogenase (the MoFe protein):
N2 + 8H+ + 8e− + 16 ATP → 2NH3 + H2 + 16 ADP + 16 Pi
Ferredoxin supplies the electrons, and each electron passed from the Fe protein costs two ATP. Nitrogenase is irreversibly damaged by oxygen, so root nodules contain leghaemoglobin, which binds O2 and keeps the local oxygen level low while still supplying oxygen for respiration.
(c) Krebs cycle (6 marks)
The Krebs cycle, also called the citric acid cycle or tricarboxylic acid (TCA) cycle, was described by Hans Krebs in 1937. It is the final common pathway for oxidising acetyl-CoA from carbohydrates, fats and amino acids, and it runs in the mitochondrial matrix except for succinate dehydrogenase, which sits in the inner mitochondrial membrane.
- Citrate synthase condenses acetyl-CoA (2C) with oxaloacetate (4C) to form citrate (6C).
- Aconitase isomerises citrate to isocitrate through cis-aconitate.
- Isocitrate dehydrogenase oxidatively decarboxylates isocitrate to α-ketoglutarate (5C), releasing CO2 and NADH.
- The α-ketoglutarate dehydrogenase complex converts α-ketoglutarate to succinyl-CoA (4C), releasing the second CO2 and NADH.
- Succinyl-CoA synthetase splits the thioester bond to give succinate and one GTP (or ATP) by substrate-level phosphorylation.
- Succinate dehydrogenase oxidises succinate to fumarate and reduces FAD to FADH2.
- Fumarase hydrates fumarate to L-malate.
- Malate dehydrogenase oxidises malate to oxaloacetate and forms the third NADH, so the cycle can turn again.
Yield per acetyl-CoA: 3 NADH, 1 FADH2, 1 GTP and 2 CO2. Through oxidative phosphorylation this equals about 10 ATP (2.5 per NADH and 1.5 per FADH2), or 20 ATP for the two acetyl-CoA formed from one glucose.
Regulation happens at citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase. High NADH, ATP and succinyl-CoA slow the cycle, while ADP and Ca2+ activate isocitrate dehydrogenase.
Why this sits in an amino acid course: the cycle is amphibolic. Glutamate enters as α-ketoglutarate and aspartate as oxaloacetate by transamination, and the carbon skeletons of glucogenic amino acids feed its intermediates. Fumarate released by the urea cycle also joins it, a link often called the Krebs bicycle.
Inborn errors of metabolism, and kwashiorkor versus marasmus
Question 2 (a): What are inborn errors of metabolism? Explain any two of them. (2 × 3½ = 7)
Question 2 (b): Distinguish between kwashiorkor and marasmus. (7)
(a) Inborn errors of metabolism
Inborn errors of metabolism (IEM) are inherited disorders in which a gene mutation causes the absence or reduced activity of one enzyme, transporter or cofactor. The substrate before the block builds up, the product after it runs short, and minor side pathways make abnormal metabolites. Sir Archibald Garrod introduced the term in 1908, using alkaptonuria as his model. Most IEMs are autosomal recessive.
1. Phenylketonuria (PKU)
Classical PKU is caused by deficiency of phenylalanine hydroxylase, the liver enzyme that converts phenylalanine to tyrosine with tetrahydrobiopterin (BH4) as cofactor. Phenylalanine accumulates in blood and is diverted to phenylpyruvate, phenyllactate and phenylacetate, which appear in urine and give it a mousy odour.
Untreated PKU causes intellectual disability, seizures and fair skin and hair, because tyrosine shortage lowers melanin. About 1 to 2 per cent of cases are non-classical PKU, caused by defects in BH4 synthesis or recycling. Newborn screening such as the Guthrie test allows early diagnosis, and a low-phenylalanine diet from infancy prevents brain damage; tyrosine becomes essential for these patients.
2. Alkaptonuria
Caused by deficiency of homogentisate 1,2-dioxygenase in the tyrosine breakdown pathway. Homogentisic acid accumulates and is excreted, and the urine turns dark brown or black on standing as it oxidises. Over the years the pigment deposits in cartilage and connective tissue (ochronosis), giving bluish-black pigmentation of the ears and eyes and arthritis of the spine and large joints.
Management includes a protein-restricted diet and the drug nitisinone, which blocks an earlier enzyme of the pathway (4-hydroxyphenylpyruvate dioxygenase) and so reduces homogentisic acid formation.
(b) Kwashiorkor and marasmus
Kwashiorkor and marasmus are the two main clinical forms of protein-energy malnutrition (PEM), seen mostly in young children. Marasmus results from a long-term shortage of both energy and protein, whereas kwashiorkor results mainly from protein deficiency when energy intake, often from starchy foods, is relatively adequate.
| Basis | Kwashiorkor | Marasmus |
|---|---|---|
| Main deficiency | Protein, with relatively adequate calories | Both calories and protein (overall starvation) |
| Usual age | 1 to 4 years, often after weaning | Under 1 year, in early infancy |
| Oedema | Present; the hallmark sign | Absent |
| Appearance | Moon face and puffy limbs; wasting hidden by oedema | Skin and bones, old-man face, severe wasting |
| Subcutaneous fat | Partly preserved | Almost completely lost |
| Liver | Enlarged fatty liver | Usually normal, no fatty infiltration |
| Serum albumin | Markedly low | Normal or mildly reduced |
| Skin and hair | Flaky-paint dermatosis; thin, pale hair with flag sign | Dry, loose, wrinkled skin; milder hair changes |
| Weight for age | 60 to 80 per cent of expected | Below 60 per cent of expected |
| Behaviour | Apathetic and irritable, poor appetite | Alert but hungry |
| Hormonal picture | Relatively higher insulin, so less muscle protein is mobilised | High cortisol mobilises muscle protein and keeps albumin near normal |
Oedema appears only in kwashiorkor because low albumin reduces plasma oncotic pressure, so fluid moves into the tissues. The fatty liver follows because too little apolipoprotein is made to export triacylglycerol as VLDL. A child below 60 per cent weight for age who also has oedema has marasmic kwashiorkor under the Wellcome classification.
Treatment follows the WHO approach for both: correct dehydration, infection and electrolyte imbalance first, then refeed gradually with therapeutic milks (F-75, followed by F-100) to avoid refeeding problems.
3. Questions Answered Only in the Full File
These six questions from the June 2026 paper are reproduced exactly as printed. Their answers are not on this page.
Question 3 (a): Explain regulatory metabolites. Differentiate between neurotransmitters and hormones. (5)
Question 3 (b): Describe the biosynthesis of the serine and pyruvate family of amino acids. (9)
Question 4 (a): Discuss pyrimidine nucleotide degradation. (8)
Question 4 (b): Differentiate between white and brown adipose tissue. (6)
Question 5 (a): Justify why the liver is called the metabolic hub of the body. (7)
Question 5 (b): Explain the degradation of the purine nucleotides. (7)
Question 6 (a): Differentiate between erythropoietic and intermittent protoporphyria. (5)
Question 6 (b): Explain haem biosynthesis. (9)
Question 7 (a): Describe the general characteristics of ribonucleotide reductase (RNR) and the flow of electrons to RNR. (4 + 6)
Question 7 (b): Explain the biosynthesis of nucleotide coenzymes. (4)
Question 8 (a): Write short notes on the following. (2 × 3½ = 7)
(i) SCID (ii) Gout
Question 8 (b): Differentiate between the de novo and salvage pathways of nucleotide synthesis. (7)
Among them sit two 9-mark questions, the serine and pyruvate family pathway and haem biosynthesis, which are the longest answers in the paper and the ones students most often lose marks on.
4. Block and Unit Syllabus
BBCCT 113 has 4 blocks and 13 units: nitrogen metabolism, amino acid biosynthesis, nucleotide biosynthesis and nucleotide degradation.
The unit focus below paraphrases IGNOU's own block descriptions, so match exact unit titles against your BBCCT 113 Study Material as you revise.
| Block | Unit | Unit focus | Key exam topics |
|---|---|---|---|
| Block 1: Nitrogen Metabolism | Unit 1 | Overview of amino acid metabolism | Nitrogen cycle and biological nitrogen fixation; nitrogen balance; protein-energy malnutrition |
| Block 1: Nitrogen Metabolism | Unit 2 | Fate of amino acids derived from proteins | Transamination; oxidative deamination by glutamate dehydrogenase; urea cycle and hyperammonaemia |
| Block 1: Nitrogen Metabolism | Unit 3 | Catabolism of amino acids | Glucogenic and ketogenic amino acids; role of pyridoxal phosphate; carbon skeletons entering the Krebs cycle |
| Block 1: Nitrogen Metabolism | Unit 4 | Disorders of amino acid metabolism | Phenylketonuria; alkaptonuria; maple syrup urine disease and homocystinuria |
| Block 2: Biosynthesis of Amino Acids and Related Molecules | Unit 5 | Biosynthesis of non-essential amino acids and its regulation | Glutamate family (glutamine, proline); serine family (glycine, cysteine); pyruvate family (alanine) |
| Block 2: Biosynthesis of Amino Acids and Related Molecules | Unit 6 | Precursor functions of amino acids | Catecholamines from tyrosine; serotonin and melatonin from tryptophan; creatine and polyamines |
| Block 2: Biosynthesis of Amino Acids and Related Molecules | Unit 7 | Porphyrin metabolism and haem biosynthesis | ALA synthase and the eight steps to haem; porphyrias; haem degradation to bilirubin |
| Block 3: Biosynthesis of Nucleotides | Unit 8 | Purine nucleotide synthesis, de novo and salvage | IMP assembly on PRPP; salvage by HGPRT and APRT; feedback regulation |
| Block 3: Biosynthesis of Nucleotides | Unit 9 | Pyrimidine nucleotide synthesis, de novo and salvage | CPS II and aspartate transcarbamoylase; ribonucleotide reductase and thymidylate synthase; inhibitors such as methotrexate |
| Block 3: Biosynthesis of Nucleotides | Unit 10 | Nucleotide-containing coenzymes | NAD+ and NADP+; FMN and FAD; coenzyme A |
| Block 4: Nucleotide Degradation | Unit 11 | Degradation of purine and pyrimidine nucleotides | Xanthine oxidase and uric acid formation; pyrimidine breakdown to β-alanine and β-aminoisobutyrate |
| Block 4: Nucleotide Degradation | Unit 12 | Disorders of nucleotide metabolism | Gout; Lesch-Nyhan syndrome; SCID due to adenosine deaminase deficiency |
| Block 4: Nucleotide Degradation | Unit 13 | Integration of metabolism and organ profiles | Liver as metabolic hub; white and brown adipose tissue; fuel supply of the brain |
Block 4 is small but scores well: in June 2026 it supplied parts of Questions 4, 5 and 8, so a student strong on degradation and organ integration can build three of the five answers needed.
5. Question Paper Pattern and Marks
The June 2026 paper had 8 questions of 14 marks each, and students had to attempt any five in 3 hours for 70 marks.
| Question | Marks split | Topics | Block |
|---|---|---|---|
| Q1 | 5 + 3 + 6 | Nitrogen cycle, nitrogen fixation, Krebs cycle | Block 1 |
| Q2 | 7 + 7 | Inborn errors; kwashiorkor versus marasmus | Block 1 |
| Q3 | 5 + 9 | Regulatory metabolites; serine and pyruvate families | Block 2 |
| Q4 | 8 + 6 | Pyrimidine degradation; white versus brown fat | Block 4 |
| Q5 | 7 + 7 | Liver as metabolic hub; purine degradation | Block 4 |
| Q6 | 5 + 9 | Erythropoietic versus intermittent protoporphyria; haem synthesis | Block 2 |
| Q7 | (4 + 6) + 4 | Ribonucleotide reductase; nucleotide coenzymes | Block 3 |
| Q8 | 7 + 7 | SCID and gout; de novo versus salvage | Blocks 3 and 4 |
The pattern is not fixed. The December 2023 paper used ten questions of 10 marks each with any seven to attempt, while June 2023, December 2025 and June 2026 all used eight questions of 14 marks. Always check the note on your own paper, and compare sessions through our IGNOU Previous Year Question Paper collection.
Blocks 2 and 4 carried the heaviest single parts this time, with two 9-mark questions and an 8-mark question.
6. Most Repeated Topics Across Four Official Papers
Across four official BBCCT 113 papers, the liver as metabolic hub, nitrogen fixation and nucleotide disorders such as gout and SCID appeared every single time.
| Topic | Sessions asked | Count (of 4) | June 2026 question |
|---|---|---|---|
| Liver as the metabolic hub | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q5(a) |
| Biological nitrogen fixation and nitrogen cycle | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q1(a) and Q1(b) (Sample 1) |
| Inborn errors of amino acid metabolism | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q2(a) (Sample 2) |
| Gout, Lesch-Nyhan syndrome or SCID | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q8(a) |
| De novo and salvage nucleotide synthesis | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q8(b) |
| Biosynthesis of an amino acid family | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q3(b) |
| Haem biosynthesis, porphyrias or haem degradation | Jun 2023, Dec 2023, Dec 2025, Jun 2026 | 4 | Q6(a) and Q6(b) |
| Ribonucleotide reductase and deoxyribonucleotides | Dec 2023, Dec 2025, Jun 2026 | 3 | Q7(a) |
| Nucleotide degradation (purine or pyrimidine) | Jun 2023, Dec 2025, Jun 2026 | 3 | Q4(a), Q5(b) |
| Hormones, neurotransmitters or catecholamines | Dec 2023, Dec 2025, Jun 2026 | 3 | Q3(a) |
| White and brown adipose tissue | Dec 2023, Jun 2026 | 2 | Q4(b) |
| Protein-energy malnutrition | Dec 2023, Jun 2026 | 2 | Q2(b) (Sample 2) |
| Nucleotide coenzymes such as coenzyme A | Jun 2023, Jun 2026 | 2 | Q7(b) |
| Urea cycle | Jun 2023, Dec 2025 | 2 | — |
We counted only papers we could open on IGNOU's own websites. The June 2024, December 2024 and June 2025 papers were not available to us for this check, so this is a four-paper picture, not a five-year one.
The urea cycle row matters for December 2026: it was asked twice before but skipped in June 2026, which makes it a strong candidate to return. For a wider shortlist across courses, see our IGNOU Solved Guess Paper page.
7. How Our Answers Are Written and Checked
Every BBCCT 113 answer is written from the IGNOU block material and reviewed before it goes into the file.
We start from the printed marks. A 3-mark note such as nitrogen fixation gets a definition, the organisms and the nitrogenase equation; a 9-mark pathway such as haem synthesis gets every step with its enzyme, cofactor and cellular location, because that is where examiners give step marks.
Difference questions, which make up five parts of this paper, are answered with a comparison table followed by one short paragraph explaining the most important contrast, as in the kwashiorkor answer above. Pathways are written as numbered steps you can redraw as a flow chart.
Before any answer is released, the reviewer checks enzyme names, equations and ATP figures against the course blocks and compares the question with earlier sessions of the BSCBCH Question Paper set, so repeated topics are answered in the depth IGNOU has asked for before.
8. Solved File Index with BBCCL 114 Lab Links
BBCCT 113 is paired with the 2-credit BBCCL 114 laboratory course, whose urea, uric acid, creatine, creatinine, ALT and AST exercises connect to several June 2026 questions.
| Question | Topic | Course unit | BBCCL 114 lab link | Where the answer is |
|---|---|---|---|---|
| Q1 | Nitrogen cycle, nitrogen fixation, Krebs cycle | Units 1 and 3 | Urea estimation shows how fixed nitrogen finally leaves the body | Sample 1 above |
| Q2 | Inborn errors; kwashiorkor and marasmus | Units 1 and 4 | Blood urea falls in protein deficiency, a point tested in viva | Sample 2 above |
| Q3 | Regulatory metabolites; serine and pyruvate families | Units 5 and 6 | Serum ALT assay measures alanine to pyruvate transamination | Full file |
| Q4 | Pyrimidine degradation; white and brown fat | Units 11 and 13 | — (theory only) | Full file |
| Q5 | Liver as metabolic hub; purine degradation | Units 11 and 13 | AST and ALT as liver markers; uric acid estimation | Full file |
| Q6 | Protoporphyrias; haem biosynthesis | Unit 7 | — (theory only) | Full file |
| Q7 | Ribonucleotide reductase; nucleotide coenzymes | Units 9 and 10 | — (theory only) | Full file |
| Q8 | SCID and gout; de novo and salvage synthesis | Units 8 and 12 | Serum uric acid estimation, the key test for gout | Full file |
The lab areas come from IGNOU's own BBCCL 114 course description; check your lab manual for the exact experiment titles. The solved file answers the theory paper only; it is not a lab record.
9. Programmes That Include BBCCT 113
BBCCT 113 Metabolism of Amino Acids and Nucleotides is a core theory course of the IGNOU B.Sc. (Hons.) Biochemistry programme.
In the IGNOU B.Sc. (Hons.) Biochemistry (BSCBCH) structure, the 4-credit theory course is listed with its 2-credit lab BBCCL 114 as courses to be taken together, and the June 2026 paper is printed under the BSCBCH name. Learners in other IGNOU biochemistry degrees may also carry this course code, so confirm it against your own programme guide before you order.
BBCCT 113 builds directly on BBCCT 109 Metabolism of Carbohydrates and Lipids, since the Krebs cycle and fat metabolism appear again here. IGNOU has also adapted some BBCCT 113 units into MBC-005 Concepts and Connections in Metabolism of its M.Sc. Biochemistry, so the same pathways return at postgraduate level.
10. How to Get the Full Solved Question Paper
The full BBCCT 113 Solved Question Paper for June 2026 is available on WhatsApp 9899436384, with complete answers to all 8 questions.
Send a message with the course code BBCCT 113 and the session June 2026. Our team confirms the details and shares the file, which has the 2 answers you read above plus 6 answers that are not on this page, from regulatory metabolites in Question 3 to de novo and salvage pathways in Question 8.
If you are also preparing for December 2026, mention it in your message. The file then doubles as revision, and we can point you to the answers whose topics have repeated most.
11. BBCCT 113 FAQs
These answers cover the questions BBCCT 113 students ask us most about the June 2026 paper and the solved file.
What does the Solved Question Paper June 2026 contain?
It contains complete answers to all 8 questions of the IGNOU June 2026 BBCCT 113 paper, written to the marks shown against each part. Two answers, Question 1 and Question 2, are on this page so you can judge the quality. The other six answers, from regulatory metabolites to de novo and salvage pathways, are available only in the full file sent on WhatsApp.
How do I get the full solved file on WhatsApp?
Send a WhatsApp message to 9899436384 with the course code BBCCT 113 and the session June 2026. Our team replies with the details, and once confirmed you receive the full solved file with answers to all 8 questions. That is the 2 answers already shown on this page plus 6 more that appear only in the file, covering Questions 3 to 8.
Which BBCCT 113 topics repeat most often in IGNOU papers?
Across the four official papers we checked (June 2023, December 2023, December 2025 and June 2026), four areas appeared every time: the liver as metabolic hub, nitrogen fixation, inborn errors of amino acid metabolism and disorders such as gout or SCID. Haem metabolism, de novo versus salvage synthesis and amino acid biosynthesis families also appeared in all four papers.
How many questions must I attempt in the BBCCT 113 exam?
The June 2026 paper asked students to attempt any five of eight questions, with every question carrying 14 marks for a total of 70 in three hours. Most questions have two parts, such as 7 + 7 or 5 + 9, so plan your time by marks. The December 2023 paper used a different pattern of seven out of ten questions.
Are the answers written to the marks printed on the paper?
Yes. Each answer is sized to its marks, so a 3-mark note on biological nitrogen fixation stays short while a 9-mark answer on haem biosynthesis goes step by step with enzymes. Difference questions, such as kwashiorkor versus marasmus, use comparison tables, and pathway answers list reactions in order so you can reproduce them in the exam.
Is BBCCT 113 linked to the BBCCL 114 practical course?
Yes. IGNOU pairs BBCCT 113 with the 2-credit laboratory course BBCCL 114, and the prospectus says the two are taken together. The lab covers estimation of urea, uric acid, creatine and creatinine, and assays of the serum transaminases AST and ALT, which connect directly to several theory questions. The file index on this page shows the lab link for each question.
Which programme studies BBCCT 113?
BBCCT 113 is a 4-credit core theory course of the IGNOU B.Sc. (Hons.) Biochemistry programme (BSCBCH), and the June 2026 paper is printed under that programme name. Learners in other IGNOU biochemistry degrees may also carry this course code, so check your own programme guide before you order.
Can I use the June 2026 answers for the December 2026 exam?
Yes, they are useful revision for December 2026 because BBCCT 113 repeats topics heavily. Liver as metabolic hub, purine degradation, haem biosynthesis, gout and SCID have each come up in more than one of the four papers we checked. Studying these complete answers prepares you for the same topics even when IGNOU changes the wording of the question.
12. Who Wrote and Checked the BBCCT 113 Answers
The BBCCT 113 answers were written by the Unnati Educations biochemistry team and reviewed by Sheetal Kirola.
Prateek Talwar, founder of Unnati Educations, leads the IGNOU science solved-paper series and prepares answers from the course blocks and the official term-end paper. Sheetal Kirola, Academic Head (M.Ed.), checks every enzyme name, equation and ATP figure against the course blocks before release.