Download PDF – RRB PH UT26 – Biochemistry Practice Test 1: Carbohydrate, Lipid & Protein Metabolism

RRB PH UT26 – Biochemistry Practice Test 1: Carbohydrate, Lipid & Protein Metabolism

Q1. Gaucher disease is caused by deficiency of which enzyme?

A) Galactocerebrosidase

B) Hexosaminidase B

C) Glucocerebrosidase (Acid beta-glucosidase)

D) Arylsulfatase A

Q1. गौचर रोग (Gaucher disease) किस एंजाइम की कमी से होता है?

A) गैलेक्टोसेरेब्रोसिडेज

B) हेक्सोसामिनिडेज बी

C) ग्लूकोसेरेब्रोसिडेज (एसिड बीटा-ग्लूकोसिडेज)

D) एरील्सल्फेटेज ए

Answer: (C)

Gaucher disease is caused by an autosomal recessive deficiency of the lysosomal enzyme glucocerebrosidase (acid beta-glucosidase), which hydrolyzes glucosylceramide to ceramide and glucose. Undegraded glucocerebroside accumulates in monocyte-macrophage lineages, producing characteristic lipid-engorged 'Gaucher cells' with a crumpled-tissue-paper appearance under microscopy, causing hepatosplenomegaly, anemia, and skeletal bone crises.

गौचर रोग ग्लूकोसेरेब्रोसिडेज (एसिड बीटा-ग्लूकोसिडेज) की कमी से होता है; जिससे मैक्रोफेज में ग्लूकोसिलसेरामाइड जमा हो जाता है।

Q2. MSUD results from deficiency of which enzyme complex?

A) Homogentisate oxidase

B) Branched-chain alpha-keto acid dehydrogenase complex

C) Phenylalanine hydroxylase

D) Fumarylacetoacetate hydrolase

Q2. MSUD (मेपल सिरप यूरिन डिजीज) किस एंजाइम सम्मिश्र (enzyme complex) की कमी से होता है?

A) होमोजेंटिसिट ऑक्सीडेज

B) ब्रांच्ड-चेन अल्फा-कीटो एसिड डिहाइड्रोजनेज सम्मिश्र

C) फेनिलएलनिन हाइड्रॉक्सिलेज

D) फ्यूमरिलएसीटोएसीटेट हाइड्रॉलेज

Answer: (B)

Maple Syrup Urine Disease (MSUD) is caused by a congenital deficiency of the mitochondrial branched-chain alpha-keto acid dehydrogenase multienzyme complex. This defect impairs the degradation of branched-chain amino acids (leucine, isoleucine, and valine), leading to toxic accumulation of these amino acids and their alpha-keto acids in plasma and urine, which imparts a distinctive sweet, burnt sugar or maple syrup odor to urine and causes severe ketoacidosis and cerebral edema.

MSUD ब्रांच्ड-चेन अल्फा-कीटो एसिड डिहाइड्रोजनेज सम्मिश्र की कमी से होता है; जिससे ल्यूसीन (leucine), आइसोल्यूसीन और वेलिन (valine) का चयापचय बाधित होता है।

Q3. Which apolipoprotein activates lipoprotein lipase (LPL)?

A) Apolipoprotein B-100

B) Apolipoprotein C-II

C) Apolipoprotein E

D) Apolipoprotein A-I

Q3. लिपोप्रोटीन लाइपेज (LPL) को कौन-सा एपोलिपोप्रोटीन (apolipoprotein) सक्रिय करता है?

A) एपोलिपोप्रोटीन B-100

B) एपोलिपोप्रोटीन C-II

C) एपोलिपोप्रोटीन E

D) एपोलिपोप्रोटीन A-I

Answer: (B)

Apolipoprotein C-II (Apo C-II) is a structural component of chylomicrons and VLDL acquired from circulating HDL. Apo C-II acts as an obligate cofactor and allosteric activator of endothelial lipoprotein lipase (LPL) in the capillary beds of adipose tissue and cardiac/skeletal muscle, hydrolyzing core triglycerides into free fatty acids and glycerol. Congenital Apo C-II deficiency causes severe familial Type I hyperlipoproteinemia.

Apo C-II केशिका (capillary) लिपोप्रोटीन लाइपेज (LPL) का सहकारक/सक्रियकर्ता (cofactor/activator) है और ट्राइग्लिसराइड्स के हाइड्रोलिसिस में आवश्यक है।

Q4. Which vitamin B12 coenzyme converts methylmalonyl-CoA to succinyl-CoA?

A) 5'-Deoxyadenosylcobalamin

B) Methylcobalamin

C) Cyanocobalamin

D) Hydroxocobalamin

Q4. मिथाइलमैलोनिल-CoA को सक्सिनिल-CoA में बदलने के लिए विटामिन B12 का कौन-सा सहएंजाइम (coenzyme) आवश्यक है?

A) 5'-डीऑक्सीएडेनोसिलकोबालामिन

B) मिथाइलकोबालामिन

C) साइनोकोबालामिन

D) हाइड्रॉक्सोकोबालामिन

Answer: (A)

Vitamin B12 functions in the human body in two coenzyme forms: (1) 5'-Deoxyadenosylcobalamin, which serves as the coenzyme for mitochondrial methylmalonyl-CoA mutase, converting methylmalonyl-CoA to succinyl-CoA; and (2) Methylcobalamin, which serves as the methyl donor for cytoplasmic methionine synthase during the remethylation of homocysteine to methionine.

5'-डीऑक्सीएडेनोसिलकोबालामिन माइटोकॉन्ड्रियल मिथाइलमैलोनिल-CoA म्यूटेज का सहएंजाइम है; यह मिथाइलमैलोनिल-CoA को सक्सिनिल-CoA में बदलता है।

Q5. What is the classic triad of pellagra?

A) Night blindness, xerophthalmia, and Bitot spots

B) Ataxia, nystagmus, and ophthalmoplegia

C) Osteomalacia, rickets, and tetany

D) Dermatitis, diarrhea, and dementia

Q5. पेलाग्रा (Pellagra) की प्रमुख त्रयी (classic triad) क्या है?

A) रतौंधी (Night blindness), ज़ेरोप्थाल्मिया (xerophthalmia) और बिटोट स्पॉट

B) गतिभंग (Ataxia), निस्टागमस (nystagmus) और ऑप्थाल्मोप्लेजिया

C) अस्थिमृदुता (Osteomalacia), रिकेट्स और टिटैनी

D) डर्मेटाइटिस, डायरिया और डिमेंशिया (Dermatitis, diarrhea, and dementia)

Answer: (D)

Pellagra is caused by a deficiency of niacin (Vitamin B3) or its metabolic precursor tryptophan. Niacin forms NAD+ and NADP+, vital cofactors for cellular hydride transfer. Pellagra manifests as the classic '3 Ds': photosensitive symmetrical dermatitis (Casal's necklace), gastrointestinal inflammation causing chronic watery diarrhea, and progressive encephalopathic dementia. Untreated pellagra culminates in death.

नियासिन (Niacin) की कमी से पेलाग्रा होता है, जिसकी प्रमुख त्रयी (classic triad) डर्मेटाइटिस (त्वचाशोथ), डायरिया (दस्त) और डिमेंशिया (मनोभ्रंश) है।

Q6. Which organ cannot use ketone bodies because it lacks thiophorase?

A) Liver

B) Brain

C) Renal cortex

D) Skeletal muscle

Q6. थियोफोरेज (Thiophorase) एंजाइम की कमी के कारण कौन-सा अंग कीटोन बॉडीज (ketone bodies) का उपयोग नहीं कर सकता?

A) यकृत (Liver)

B) मस्तिष्क (Brain)

C) वृक्क वल्कुट (Renal cortex)

D) कंकाल पेशी (Skeletal muscle)

Answer: (A)

The liver is the exclusive primary site of ketogenesis, synthesizing acetoacetate and beta-hydroxybutyrate from excess acetyl-CoA. However, hepatic mitochondria completely lack the enzyme thiophorase (beta-ketoacyl-CoA transferase / succinyl-CoA:acetoacetate CoA transferase) required to activate acetoacetate into acetoacetyl-CoA. Consequently, the liver cannot oxidize ketone bodies and exports them to extrahepatic tissues.

यकृत कीटोन बॉडीज बनाता है, लेकिन थियोफोरेज एंजाइम की कमी के कारण उनका ऑक्सीकरण (oxidation) नहीं कर सकता; इसलिए यकृत उनका उपयोग नहीं करता।

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