Keshan's disease is due to deficiency of:
Site of 25-hydroxylation of cholecalciferol
Active form of Vitamin D is:
Glutathione reductase assay is helpful in assessing the deficiency of
All are true regarding vitamin D, except ?
During the dark phase of visual cycle, which form of vitamin A combines with opsin to make Rhodopsin:
All of the following statements are true except:
Which of the following acts via the steroid-thyroid receptor superfamily (nuclear receptors)?
Which of the following is absolutely essential for wound healing?
Which vitamin deficiency is associated with night blindness and impaired immunity?
Explanation: **Selenium (Correct Answer)** - **Keshan disease** is an endemic cardiomyopathy characterized by multifocal myocyte necrosis, which has been directly linked to a severe dietary deficiency of **selenium**. - Selenium is an essential component of **glutathione peroxidase**, an enzyme critical for protecting cells against oxidative damage. - The disease is named after Keshan County in China where it was first identified in selenium-deficient regions. *Iron (Incorrect)* - **Iron deficiency** primarily leads to **anemia**, characterized by fatigue, pallor, and weakness due to insufficient hemoglobin production. - It does not directly cause the specific cardiomyopathy seen in Keshan disease. *Zinc (Incorrect)* - **Zinc deficiency** can cause a range of symptoms including impaired immune function, skin lesions (acrodermatitis enteropathica), hair loss, and growth retardation. - It is not associated with the cardiac manifestations of Keshan disease. *Copper (Incorrect)* - **Copper deficiency** can result in anemia, neutropenia, impaired immune function, and neurological dysfunction (Menkes disease). - While copper is important for various metalloenzymes, its deficiency does not cause Keshan disease.
Explanation: ***Liver*** - The **liver** is the site of **25-hydroxylation** of cholecalciferol (Vitamin D3) to form **25-hydroxycholecalciferol (calcidiol)**. - This reaction is catalyzed by **25-hydroxylase (CYP2R1)** in hepatocytes. - This is the **first step** in vitamin D activation; subsequent 1α-hydroxylation occurs in the **kidney** to form the active **calcitriol**. *Bone* - Bone is a **target organ** for active vitamin D (calcitriol) action, not a site of hydroxylation. - It responds to calcitriol for calcium homeostasis and bone remodeling. *Pancreas* - The pancreas has no role in vitamin D metabolism. - Its primary functions are digestive enzyme secretion and endocrine regulation (insulin, glucagon). *Heart* - The heart does not perform vitamin D hydroxylation. - While vitamin D receptors exist in cardiac tissue, the organ does not metabolize vitamin D.
Explanation: ***Calcitriol*** - **Calcitriol** (1,25-dihydroxycholecalciferol) is the **biologically active form of vitamin D**. - It is produced primarily in the kidneys from calcifediol and is responsible for regulating **calcium and phosphate levels** in the body. *Calcifediol* - **Calcifediol** (25-hydroxyvitamin D) is the main circulating form of vitamin D, produced in the liver from cholecalciferol. - It is **not the active form**; rather, it is a precursor that needs further hydroxylation in the kidneys to become calcitriol. *Paricalcitol* - **Paricalcitol** is a **synthetic vitamin D analog** used therapeutically to prevent and treat secondary hyperparathyroidism. - It is not the naturally occurring active form of vitamin D in the body. *Cholecalciferol* - **Cholecalciferol** (vitamin D3) is the form of vitamin D synthesized in the skin upon exposure to sunlight or obtained from the diet. - It is a **precursor** to the active form and requires two hydroxylation steps (in the liver and kidneys) to become calcitriol.
Explanation: ***Riboflavin*** - The **glutathione reductase assay** measures the activity of the enzyme glutathione reductase, which uses **FAD** (derived from riboflavin) as a coenzyme. - A significant increase in enzyme activity upon addition of FAD indicates **riboflavin deficiency**, as the enzyme was previously operating at suboptimal levels due to insufficient FAD. *Niacin* - Niacin is a precursor for **NAD+** and **NADP+**, which are involved in many redox reactions, but not directly as a coenzyme for glutathione reductase. - Deficiency leads to **pellagra**, characterized by dermatitis, diarrhea, and dementia. *Pyridoxine* - Pyridoxine (vitamin B6) is a precursor for **pyridoxal phosphate (PLP)**, a coenzyme involved in amino acid metabolism. - It is not directly linked to the function of glutathione reductase. *Vit B5* - Vitamin B5 (pantothenic acid) is a component of **coenzyme A (CoA)**, crucial for fatty acid synthesis and degradation, and the citric acid cycle. - It does not directly affect the activity of glutathione reductase.
Explanation: ***1-hydroxylation in liver*** - The **1-alpha-hydroxylation** of 25-hydroxyvitamin D (calcidiol) primarily occurs in the **kidneys** to form the active form, **calcitriol (1,25-dihydroxyvitamin D)**. - The liver is responsible for the **25-hydroxylation** of vitamin D to calcidiol, not the 1-hydroxylation step. *Sunlight is important* - Exposure to **ultraviolet B (UVB) rays** from sunlight is crucial for the endogenous synthesis of **vitamin D3 (cholecalciferol)** in the skin from 7-dehydrocholesterol. - Insufficient sun exposure can lead to **vitamin D deficiency**, especially in individuals with darker skin or those living at higher latitudes. *Active form is calcitriol* - **Calcitriol (1,25-dihydroxyvitamin D)** is the hormonally active form of vitamin D, playing a key role in **calcium and phosphate homeostasis**. - It acts on target tissues like the intestine, bone, and kidney to regulate mineral metabolism. *RDA for children is 400 IU* - The recommended dietary allowance (RDA) for **infants and children** is typically **400 International Units (IU)** of vitamin D per day. - This recommendation helps prevent **rickets** in children and supports healthy bone development.
Explanation: ***11-cis-Retinaldehyde*** - In the **dark phase** of the visual cycle, **11-cis-retinaldehyde** (retinal) is regenerated and combines with **opsin** to form **rhodopsin**. - This molecule is crucial for initiating the visual transduction pathway in **rod cells** when light is detected. *11-cis-Retinol* - **11-cis-Retinol** is an intermediate in the regeneration of 11-cis-retinaldehyde from all-trans-retinol, but it does not directly bind to opsin to form rhodopsin. - It is converted to 11-cis-retinaldehyde by the enzyme **11-cis-retinol dehydrogenase**. *all trans-Retinol* - **All-trans-retinol** is the form of vitamin A transported to the eye and is also an intermediate in the visual cycle, but it does not combine directly with opsin. - It is converted to all-trans-retinaldehyde after the absorption of light and then subsequently isomerized to 11-cis-retinol. *All trans-Retinaldehyde* - **All-trans-retinaldehyde** is formed when **rhodopsin** absorbs light, causing the isomerization of 11-cis-retinaldehyde. - This molecule is then released from opsin and subsequently reduced to all-trans-retinol before being recycled back to 11-cis-retinaldehyde in the pigment epithelium.
Explanation: ***25(OH)D3 is the most active form of vitamin D*** - This statement is incorrect. While **25(OH)D3 (calcifediol)** is the major circulating form of vitamin D, it is not the most active form. - The most active form of vitamin D is **1,25(OH)2D3 (calcitriol)**, which is formed by the 1-alpha hydroxylation of calcifediol in the kidneys. *25–α hydroxylation takes place in liver* - This statement is true. The initial hydroxylation of **vitamin D3 (cholecalciferol)** at the 25-position occurs in the liver, forming 25(OH)D3 (calcifediol). - This step is catalyzed by the enzyme **25-hydroxylase**. *1–α hydroxylation takes place in kidney* - This statement is true. The 25(OH)D3 produced in the liver is then transported to the kidneys, where it undergoes a second hydroxylation at the 1-alpha position. - This step, catalyzed by **1-alpha-hydroxylase**, forms the biologically active hormone 1,25(OH)2D3 (calcitriol). *Daily requirement in the absence of sun–light is 450-600 IU/day* - This statement is generally true. The recommended daily allowance (RDA) for vitamin D in adults, especially in the absence of sufficient sun exposure, typically ranges from **400 to 800 IU (international units)**, with 600 IU/day being a common guideline. - This requirement can vary based on age, geographical location, and other individual factors.
Explanation: ***Vitamin D3*** - **Vitamin D3** (calcitriol) is a **steroid hormone** that acts by binding to the **vitamin D receptor (VDR)**, which is a member of the **steroid-thyroid receptor superfamily** of nuclear receptors. - This binding leads to gene transcription modulation, affecting calcium and phosphate homeostasis. *GH* - **Growth Hormone (GH)** acts primarily through **tyrosine kinase-associated receptors** (specifically, the JAK/STAT pathway), not nuclear receptors. - It's a **peptide hormone** that regulates growth, metabolism, and body composition. *Enkephalins* - **Enkephalins** are **opioid peptides** that bind to **G protein-coupled receptors (GPCRs)** on the cell surface. - They are involved in pain modulation and do not act via nuclear receptors. *Insulin* - **Insulin** is a **peptide hormone** that primarily acts via **receptor tyrosine kinases (RTKs)**, not nuclear receptors. - Upon binding, it initiates a signaling cascade involving phosphorylation events, regulating glucose metabolism.
Explanation: ***Vit C*** - **Vitamin C** is absolutely essential for wound healing because it is a crucial cofactor for **collagen synthesis**, specifically for the hydroxylation of proline and lysine residues. - Without adequate vitamin C, strong, stable **collagen fibers** cannot be formed, leading to impaired wound tensile strength and delayed healing. *Balanced diet* - While a **balanced diet** provides overall nutritional support for wound healing, it is a general principle, not a single, absolutely essential nutrient in the same way **Vitamin C** is for a specific biochemical process. - A balanced diet incorporates many components, but specifically points to **Vitamin C's** role makes it more specific and thereby the correct answer. *Vit D* - **Vitamin D** plays a role in bone health and immune function but is not directly involved in the **collagen synthesis** or immediate structural integrity of new tissue formation in wound healing to the same critical extent as Vitamin C. - Its effects on wound healing are more indirect, through modulation of inflammation and cell proliferation, rather than being an "absolutely essential" direct component of the healing process. *Carbohydrates* - **Carbohydrates** are important for providing energy for cellular activities during wound healing. - However, they are not directly involved in the **structural integrity** or **collagen formation** of the healing tissue itself, unlike Vitamin C.
Explanation: ***Vitamin A*** - **Vitamin A deficiency** is a classic cause of **night blindness** (nyctalopia) due to its role in the formation of **rhodopsin**, a light-sensitive pigment in the retina. - It also plays a crucial role in maintaining **immune function**, particularly in the integrity of epithelial tissues and normal lymphocyte activity. *Vitamin K* - **Vitamin K** is primarily involved in **blood clotting** (coagulation) through its role in the synthesis of clotting factors. - Deficiency leads to **bleeding disorders** and has no direct association with night blindness or significant impaired immunity. *Vitamin C* - **Vitamin C** (ascorbic acid) is essential for **collagen synthesis**, acting as an antioxidant and playing a role in immune defense. - Severe deficiency causes **scurvy**, characterized by bleeding gums, poor wound healing, and fatigue, but not night blindness. *Vitamin D* - **Vitamin D** is crucial for **calcium and phosphate metabolism**, bone health, and immune regulation. - Deficiency can lead to **rickets** in children and **osteomalacia** in adults, and while it impacts immunity, it does not cause night blindness.
Fat-Soluble Vitamins: A, D, E, K
Practice Questions
Vitamin A and Vision
Practice Questions
Vitamin D and Calcium Metabolism
Practice Questions
Vitamin E and Antioxidant Functions
Practice Questions
Vitamin K and Blood Coagulation
Practice Questions
Water-Soluble Vitamins: B Complex and C
Practice Questions
Thiamine (B1) and Pyruvate Dehydrogenase
Practice Questions
Riboflavin (B2) and Flavin Coenzymes
Practice Questions
Niacin and NAD/NADP
Practice Questions
Vitamin B6 and Transamination
Practice Questions
Folate and Vitamin B12 in One-Carbon Metabolism
Practice Questions
Vitamin C and Collagen Synthesis
Practice Questions
Get full access to all questions, explanations, and performance tracking.
Start For Free