Which hormone is NOT increased in stress?
Which hormone acts on cytoplasmic membrane receptor?
Hormone associated with satiety is
Which of the following hormones is mainly responsible for skeletal maturation of long bones during puberty?
Intracellular receptors are found in all except
Which of the following is called hunger hormone?
Growth hormone secretion is decreased by
A shift to the right in the biological activity dose- response curve for a hormone with no accompanying change in the maximal response indicates:
Estrogen administration in a menopausal woman increases the:
Which among the following is the function of ghrelin?
Explanation: ***Insulin*** - Insulin levels generally **decrease** during acute stress. This allows for increased availability of glucose for tissues, such as the brain and muscles, during "fight or flight" responses. - The sympathetic nervous system activity during stress **inhibits insulin secretion** from pancreatic beta cells. *Glucagon* - **Glucagon levels increase** during stress to promote **hepatic glucose production** (glycogenolysis and gluconeogenesis), ensuring a readily available energy supply. - This rise in glucagon is part of the counter-regulatory response to maintain blood glucose stability during stressful conditions. *Cortisol* - **Cortisol levels significantly increase** during stress as part of the **hypothalamic-pituitary-adrenal (HPA) axis** activation. - Cortisol mobilizes energy stores, suppresses the immune system, and prepares the body for prolonged stress. *Epinephrine* - **Epinephrine (adrenaline) levels increase rapidly** during acute stress as part of the **sympathetic nervous system** response. - It triggers the "fight or flight" response, increasing heart rate, blood pressure, and diverting blood flow to essential organs, while also promoting glucose release.
Explanation: ***TSH*** - **TSH** (**Thyroid-Stimulating Hormone**) is a **peptide hormone** that cannot pass through the lipid bilayer of the cell membrane due to its large, hydrophilic nature. - Therefore, TSH binds to specific **G protein-coupled receptors** located on the **cytoplasmic membrane** of thyroid follicular cells to exert its effects. *Thyroxine* - **Thyroxine** (T4) is a **thyroid hormone** derived from the amino acid tyrosine (an iodinated tyrosine derivative), which is **lipophilic** and can easily cross the cell membrane. - It primarily binds to **intracellular receptors** in the nucleus to regulate gene expression. *Androgen* - **Androgens** are **steroid hormones** (e.g., testosterone) that are **lipophilic** and readily diffuse across the cell membrane. - They act on **intracellular androgen receptors** located in the cytoplasm or nucleus. *Cortisol* - **Cortisol** is a **steroid hormone** that is **lipophilic** and can freely pass through the cell membrane. - It primarily binds to **intracellular glucocorticoid receptors** within the cytoplasm, forming a complex that translocates to the nucleus to modulate gene transcription.
Explanation: ***α-MSH*** - **Alpha-Melanocyte-stimulating hormone (α-MSH)** is a key neuropeptide involved in the **satiety pathway**. - It acts on **MC4 receptors** in the hypothalamus, leading to a decrease in food intake and an increase in energy expenditure. *Neuropeptide-Y* - **Neuropeptide-Y (NPY)** is a potent **orexigenic (appetite-stimulating)** peptide produced in the hypothalamus. - It promotes food intake and reduces energy expenditure, thereby **increasing hunger**. *Ghrelin* - **Ghrelin** is a hormone primarily produced in the stomach, often referred to as the "**hunger hormone**." - It stimulates appetite, increasing food intake and **promoting weight gain**. *Orexin* - **Orexin (also known as hypocretin)** is a neuropeptide produced in the hypothalamus that regulates **arousal, wakefulness, and appetite**. - While it has a role in regulating feeding, its primary function is more related to **increasing wakefulness and promoting food-seeking behavior** rather than directly signaling satiety.
Explanation: ***Estrogen*** - Estrogen is crucial for **epiphyseal plate fusion** in both sexes, leading to the cessation of longitudinal bone growth. - While growth hormone initiates growth, estrogen is the primary signal for its **termination and skeletal maturation**. *Growth hormone* - **Growth hormone (GH)** is essential for stimulating longitudinal bone growth by promoting the proliferation of chondrocytes in the **epiphyseal plates**. - However, GH primarily drives *growth*, not the final *maturation and closure* of the growth plates. *Testosterone/estrogen ratio* - The ratio itself is not the direct hormonal signal for **skeletal maturation**. - While testosterone is converted to estrogen in males, it is the **estrogen** produced that mediates epiphyseal fusion. *Testosterone* - In males, testosterone promotes bone growth and increased bone density, but its effect on skeletal maturation is largely mediated through its **aromatization to estrogen**. - **High levels of testosterone** in puberty lead to increased estrogen, which then signals the closure of the growth plates.
Explanation: ***Insulin*** - **Insulin** is a **peptide hormone** that cannot easily cross the cell membrane. It binds to a specific **extracellular receptor** on the cell surface, initiating a signaling cascade. - Its receptor is a **transmembrane protein** with an extracellular ligand-binding domain and an intracellular tyrosine kinase domain. *Androgen* - **Androgens** are **steroid hormones** that are lipid-soluble and can readily diffuse across the cell membrane to bind to **intracellular receptors** in the cytoplasm or nucleus. - The androgen-receptor complex then translocates to the nucleus to regulate gene expression. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that, despite being an amine derivative, is lipophilic and can enter cells to bind to **intracellular receptors** located in the nucleus. - These nuclear receptors regulate gene transcription involved in metabolism, growth, and development. *Corticosteroids* - **Corticosteroids** are **steroid hormones** that are lipid-soluble and diffuse through the cell membrane to bind to **intracellular receptors**, primarily in the cytoplasm. - The activated receptor-hormone complex then moves into the nucleus to influence gene expression.
Explanation: ***Ghrelin*** - **Ghrelin** is often referred to as the **"hunger hormone"** because it stimulates appetite, increases food intake, and promotes fat storage. - It is primarily produced in the **stomach** and its levels rise before meals and decrease after meals. *Insulin* - **Insulin** is a hormone primarily involved in regulating **blood glucose levels** by facilitating glucose uptake into cells. - It does not directly induce hunger but rather signals satiety and energy storage. *Leptin* - **Leptin** is known as the **"satiety hormone"** because it suppresses appetite and signals to the brain that the body has sufficient energy stores. - It is produced by **adipose tissue** (fat cells) and helps regulate long-term energy balance. *Cortisol* - **Cortisol** is a **stress hormone** involved in the body's 'fight or flight' response, influencing metabolism, immune function, and inflammation. - While chronic stress and elevated cortisol can indirectly affect appetite and food cravings, it is not primarily known as a hunger or satiety hormone.
Explanation: ***Glucose*** - **High blood glucose levels** act as a negative feedback signal to the **hypothalamus** and **anterior pituitary**, inhibiting the release of Growth Hormone-Releasing Hormone (GHRH) and Growth Hormone (GH), respectively. - This physiological response helps to prevent excessive growth and metabolism when energy substrates are readily available. *Exercise* - **Physical exercise**, particularly intense activity, is a powerful stimulus for **GH secretion**, likely due to increased sympathetic activity and changes in circulating metabolites. - This GH surge during exercise contributes to **fat mobilization** and **muscle protein synthesis**. *Stress* - Both **physical and psychological stress** can significantly stimulate **GH release**, mediated by increased activity of the **hypothalamic-pituitary-adrenal (HPA) axis** and adrenaline. - GH's role here is to mobilize energy resources to cope with the stressful situation. *Glucagon* - **Glucagon**, a hormone primarily known for raising blood glucose, also has a direct stimulatory effect on **GH secretion**, especially during periods of low glucose or fasting. - This effect is utilized in certain diagnostic tests for GH deficiency.
Explanation: ***Decreased sensitivity*** - A **right shift** in the dose-response curve means a **higher concentration** of the hormone is required to achieve the same effect, indicating reduced sensitivity. - No change in the **maximal response** implies the system can still reach the same peak effect, but it needs more hormone. *Increased sensitivity and decreased responsiveness* - **Increased sensitivity** would be represented by a **left shift** in the dose-response curve, meaning less hormone is needed for a given effect. - **Decreased responsiveness** implies a reduction in the **maximal effect**, which is stated as unchanged in the question. *Increased responsiveness* - **Increased responsiveness** would mean a **higher maximal effect** can be achieved or a steeper slope in the dose-response curve, neither of which is described. - A right shift is related to the dose required for an effect, not the magnitude of the maximal effect. *Decreased responsiveness and decreased sensitivity* - While **decreased sensitivity** is correct, **decreased responsiveness** is incorrect because the question specifies "no accompanying change in the maximal response." - **Decreased responsiveness** would be indicated by a **lower maximal effect (Emax)**, which is not the case here.
Explanation: ***Bone mass*** - Estrogen plays a crucial role in maintaining **bone density** by inhibiting osteoclast activity and promoting osteoblast function. - In menopausal women, estrogen administration counteracts bone loss and thus **increases bone mass**, reducing the risk of osteoporosis. *Gonadotropin secretion* - In menopausal women, **gonadotropin-releasing hormone (GnRH)** and subsequent **FSH and LH levels are elevated** due to the absence of ovarian estrogen feedback. - Estrogen administration would exert a **negative feedback** on the hypothalamus and pituitary, thereby **decreasing**, not increasing, gonadotropin secretion. *Muscle mass* - While estrogen has some anabolic effects, **androgens** (like testosterone) are the primary hormones responsible for significantly increasing muscle mass. - Estrogen administration to menopausal women is not a primary intervention for increasing muscle mass; its effects on this parameter are generally **modest or negligible**. *LDL cholesterol* - Estrogen generally has a **favorable effect on lipid profiles**, typically leading to a **decrease in LDL cholesterol** and an increase in HDL cholesterol. - Therefore, estrogen administration would generally **reduce**, not increase, LDL cholesterol levels.
Explanation: ***Stimulation of appetite*** - **Ghrelin** is often referred to as the **"hunger hormone"** because its primary function is to stimulate appetite. - Levels of ghrelin typically rise before meals and decrease after eating, signaling the brain to initiate food intake. *Suppression of appetite* - Hormones like **leptin** and **cholecystokinin (CCK)** are known to suppress appetite, acting as satiety signals. - Ghrelin has the opposite effect, promoting feelings of hunger rather than fullness. *Stimulation of sleep* - While ghrelin levels can influence **sleep-wake cycles** through its effects on the **hypothalamus**, its primary and most direct function is not the stimulation of sleep. - Sleep regulation is a complex process involving multiple neurotransmitters and hormones distinct from ghrelin's main role in hunger. *Regulation of gastric motility* - Although ghrelin can have some effects on **gastrointestinal motility**, its main function is not to regulate it. - Gastric motility is primarily influenced by hormones like **motilin** and the **enteric nervous system**.
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