Stress hyperglycemia occurs due to all except -
Which of the following statements best describes the mechanism of action of insulin on target cells?
Agent that acts through tyrosine kinase receptor is
Which of the following is not a peptide/protein -
Which of the following is called hunger hormone?
All the following hormones have receptors on the plasma membrane of target tissues except:
Which hormone is NOT increased in stress?
Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?
All of the following are increased in Acute stress except
All of these cause hyperglycemia except:
Explanation: ***Decreased level of norepinephrine*** - **Norepinephrine** is a **catecholamine** that generally **increases blood glucose** by stimulating **glycogenolysis** and **gluconeogenesis**. - Therefore, a *decrease* in norepinephrine would *reduce* stress-induced hyperglycemia, making this the exception. *Increased level of ACTH* - **ACTH (Adrenocorticotropic Hormone)** stimulates the adrenal glands to release **cortisol**, which contributes significantly to stress hyperglycemia. - Increased ACTH levels therefore *promote* hyperglycemia in stress. *Insulin resistance* - **Insulin resistance** is a common feature during stress, where target cells become less responsive to insulin's effects. - This reduced insulin sensitivity leads to higher circulating glucose levels, contributing to hyperglycemia. *Increased level of cortisol* - **Cortisol** is a key **stress hormone** that promotes **gluconeogenesis** (production of glucose from non-carbohydrate sources) and **glycogenolysis** (breakdown of glycogen to glucose). - Elevated cortisol levels directly lead to an increase in blood glucose, causing hyperglycemia.
Explanation: ***Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.*** - **Insulin** is a **peptide hormone** and cannot freely pass through the lipid bilayer, thus it binds to a **transmembrane receptor** on the cell surface. - This binding leads to the activation of the receptor's intrinsic **tyrosine kinase activity** in the intracellular domain, initiating a signaling cascade. *Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.* - This mechanism describes the action of **steroid hormones**, which are lipid-soluble and can cross the cell membrane, binding to **intracellular receptors**. - **Insulin** acts via a **cell surface receptor** and its downstream effects are mediated through signal transduction pathways, not direct nuclear translocation. *Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.* - This mechanism is characteristic of **G-protein coupled receptors (GPCRs)**, which activate or inhibit enzymes like adenylate cyclase via G-proteins to produce second messengers like cyclic AMP. - The **insulin receptor** is a **receptor tyrosine kinase**, not a GPCR, and does not directly activate adenylate cyclase via Gs protein. *Insulin enters the cell and causes the release of calcium ions from intracellular stores.* - While some hormones and neurotransmitters can trigger the release of intracellular **calcium ions**, this is typically mediated by specific pathways (e.g., GPCRs linked to phospholipase C). - **Insulin** does not directly enter target cells to cause calcium release; its actions are primarily mediated through receptor tyrosine kinase signaling pathways.
Explanation: ***Insulin*** - **Insulin** binds to its receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and the activation of intracellular signaling pathways. - This activation is crucial for glucose uptake and metabolism by various cells in the body. *MSH* - **Melanocyte-stimulating hormone (MSH)** acts primarily through **G protein-coupled receptors**, specifically melanocortin receptors. - These receptors activate adenylyl cyclase, leading to an increase in intracellular cAMP. *TSH* - **Thyroid-stimulating hormone (TSH)** also acts via a **G protein-coupled receptor** on thyroid follicular cells. - Its binding stimulates adenylyl cyclase, increasing cAMP and thus thyroid hormone synthesis and release. *TRH* - **Thyrotropin-releasing hormone (TRH)** binds to **G protein-coupled receptors** on pituitary thyrotrophs. - This interaction activates the phospholipase C pathway, leading to the release of TSH.
Explanation: ***Glucocorticoids*** - **Glucocorticoids** are **steroid hormones** derived from cholesterol, making them **lipids**, not peptides or proteins. - They exert their effects by binding to **intracellular receptors** to regulate gene expression. *Growth hormone* - **Growth hormone (GH)** is a **peptide hormone** produced by the anterior pituitary gland. - It plays a crucial role in **growth**, cell reproduction, and metabolism. *PTH* - **Parathyroid hormone (PTH)** is a **peptide hormone** secreted by the parathyroid glands. - It primarily regulates **calcium** and phosphate levels in the blood. *Insulin* - **Insulin** is a **peptide hormone** produced by the beta cells of the pancreatic islets. - Its main function is to regulate **glucose metabolism** by facilitating glucose uptake into cells.
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: ***Estradiol*** - **Estradiol** is a **steroid hormone** derived from cholesterol, making it **lipid-soluble**. - Due to its lipid solubility, estradiol can readily pass through the **plasma membrane** and bind to **intracellular receptors** in the cytoplasm or nucleus. *Epinephrine* - **Epinephrine** is a **catecholamine hormone** and is **water-soluble**. - Water-soluble hormones cannot cross the lipid bilayer of the plasma membrane and thus bind to **receptors located on the cell surface**. *Glucagon* - **Glucagon** is a **peptide hormone** and is **water-soluble**. - Like other peptide hormones, it binds to **specific receptors embedded in the plasma membrane** to elicit its cellular effects via second messenger systems. *Thyrotropin* - **Thyrotropin**, also known as **Thyroid-Stimulating Hormone (TSH)**, is a **glycoprotein hormone** and is **water-soluble**. - TSH exerts its action by binding to **receptors on the plasma membrane** of thyroid follicular cells.
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: ***TCA (Tricarboxylic Acid Cycle)*** - The **TCA cycle** (also called Krebs cycle or citric acid cycle) is the **final common oxidative pathway** where all three macronutrients converge - **Carbohydrates** → Pyruvate → **Acetyl-CoA** (via pyruvate dehydrogenase) - **Lipids** → Fatty acids → **Acetyl-CoA** (via beta-oxidation) - **Proteins** → Amino acids → **Acetyl-CoA or TCA intermediates** (via deamination/transamination) - Complete oxidation of acetyl-CoA occurs in the TCA cycle, producing **NADH, FADH2, and GTP** for energy production *Gluconeogenesis* - This is a **biosynthetic pathway** that synthesizes glucose from non-carbohydrate precursors (lactate, glycerol, amino acids) - It is an **anabolic process**, not the catabolic final common pathway for energy production from all macronutrients *Glycolysis* - **Carbohydrate-specific pathway** that converts glucose to pyruvate - It is only the initial breakdown pathway for carbohydrates, not the common pathway where lipids and proteins also converge - Pyruvate from glycolysis must enter TCA cycle for complete oxidation *HMP pathway (Pentose Phosphate Pathway)* - Parallel pathway to glycolysis that generates **NADPH** (for biosynthesis and antioxidant defense) and **ribose-5-phosphate** (for nucleotide synthesis) - Processes only **glucose-6-phosphate** from carbohydrate metabolism - Not involved in lipid or protein metabolism integration
Explanation: ***Insulin*** - During acute stress, **insulin secretion is actively suppressed** by catecholamines (epinephrine and norepinephrine) acting on **alpha-2 adrenergic receptors** on pancreatic beta cells. - This suppression is crucial for the stress response, as it allows **unopposed action of counter-regulatory hormones** to mobilize glucose and raise blood glucose levels. - The body prioritizes **immediate energy availability** (high blood glucose) over storage, making insulin the hormone that is **decreased, not increased**, during acute stress. *Growth hormone* - **Growth hormone** is a counter-regulatory hormone that **increases during acute stress** to mobilize energy stores, particularly by promoting lipolysis and gluconeogenesis. - Its actions contribute to the stress-induced elevation of **blood glucose levels**. *Epinephrine* - **Epinephrine** (adrenaline) is a primary catecholamine released during acute stress, leading to a rapid **fight or flight response**. - It significantly **increases heart rate**, blood pressure, and **glucose mobilization** through glycogenolysis and gluconeogenesis. *Glucagon* - **Glucagon** is a key hormone involved in **maintaining glucose homeostasis** and is significantly **increased during acute stress**. - It primarily acts on the liver to **stimulate glycogenolysis** and **gluconeogenesis**, thereby raising blood glucose levels to provide energy.
Explanation: ***Insulin*** - Insulin's primary function is to **lower blood glucose levels** by facilitating glucose uptake into cells and promoting glycogen synthesis. - It counters the effects of hormones that elevate blood sugar, directly leading to a **decrease in hyperglycemia**. *Catecholamines* - **Catecholamines** (e.g., epinephrine, norepinephrine) increase blood glucose by promoting **glycogenolysis** and **gluconeogenesis**. - They also **inhibit insulin secretion**, further contributing to elevated blood sugar. *Cortisol* - **Cortisol** is a **glucocorticoid** that raises blood glucose by increasing **gluconeogenesis** and reducing peripheral **glucose utilization**. - It can also decrease insulin sensitivity, leading to **hyperglycemia**. *GH* - **Growth hormone (GH)** can induce **insulin resistance** in peripheral tissues, which leads to reduced glucose uptake. - It also promotes **gluconeogenesis**, both contributing to elevated blood glucose levels.
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