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Questions and Answers
Consider a cell rendered incapable of producing cyclic AMP. Which of the following hormonal mechanisms would remain functional in this compromised cellular environment?
Consider a cell rendered incapable of producing cyclic AMP. Which of the following hormonal mechanisms would remain functional in this compromised cellular environment?
- Direct genomic regulation by steroid hormones via intracellular receptor complexes. (correct)
- Signal transduction initiated by protein hormones binding to membrane receptors coupled with G-protein activation.
- Hormone signaling through inositol triphosphate ($IP_3$) and diacylglycerol (DAG) pathways.
- Activation of receptor tyrosine kinases (RTKs) leading to a phosphorylation cascade.
A researcher discovers a novel synthetic hormone analog that, unlike endogenous steroid hormones, is unable to form a stable complex with its cytoplasmic receptor. However, it still elicits a biological response characteristic of the hormone. What is the most likely mechanism of action for this analog?
A researcher discovers a novel synthetic hormone analog that, unlike endogenous steroid hormones, is unable to form a stable complex with its cytoplasmic receptor. However, it still elicits a biological response characteristic of the hormone. What is the most likely mechanism of action for this analog?
- It inhibits proteins that normally repress transcription of hormone-sensitive genes.
- It directly binds to DNA response elements independent of receptor interaction.
- It activates a cell surface receptor, triggering a second messenger cascade. (correct)
- It is converted into a form that can bind to the nuclear receptor.
In a cellular context where protein kinase A (PKA) is constitutively active, how would the introduction of a protein hormone that typically acts via the two-messenger mechanism (cAMP) affect the cellular response, assuming other regulatory mechanisms remain intact?
In a cellular context where protein kinase A (PKA) is constitutively active, how would the introduction of a protein hormone that typically acts via the two-messenger mechanism (cAMP) affect the cellular response, assuming other regulatory mechanisms remain intact?
- The cellular response would be attenuated due to receptor desensitization.
- The cellular response would be completely abolished due to feedback inhibition.
- Potentially no change in the cellular response, since PKA is already maximally activated. (correct)
- The cellular response would be significantly amplified due to synergistic activation.
A cell line is engineered to express a mutant adenylyl cyclase that is unresponsive to G-protein activation. Exposure of these cells to a protein hormone that normally elevates cAMP levels would result in which outcome?
A cell line is engineered to express a mutant adenylyl cyclase that is unresponsive to G-protein activation. Exposure of these cells to a protein hormone that normally elevates cAMP levels would result in which outcome?
Consider a scenario where a cell simultaneously receives signals from both a steroid hormone and a protein hormone that acts via cAMP. If the steroid hormone increases the expression of a specific phosphodiesterase (PDE) isoform, how would this affect the cell's response to the protein hormone over time?
Consider a scenario where a cell simultaneously receives signals from both a steroid hormone and a protein hormone that acts via cAMP. If the steroid hormone increases the expression of a specific phosphodiesterase (PDE) isoform, how would this affect the cell's response to the protein hormone over time?
Given the intricate interplay between the hypothalamus and the posterior pituitary, under what specific physiological condition would the release of both ADH and oxytocin be simultaneously and maximally stimulated, considering the necessity for distinct yet concurrent hypothalamic activation patterns?
Given the intricate interplay between the hypothalamus and the posterior pituitary, under what specific physiological condition would the release of both ADH and oxytocin be simultaneously and maximally stimulated, considering the necessity for distinct yet concurrent hypothalamic activation patterns?
In a hypothetical scenario where a novel synthetic peptide selectively and reversibly inhibits the action of all known hypothalamic releasing hormones at the level of the anterior pituitary, what would be the MOST immediate and direct consequence on the endocrine profile, assuming no compensatory mechanisms are in place?
In a hypothetical scenario where a novel synthetic peptide selectively and reversibly inhibits the action of all known hypothalamic releasing hormones at the level of the anterior pituitary, what would be the MOST immediate and direct consequence on the endocrine profile, assuming no compensatory mechanisms are in place?
Considering the diverse chemical structures of hormones produced by endocrine glands, which of the following hormones would MOST likely exhibit the FASTEST onset of action following its release into the circulation, and why?
Considering the diverse chemical structures of hormones produced by endocrine glands, which of the following hormones would MOST likely exhibit the FASTEST onset of action following its release into the circulation, and why?
If a patient presents with symptoms indicative of both diabetes insipidus and a deficiency in milk ejection reflex, which of the following scenarios BEST explains the potential underlying pathophysiology, considering the anatomical relationship between the hypothalamus and the pituitary gland?
If a patient presents with symptoms indicative of both diabetes insipidus and a deficiency in milk ejection reflex, which of the following scenarios BEST explains the potential underlying pathophysiology, considering the anatomical relationship between the hypothalamus and the pituitary gland?
Following chronic administration of an exogenous glucocorticoid, such as dexamethasone, what intricate sequence of events would predictably occur within the hypothalamic-pituitary-adrenal (HPA) axis, considering both short-loop and long-loop feedback mechanisms, and how would this manifest in the circulating levels of relevant hormones?
Following chronic administration of an exogenous glucocorticoid, such as dexamethasone, what intricate sequence of events would predictably occur within the hypothalamic-pituitary-adrenal (HPA) axis, considering both short-loop and long-loop feedback mechanisms, and how would this manifest in the circulating levels of relevant hormones?
A patient presents with chronic hyponatremia, exhibiting symptoms of muscle weakness and neurological deficits. Endocrine evaluation reveals suppressed aldosterone levels despite elevated plasma renin activity. Further investigation uncovers a mutation affecting the mineralocorticoid receptor's interaction with heat shock proteins. Which of the following best describes the most likely underlying pathophysiological mechanism?
A patient presents with chronic hyponatremia, exhibiting symptoms of muscle weakness and neurological deficits. Endocrine evaluation reveals suppressed aldosterone levels despite elevated plasma renin activity. Further investigation uncovers a mutation affecting the mineralocorticoid receptor's interaction with heat shock proteins. Which of the following best describes the most likely underlying pathophysiological mechanism?
A researcher is investigating the effects of a novel synthetic analog of growth hormone-releasing hormone (GHRH) on somatotrope activity in vitro. Initial experiments demonstrate a significant increase in intracellular cAMP levels and subsequent GH secretion. However, prolonged exposure leads to a paradoxical reduction in GH responsiveness. Which of the following mechanisms most accurately explains this desensitization phenomenon?
A researcher is investigating the effects of a novel synthetic analog of growth hormone-releasing hormone (GHRH) on somatotrope activity in vitro. Initial experiments demonstrate a significant increase in intracellular cAMP levels and subsequent GH secretion. However, prolonged exposure leads to a paradoxical reduction in GH responsiveness. Which of the following mechanisms most accurately explains this desensitization phenomenon?
A 35-year-old female presents with galactorrhea and amenorrhea. Her prolactin levels are markedly elevated, but a pituitary MRI is unremarkable. Further endocrine testing reveals normal TSH and FSH levels. However, dynamic testing with a dopamine agonist fails to suppress prolactin secretion, and the patient reports chronic use of a centrally-acting antiemetic. Which of the following mechanisms best accounts for the observed hyperprolactinemia?
A 35-year-old female presents with galactorrhea and amenorrhea. Her prolactin levels are markedly elevated, but a pituitary MRI is unremarkable. Further endocrine testing reveals normal TSH and FSH levels. However, dynamic testing with a dopamine agonist fails to suppress prolactin secretion, and the patient reports chronic use of a centrally-acting antiemetic. Which of the following mechanisms best accounts for the observed hyperprolactinemia?
A researcher is studying the molecular mechanisms of thyroid hormone action in a cell line lacking a functional thyroid hormone receptor (TR). Introduction of a plasmid expressing a chimeric protein consisting of the DNA-binding domain of a yeast transcription factor fused to the ligand-binding domain of TRα1 restores T3-dependent gene expression. However, mutation of a specific lysine residue within the TRα1 ligand-binding domain abolishes this effect. This lysine residue is most likely involved in which of the following processes?
A researcher is studying the molecular mechanisms of thyroid hormone action in a cell line lacking a functional thyroid hormone receptor (TR). Introduction of a plasmid expressing a chimeric protein consisting of the DNA-binding domain of a yeast transcription factor fused to the ligand-binding domain of TRα1 restores T3-dependent gene expression. However, mutation of a specific lysine residue within the TRα1 ligand-binding domain abolishes this effect. This lysine residue is most likely involved in which of the following processes?
A patient with a history of hypoparathyroidism secondary to thyroidectomy presents with recurrent episodes of muscle cramps, tetany, and seizures. Despite adequate calcium and vitamin D supplementation, his serum calcium levels remain consistently low. Further investigation reveals significantly decreased renal expression of the calcium-sensing receptor (CaSR). Which of the following best explains the observed resistance to PTH?
A patient with a history of hypoparathyroidism secondary to thyroidectomy presents with recurrent episodes of muscle cramps, tetany, and seizures. Despite adequate calcium and vitamin D supplementation, his serum calcium levels remain consistently low. Further investigation reveals significantly decreased renal expression of the calcium-sensing receptor (CaSR). Which of the following best explains the observed resistance to PTH?
A researcher is investigating the effects of chronic exposure to a novel endocrine-disrupting chemical (EDC) on pancreatic beta-cell function. In vitro studies demonstrate that EDC exposure leads to impaired glucose-stimulated insulin secretion (GSIS) despite normal insulin content. Further analysis reveals decreased expression of the glucose transporter GLUT2 and reduced activity of glucokinase. Which of the following mechanisms most likely underlies the EDC-induced beta-cell dysfunction?
A researcher is investigating the effects of chronic exposure to a novel endocrine-disrupting chemical (EDC) on pancreatic beta-cell function. In vitro studies demonstrate that EDC exposure leads to impaired glucose-stimulated insulin secretion (GSIS) despite normal insulin content. Further analysis reveals decreased expression of the glucose transporter GLUT2 and reduced activity of glucokinase. Which of the following mechanisms most likely underlies the EDC-induced beta-cell dysfunction?
A patient with longstanding type 1 diabetes mellitus develops gastroparesis and erratic glucose absorption, leading to unpredictable fluctuations in blood glucose levels. To mitigate these challenges, the endocrinologist considers prescribing pramlintide, a synthetic analog of amylin. Which of the following mechanisms of action of pramlintide is MOST relevant in addressing the specific challenges presented by this patient's condition?
A patient with longstanding type 1 diabetes mellitus develops gastroparesis and erratic glucose absorption, leading to unpredictable fluctuations in blood glucose levels. To mitigate these challenges, the endocrinologist considers prescribing pramlintide, a synthetic analog of amylin. Which of the following mechanisms of action of pramlintide is MOST relevant in addressing the specific challenges presented by this patient's condition?
A researcher is studying the effects of a novel synthetic glucocorticoid on immune cell function. The compound exhibits potent anti-inflammatory activity in vitro but displays minimal binding affinity for the canonical glucocorticoid receptor (GR). Further investigation reveals that the compound inhibits NF-κB signaling by directly binding to and activating cytosolic phospholipase A2 (cPLA2). Which of the following downstream mechanisms is most likely responsible for the observed anti-inflammatory effects?
A researcher is studying the effects of a novel synthetic glucocorticoid on immune cell function. The compound exhibits potent anti-inflammatory activity in vitro but displays minimal binding affinity for the canonical glucocorticoid receptor (GR). Further investigation reveals that the compound inhibits NF-κB signaling by directly binding to and activating cytosolic phospholipase A2 (cPLA2). Which of the following downstream mechanisms is most likely responsible for the observed anti-inflammatory effects?
A 28-year-old female presents with primary ovarian insufficiency (POI). Genetic testing reveals a heterozygous mutation in the gene encoding follicle-stimulating hormone receptor (FSHR). In vitro studies demonstrate that the mutant receptor exhibits constitutive activity in the absence of FSH binding. Which of the following mechanisms is MOST likely to contribute to the pathogenesis of POI in this patient?
A 28-year-old female presents with primary ovarian insufficiency (POI). Genetic testing reveals a heterozygous mutation in the gene encoding follicle-stimulating hormone receptor (FSHR). In vitro studies demonstrate that the mutant receptor exhibits constitutive activity in the absence of FSH binding. Which of the following mechanisms is MOST likely to contribute to the pathogenesis of POI in this patient?
In a clinical trial evaluating a novel therapeutic agent for osteoporosis, researchers observe that the drug paradoxically increases bone mineral density (BMD) in the spine but decreases BMD in the hip. Further investigation reveals that the drug acts as a selective estrogen receptor modulator (SERM) with tissue-specific effects on estrogen receptor (ER) conformation and co-regulator recruitment. Which of the following best describes the most likely mechanism underlying the observed regional differences in BMD?
In a clinical trial evaluating a novel therapeutic agent for osteoporosis, researchers observe that the drug paradoxically increases bone mineral density (BMD) in the spine but decreases BMD in the hip. Further investigation reveals that the drug acts as a selective estrogen receptor modulator (SERM) with tissue-specific effects on estrogen receptor (ER) conformation and co-regulator recruitment. Which of the following best describes the most likely mechanism underlying the observed regional differences in BMD?
A researcher is studying the effects of chronic stress on adrenal gland function in a rodent model. Animals subjected to unpredictable chronic mild stress (UCMS) exhibit elevated plasma corticosterone levels and adrenal hypertrophy. Microarray analysis of adrenal tissue reveals increased expression of the gene encoding steroid 11β-hydroxylase (CYP11B1), the enzyme responsible for the final step in corticosterone synthesis. Which of the following transcription factors is MOST likely involved in mediating the stress-induced upregulation of CYP11B1 expression.
A researcher is studying the effects of chronic stress on adrenal gland function in a rodent model. Animals subjected to unpredictable chronic mild stress (UCMS) exhibit elevated plasma corticosterone levels and adrenal hypertrophy. Microarray analysis of adrenal tissue reveals increased expression of the gene encoding steroid 11β-hydroxylase (CYP11B1), the enzyme responsible for the final step in corticosterone synthesis. Which of the following transcription factors is MOST likely involved in mediating the stress-induced upregulation of CYP11B1 expression.
A patient presents with symptoms suggestive of Cushing's syndrome. Initial testing reveals elevated levels of cortisol, but an overnight dexamethasone suppression test fails to suppress cortisol secretion. Further investigation reveals elevated levels of adrenocorticotropic hormone (ACTH). However, a high-dose dexamethasone suppression test also fails to suppress cortisol secretion. A CRH stimulation test results in a significant increase in both ACTH and cortisol levels. Which of the following is the MOST likely underlying etiology?
A patient presents with symptoms suggestive of Cushing's syndrome. Initial testing reveals elevated levels of cortisol, but an overnight dexamethasone suppression test fails to suppress cortisol secretion. Further investigation reveals elevated levels of adrenocorticotropic hormone (ACTH). However, a high-dose dexamethasone suppression test also fails to suppress cortisol secretion. A CRH stimulation test results in a significant increase in both ACTH and cortisol levels. Which of the following is the MOST likely underlying etiology?
A researcher is investigating the molecular mechanisms underlying the synergistic effects of glucocorticoids and beta-adrenergic agonists on the induction of surfactant protein A (SP-A) gene expression in fetal lung cells. Experiments demonstrate that both agents independently increase SP-A mRNA levels, but their combined effect is significantly greater than the sum of their individual effects. Further analysis reveals that glucocorticoid receptor (GR) and beta-adrenergic receptor (βAR) activation leads to enhanced recruitment of the transcriptional co-activator CREB-binding protein (CBP) to the SP-A promoter. Which of the following best describes the most likely mechanism underlying this synergistic effect?
A researcher is investigating the molecular mechanisms underlying the synergistic effects of glucocorticoids and beta-adrenergic agonists on the induction of surfactant protein A (SP-A) gene expression in fetal lung cells. Experiments demonstrate that both agents independently increase SP-A mRNA levels, but their combined effect is significantly greater than the sum of their individual effects. Further analysis reveals that glucocorticoid receptor (GR) and beta-adrenergic receptor (βAR) activation leads to enhanced recruitment of the transcriptional co-activator CREB-binding protein (CBP) to the SP-A promoter. Which of the following best describes the most likely mechanism underlying this synergistic effect?
A 60-year-old male with a history of type 2 diabetes mellitus and chronic kidney disease presents with fatigue, muscle weakness, and cardiac arrhythmias. Laboratory investigations reveal hyperkalemia, metabolic acidosis, and elevated levels of aldosterone and renin. However, administration of exogenous angiotensin II fails to stimulate aldosterone secretion. Further evaluation reveals the presence of an inactivating mutation in the gene encoding ROMK (renal outer medullary potassium channel) in the distal nephron. Which of the following best explains the underlying pathophysiology?
A 60-year-old male with a history of type 2 diabetes mellitus and chronic kidney disease presents with fatigue, muscle weakness, and cardiac arrhythmias. Laboratory investigations reveal hyperkalemia, metabolic acidosis, and elevated levels of aldosterone and renin. However, administration of exogenous angiotensin II fails to stimulate aldosterone secretion. Further evaluation reveals the presence of an inactivating mutation in the gene encoding ROMK (renal outer medullary potassium channel) in the distal nephron. Which of the following best explains the underlying pathophysiology?
A researcher is investigating the role of microRNAs (miRNAs) in the regulation of insulin secretion from pancreatic beta-cells. In vitro studies reveal that a specific miRNA, miR-124a, is highly expressed in beta-cells and negatively regulates insulin secretion. Further analysis identifies that miR-124a directly targets and downregulates the expression of a key protein involved in exocytosis of insulin granules. Which of the following proteins is MOST likely targeted by miR-124a?
A researcher is investigating the role of microRNAs (miRNAs) in the regulation of insulin secretion from pancreatic beta-cells. In vitro studies reveal that a specific miRNA, miR-124a, is highly expressed in beta-cells and negatively regulates insulin secretion. Further analysis identifies that miR-124a directly targets and downregulates the expression of a key protein involved in exocytosis of insulin granules. Which of the following proteins is MOST likely targeted by miR-124a?
Flashcards
Endocrine System
Endocrine System
A major regulatory system that maintains body functions and homeostasis through hormone secretion.
Hormones
Hormones
Chemical messengers secreted by glands that regulate various body functions.
Negative Feedback
Negative Feedback
A mechanism where the effects of a hormone decrease its secretion to maintain balance.
Pituitary Gland
Pituitary Gland
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Posterior Pituitary Gland
Posterior Pituitary Gland
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Two-messenger mechanism
Two-messenger mechanism
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Cyclic AMP
Cyclic AMP
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Hormone receptors
Hormone receptors
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Steroid hormones
Steroid hormones
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Protein synthesis activation
Protein synthesis activation
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Antidiuretic Hormone (ADH)
Antidiuretic Hormone (ADH)
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Oxytocin
Oxytocin
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Growth Hormone (GH)
Growth Hormone (GH)
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Thyroid-Stimulating Hormone (TSH)
Thyroid-Stimulating Hormone (TSH)
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Prolactin
Prolactin
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Follicle Stimulating Hormone (FSH)
Follicle Stimulating Hormone (FSH)
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Luteinizing Hormone (LH)
Luteinizing Hormone (LH)
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Thyroxine (T4) and Triiodothyronine (T3)
Thyroxine (T4) and Triiodothyronine (T3)
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Calcitonin
Calcitonin
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Parathyroid Hormone (PTH)
Parathyroid Hormone (PTH)
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Insulin
Insulin
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Glucagon
Glucagon
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Epinephrine
Epinephrine
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Cortisol
Cortisol
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Study Notes
Endocrine System Overview
- The endocrine system is a major regulating system for homeostasis and body function
- Endocrine glands are ductless, meaning they secrete hormones directly into the bloodstream
- Hormones are chemical messengers that travel throughout the body and influence various organs and tissues
- Hormone types include amines, proteins, and steroids
- Key hormones include thyroxine, epinephrine, norepinephrine, insulin, growth hormone, calcitonin, antidiuretic hormone, oxytocin, cortisol, aldosterone, estrogen, progesterone, and testosterone.
Endocrine Glands
- Pituitary gland (hypophysis): Located at the base of the brain and has anterior and posterior parts. It plays a critical role in regulating several body functions.
- Anterior pituitary (adenohypophysis): Produces hormones such as growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), prolactin, follicle-stimulating hormone (FSH), and luteinizing hormone (LH).
- Posterior pituitary (neurohypophysis): Stores and releases hormones produced by the hypothalamus, including antidiuretic hormone (ADH) and oxytocin.
- Thyroid gland: Located in the neck, produces thyroxine (T4) and triiodothyronine (T3) which are crucial for metabolic rate and growth, also produces calcitonin.
- Parathyroid glands: Four small glands located behind the thyroid gland, that produce parathyroid hormone (PTH), which regulates calcium and phosphorus levels in the body.
- Adrenal glands: Located on top of each kidney, these glands have two parts:
- Adrenal medulla: Produces epinephrine and norepinephrine (catecholamines), involved in the body's "fight-or-flight" response.
- Adrenal cortex: Produces steroid hormones, including mineralocorticoids (e.g., aldosterone), which regulate mineral balance, glucocorticoids (e.g., cortisol), which affect carbohydrate metabolism, and sex hormones (e.g., estrogen and androgens).
- Pancreas: Located in the abdomen, contains islets of Langerhans with alpha and beta cells.
- Alpha cells: Produce glucagon, which raises blood glucose levels.
- Beta cells: Produce insulin, which lowers blood glucose levels.
Hormone Secretion Regulation
- Hormone secretion is primarily regulated by negative feedback mechanisms
- Changes in the concentration of a hormone or other relevant substance (e.g., blood glucose or calcium levels) trigger feedback to the endocrine gland, influencing the amount of hormone released.
Hormone Action Mechanisms
- Two-messenger mechanism: Protein hormones bind to membrane receptors, triggering a cascade that results in the production of secondary messengers (e.g., cyclic AMP), which initiate cellular responses.
- Steroid hormone mechanism: Steroid hormones diffuse across cell membranes and bind to intracellular receptors, influencing gene expression and cellular activity.
Posterior Pituitary Hormones
- Antidiuretic hormone (ADH): Also known as vasopressin, ADH increases water reabsorption in the kidneys, regulating blood pressure and blood volume.
- Oxytocin: Oxytocin stimulates uterine contractions during childbirth and milk ejection during breastfeeding.
Anterior Pituitary Hormones
- Growth hormone (GH): Promotes growth and development, influences protein synthesis and metabolism.
- Thyroid-stimulating hormone (TSH): Stimulates the thyroid gland to produce thyroxine and triiodothyronine, influencing metabolic rate.
- Adrenocorticotropic hormone (ACTH): Stimulates the adrenal cortex to produce cortisol, which regulates stress response and metabolism.
- Prolactin: Promotes milk production in mammary glands, influenced by hormonal feedback and stimuli.
- Follicle-stimulating hormone (FSH): Supports egg development in females and sperm production in males.
- Luteinizing hormone (LH): Triggers ovulation in females and testosterone production in males.
Other Hormones (by organ)
- Thyroid: Calcitonin regulates calcium and phosphate balance in the blood.
- Pancreas: Glucagon & Insulin regulate blood sugar levels through glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (formation of glucose from non-carbohydrate sources), respectively.
- Ovaries: Estrogen & Progesterone: Involved in reproduction, secondary sex characteristics, and maintenance of the uterine lining.
- Testes: Testosterone: Involved in male reproduction, secondary sex characteristics, and muscle development.
- Adrenal Cortex: Additional steroid hormones, like aldosterone, regulate mineral balance and cortisol for stress response.
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Description
Questions cover cellular mechanisms of hormone action, including cAMP, receptor binding, PKA activity, and adenylyl cyclase. They address scenarios with compromised cellular function and novel hormone analogs to understand the signal transduction pathways involved.