Advanced Endocrine System and Hormonal Regulation Quiz

1. How do Insulin and C-Peptide levels vary with Exogenous insulin use (such as a bodybuilder trying to bulk up) versus Insulinoma and Sulfonylurea use?

Exogenous insulin use will have no effect on C-peptide levels.

Insulin and C-Peptide levels will decrease with Insulinoma and Sulfonylurea use.

Insulin and C-Peptide levels will increase with Exogenous insulin use.

2. In which organelles does cleavage of proinsulin into insulin happen and how does insulin leave the cell?

Golgi Apparatus

Peroxisomes

Lysosomes

Insulin is cleaved from proinsulin inside the secretory granules, not in lysosomes, peroxisomes, or the Golgi Apparatus. Additionally, insulin leaves the cell through exocytosis, a process where secretory granules containing insulin fuse with the plasma membrane to release insulin outside the cell.

Explanation

Insulin is cleaved from proinsulin inside the secretory granules, not in lysosomes, peroxisomes, or the Golgi Apparatus. Additionally, insulin leaves the cell through exocytosis, a process where secretory granules containing insulin fuse with the plasma membrane to release insulin outside the cell.

3. What are the structures of PREPROinsulin, PROinsulin, and insulin, and in which organelle is PREPROinsulin synthesized?

PROinsulin contains C-peptide while insulin does not.

PREPROinsulin contains only alpha and beta chains, no C-peptide.

PREPROinsulin is synthesized in the smooth endoplasmic reticulum.

Understanding the structures of PREPROinsulin, PROinsulin, and insulin, along with the organelle in which PREPROinsulin is synthesized, is crucial in differentiating between the three forms of insulin synthesis and maturation.

Explanation

Understanding the structures of PREPROinsulin, PROinsulin, and insulin, along with the organelle in which PREPROinsulin is synthesized, is crucial in differentiating between the three forms of insulin synthesis and maturation.

4. Is the bidirectional GLUT 2 transporter on B-islets of the endocrine pancreas insulin dependent or independent?

GLUT 2 transporter is dependent on insulin for its function.

GLUT 2 transporter is only found in the liver.

GLUT 2 transporter is unidirectional and only transports glucose out of cells.

The correct answer explains that the bidirectional GLUT 2 transporter is insulin independent and found in various locations including B-islets of the pancreas, small intestine, liver, and kidney.

Explanation

The correct answer explains that the bidirectional GLUT 2 transporter is insulin independent and found in various locations including B-islets of the pancreas, small intestine, liver, and kidney.

5. Which GLUT transporter is responsible for transporting Glucose vs Fructose in GI tract and which one is Insulin dependent?

GLUT4 for Glucose and GLUT1 for Fructose, both are Glucagon dependent

GLUT2 for Fructose and GLUT5 for Glucose, both are Insulin dependent

GLUT1 for Glucose and GLUT4 for Fructose, both are Insulin dependent

In the GI tract, GLUT2 is responsible for transporting Glucose while GLUT5 is responsible for transporting Fructose. Neither of these transporters are Insulin dependent. The mnemonic 'FivE for FructosE' can be used to remember the correct transporter for Fructose.

Explanation

In the GI tract, GLUT2 is responsible for transporting Glucose while GLUT5 is responsible for transporting Fructose. Neither of these transporters are Insulin dependent. The mnemonic 'FivE for FructosE' can be used to remember the correct transporter for Fructose.

6. What is the main source of energy and transporter for spermatocyte?

Sucrose and through GLUT2

*FRUCTOSE(Not glucose) and trough GLUT5.

Glucose and through GLUT4

Lactose and through SGLT1

Spermatocytes utilize fructose as their main source of energy and transporter through GLUT5, not glucose or other sugars with different transporters.

Explanation

Spermatocytes utilize fructose as their main source of energy and transporter through GLUT5, not glucose or other sugars with different transporters.

7. Which Glucose transporters are expressed in BRAIN and PLACENTA? are they insulin-dependent/independent?

GLUT2 and GLUT4 are both Insulin-Dependent and are present in BRAIN and PLACENTA.

GLUT1 and GLUT2 are both Insulin-Independent and are present in LIVER and MUSCLE.

GLUT4 and GLUT5 are both Insulin-Independent and are present in FAT and INTESTINES.

GLUT1 and GLUT3 are known to be highly expressed in the BRAIN and PLACENTA, functioning as Insulin-Independent glucose transporters with high affinity and capacity. The other incorrect options do not accurately describe the expression and insulin dependency of glucose transporters in these specific locations.

Explanation

GLUT1 and GLUT3 are known to be highly expressed in the BRAIN and PLACENTA, functioning as Insulin-Independent glucose transporters with high affinity and capacity. The other incorrect options do not accurately describe the expression and insulin dependency of glucose transporters in these specific locations.

8. How does increased insulin affect Na excretion in the kidneys?

Has no effect on Na excretion in the kidneys.

Increases it by promoting Na excretion in the urine.

*DECREASES it by causing increased reabsorption>Na Retention.

Increases it by inhibiting Na reabsorption in the kidneys.

Insulin plays a role in regulating sodium excretion in the kidneys by promoting the reabsorption of sodium, leading to decreased Na excretion and Na retention in the body.

Explanation

Insulin plays a role in regulating sodium excretion in the kidneys by promoting the reabsorption of sodium, leading to decreased Na excretion and Na retention in the body.

9. Which substance can cross the placenta: Glucose or Insulin? How can this be tested?

Neither Glucose nor Insulin

Insulin

Both Glucose and Insulin

When the mother injects insulin, it indirectly affects the glucose levels in the fetus by decreasing the glucose available in the mother's blood. This demonstrates that glucose can cross the placenta, but insulin cannot.

Explanation

When the mother injects insulin, it indirectly affects the glucose levels in the fetus by decreasing the glucose available in the mother's blood. This demonstrates that glucose can cross the placenta, but insulin cannot.

10. Why is insulin spike greater with Oral glucose when compared with IV glucose?

*Oral glucose triggers a faster response from the pancreas leading to higher insulin release.

*IV glucose bypasses the liver, where a large portion of insulin is normally degraded.

*So you should know that GIP and GLP-1 are Incretins(Hormones secreted by ENTEROendocrine cells)

*Insulin is absorbed more efficiently through the digestive system.

When glucose is taken orally, GIP and GLP-1 are released, stimulating insulin secretion more effectively than IV glucose which does not activate the incretin response.

Explanation

When glucose is taken orally, GIP and GLP-1 are released, stimulating insulin secretion more effectively than IV glucose which does not activate the incretin response.

11. Which glucose transporter is the SLOWEST at LOW glucose concentrations?

*GLUT-2.

GLUT-3

GLUT-1

GLUT-4

GLUT-2 has a low affinity for glucose, so it operates at slower rates when glucose concentrations are low compared to other glucose transporters.

Explanation

GLUT-2 has a low affinity for glucose, so it operates at slower rates when glucose concentrations are low compared to other glucose transporters.

12. How does insulin promote uptake of glucose into the cells?

Insulin acts by directly converting glucose into energy within the cells.

Insulin promotes breakdown of glycogen in the liver, leading to increased blood glucose levels.

Insulin inhibits glucose uptake into the cells by blocking the GLUT4 transporter.

Insulin promotes glucose uptake into cells by increasing the activity of specific pathways that lead to increased synthesis of proteins, lipids, glycogen, and GLUT4 transporter. It also stimulates cell growth and DNA synthesis through the RAS/MAP kinase pathway.

Explanation

Insulin promotes glucose uptake into cells by increasing the activity of specific pathways that lead to increased synthesis of proteins, lipids, glycogen, and GLUT4 transporter. It also stimulates cell growth and DNA synthesis through the RAS/MAP kinase pathway.

13. How does increased intracellular glucose lead to insulin release from B-islets of pancreas?

Through gluconeogenesis, intracellular glucose binds directly to insulin receptors on the B-islets of pancreas, triggering insulin release.

Through the activation of lipogenesis, intracellular glucose generates a signal that prompts the secretion of insulin from B-islets of pancreas.

By inhibiting the production of glucagon, intracellular glucose indirectly stimulates insulin release from B-islets of pancreas.

The correct process of how increased intracellular glucose leads to insulin release involves glycolysis, ATP levels, potassium channels, cell depolarization, calcium channels, and exocytosis of insulin-containing granules.

Explanation

The correct process of how increased intracellular glucose leads to insulin release involves glycolysis, ATP levels, potassium channels, cell depolarization, calcium channels, and exocytosis of insulin-containing granules.

14. Effects of Alpha 2 receptor activation vs B2 receptor activation on insulin release?

Alpha 2 activation INCREASES insulin release vs B2 activation DECREASES insulin release.

Alpha 2 activation DECREASES insulin release vs B2 activation DECREASES insulin release.

Alpha 2 activation INCREASES insulin release vs B2 activation also INCREASES insulin release.

Normally insulin is anabolic and decreases lipolysis. Alpha 2 activation leads to decreased insulin release and decreased lipolysis, whereas B2 activation leads to increased insulin release and increased lipolysis. Remember the direction of insulin release to predict the direction of lipolysis.

Explanation

Normally insulin is anabolic and decreases lipolysis. Alpha 2 activation leads to decreased insulin release and decreased lipolysis, whereas B2 activation leads to increased insulin release and increased lipolysis. Remember the direction of insulin release to predict the direction of lipolysis.

15. Which hormone increases production in fasting state and what effects will it have on gluconeogenesis, glycogenolysis, and lipolysis?

Epinephrine increases production in fasting state but only affects lipolysis and glycogenolysis, not gluconeogenesis.

Cortisol increases production in fasting state and primarily affects gluconeogenesis and lipolysis, but not glycogenolysis.

Insulin decreases production in fasting state and inhibits gluconeogenesis, glycogenolysis, and lipolysis.

16. How does physiology explain the development of GALACTORRHEA in a patient with HYPOthyroidism?

Hypothyroidism increases TSH levels, resulting in GALACTORRHEA through a separate pathway.

Hypothyroidism has no effect on Prolactin levels and therefore cannot cause GALACTORRHEA.

Hypothyroidism causes a decrease in Prolactin levels, leading to GALACTORRHEA.

17. Which hormones are Trophic? Those released from acidophils or basophils of pituitary?

ACTH and TSH are secreted by acidophils and are Trophic hormones

FSH and LH are secreted by acidophils and not Trophic hormones

GH and Prolactin are secreted by BASOPHILS and are Trophic hormones

Trophic hormones regulate the secretion of other hormones, while non-trophic hormones act directly on end-organs.

Explanation

Trophic hormones regulate the secretion of other hormones, while non-trophic hormones act directly on end-organs.

18. Why can some antipsychotics cause sexual dysfunction/amenorrhea?

Because they act on the thyroid gland, causing hormonal imbalances that affect sexual function and menstruation.

Because they increase dopamine levels, which directly affect sexual function and menstrual cycles.

Because they stimulate the release of GnRH, leading to an imbalance of sex hormones.

Antipsychotics can cause sexual dysfunction/amenorrhea by blocking dopamine, which normally inhibits prolactin release. This leads to hyperprolactinemia, resulting in decreased sex steroids and potential side effects like sexual dysfunction and amenorrhea.

Explanation

Antipsychotics can cause sexual dysfunction/amenorrhea by blocking dopamine, which normally inhibits prolactin release. This leads to hyperprolactinemia, resulting in decreased sex steroids and potential side effects like sexual dysfunction and amenorrhea.

19. What hormone levels can be expected with exogenous steroid use?

Suppressed CRF release, leading to suppressed release of cortisol, aldosterone, and epinephrine.

Increased CRF release, leading to increased release of ACTH, B-endorphin, and MSH.

Suppressed CRF release, leading to increased release of ACTH, B-endorphin, and MSH.

*Remember EXOgenous Steroids>Supressed CRF release>Supressed release of ACTH,B-endorphin,MSH.Normally CRF is released during stress and stimulates release of ACTH,B-endorphin,MSH.

Exogenous steroid use suppresses the release of CRF, which in turn suppresses the release of ACTH, B-endorphin, and MSH. This leads to a downregulation of the hypothalamic-pituitary-adrenal (HPA) axis activity.

Explanation

Exogenous steroid use suppresses the release of CRF, which in turn suppresses the release of ACTH, B-endorphin, and MSH. This leads to a downregulation of the hypothalamic-pituitary-adrenal (HPA) axis activity.

20. What hormonal increase could cause deficiency of GH?

Decrease in FSH

Decrease in GHRH

Increase in GNRH

Increase in SOMATOSTATIN can lead to deficiencies in GH levels, as it stops the production of many hormones including GH. GHRH is actually responsible for the release of GH, so a decrease in GHRH can cause a deficiency in GH. GNRH is involved in the release of gonadotropins, not GH. FSH is a gonadotropin hormone and not directly related to GH production.

Explanation

Increase in SOMATOSTATIN can lead to deficiencies in GH levels, as it stops the production of many hormones including GH. GHRH is actually responsible for the release of GH, so a decrease in GHRH can cause a deficiency in GH. GNRH is involved in the release of gonadotropins, not GH. FSH is a gonadotropin hormone and not directly related to GH production.

21. Patient with HIV develops LIPODYSTROPHY as a side effect of protease inhibitors, Tesamorelin was given to patient for treatment. Tesamorelin is an analog of a hormone released from where and in response to what?

Tesamorelin is a Thyroid Stimulating Hormone analog.

*Tesamorelin is Growth Hormone RELEASING HORMONE(NOT GH analog) analog.

Tesamorelin is a direct analog of Growth Hormone.

Tesamorelin is a Cortisol releasing hormone analog.

22. What are the effects of growth hormone (GH) on bone in children versus adults, and through which process does it increase muscle mass?

In children, GH promotes bone mineralization, while in adults it decreases bone density. Muscle mass is increased through hypertonicity.

Growth hormone (GH) has different effects on bone in children versus adults, with children experiencing linear growth and adults experiencing lateral growth or thickening of bones. Muscle mass is increased through hypertrophy, not hyperplasia. GH primarily acts through IGF1, secreted from the liver, to mediate its effects.

Explanation

Growth hormone (GH) has different effects on bone in children versus adults, with children experiencing linear growth and adults experiencing lateral growth or thickening of bones. Muscle mass is increased through hypertrophy, not hyperplasia. GH primarily acts through IGF1, secreted from the liver, to mediate its effects.

23. What are the effects of GH on Glycogenolysis, Gluconeogenesis, and Lipolysis? What are the stimuli for GH secretion and inhibitors? Why is GH considered diabetogenic?

GH has no effect on Glycogenolysis, Gluconeogenesis, and Lipolysis. GH secretion is only stimulated by puberty.

GH only promotes Lipolysis but not Glycogenolysis or Gluconeogenesis. GH secretion is inhibited by deep sleep and amino acids.

GH decreases Glycogenolysis, Gluconeogenesis, and Lipolysis. GH secretion is stimulated by simple sugars (glucose) and inhibited by exercise.

GH is known to have catabolic effects on glycogenolysis, gluconeogenesis, and lipolysis, despite being an anabolic hormone. This can be confusing but it is a key concept in understanding the hormone's physiological actions.

Explanation

GH is known to have catabolic effects on glycogenolysis, gluconeogenesis, and lipolysis, despite being an anabolic hormone. This can be confusing but it is a key concept in understanding the hormone's physiological actions.

24. Why does lack of sleep promote weight gain?

Lack of sleep has no effect on hormones related to hunger or satiety.

Lack of sleep increases metabolism, leading to weight gain.

Lack of sleep causes a decrease in appetite, resulting in less food intake.

The correct answer explains how lack of sleep affects hormones related to hunger and satiety, ultimately leading to weight gain.

Explanation

The correct answer explains how lack of sleep affects hormones related to hunger and satiety, ultimately leading to weight gain.

25. How does Gherlin increase the release of GH Hormone?

A) Gherlin inhibits the release of GH by binding directly to pituitary gland receptors.

C) Gherlin increases the release of GH by interacting with the thyroid gland receptors.

B) Gherlin stimulates the release of GH by acting on the adrenal cortex.

*Gherlin promotes release of GH by activatingG-protein coupled receptor known as GH secretagog receptor.

Gherlin promotes the release of GH by activating the GH secretagog receptor, not by inhibiting release or by acting on other glands. This receptor activation leads to increased GH secretion.

Explanation

Gherlin promotes the release of GH by activating the GH secretagog receptor, not by inhibiting release or by acting on other glands. This receptor activation leads to increased GH secretion.

26. What can cause obesity and hypogonadism in a child who fights with other children for food?

Genetic predisposition to being overweight and lack of physical activity

High levels of physical activity and a healthy diet

Emotional eating due to stress and anxiety

Obesity and hypogonadism in a child who is aggressive over food can be caused by specific hormonal imbalances and genetic conditions, rather than general factors like lack of physical activity or emotional eating.

Explanation

Obesity and hypogonadism in a child who is aggressive over food can be caused by specific hormonal imbalances and genetic conditions, rather than general factors like lack of physical activity or emotional eating.