Lab 4: Endocrine System, Hormonal Pathways, and Disorders

1. Major Structures and Functions of the Endocrine System

• The endocrine system consists of glands and organs that secrete hormones to regulate various physiological processes.

• Major glands include:

  • Hypothalamus: Links the nervous and endocrine systems; releases hormones that regulate the pituitary.

  • Pituitary Gland: Often called the "master gland," it releases hormones that control other endocrine glands (e.g., thyroid, adrenal, gonads).

  • Thyroid Gland: Regulates metabolism through the secretion of thyroid hormones (T3, T4).

  • Adrenal Glands: Release hormones like cortisol, aldosterone, and adrenaline to manage stress, metabolism, and sodium balance.

  • Pancreas: Regulates blood glucose through insulin and glucagon.

  • Gonads (Testes and Ovaries): Produce sex hormones (testosterone, estrogen, progesterone) responsible for reproduction and secondary sexual characteristics.

2. Roles of Negative and Positive Feedback in Hormone Release and Homeostasis

• Negative feedback: A process where the release of a hormone is inhibited by its own action or by a product of the pathway (e.g., the hypothalamic-pituitary-thyroid axis). This maintains balance (homeostasis).

  • Example: Increased thyroid hormone (T3, T4) levels inhibit the release of TRH from the hypothalamus and TSH from the anterior pituitary, reducing thyroid hormone production.

• Positive feedback: A mechanism where the release of a hormone stimulates further release of that hormone, amplifying the response.

  • Example: During childbirth, oxytocin release increases uterine contractions, which further stimulate oxytocin release in a positive feedback loop.

3. Analyze Data and Identify Unknown Hormones Based on Their Effects in Virtual Rats

• Key concept: When studying the endocrine system in virtual or experimental models (like rats), it's important to analyze the effects of hormone changes on behaviors, metabolism, and organ function.

• Steps:

  1. Examine physiological responses (weight gain/loss, activity level, blood pressure, etc.).

  2. Identify patterns that match known effects of certain hormones (e.g., cortisol causes immune suppression, T3/T4 affect metabolism).

  3. Use control and experimental conditions to link the observed effects to specific hormonal imbalances.

4. Hormonal Disorders

• Addison's Disease:

  • Cause: Insufficient production of cortisol and sometimes aldosterone from the adrenal glands (often due to autoimmune destruction).

  • Symptoms: Fatigue, weight loss, hyperpigmentation of the skin, low blood pressure, salt cravings.

  • Treatment: Hormone replacement therapy (e.g., corticosteroids like hydrocortisone).

• Graves’ Disease:

  • Cause: Autoimmune disorder where the body produces antibodies that stimulate the thyroid gland to release excess thyroid hormones (hyperthyroidism).

  • Symptoms: Weight loss, hyperthermia (heat intolerance), anxiety, increased heart rate, bulging eyes (exophthalmos).

  • Treatment: Antithyroid medications (e.g., methimazole), radioactive iodine therapy, or thyroidectomy in severe cases.

5. HGT, HPA, and HPG Axis

• HGT Axis (Hypothalamic-Gonadal-Thyroid):

  • Hormones released:

    • Hypothalamus: TRH (Thyrotropin-releasing hormone).

    • Anterior Pituitary: TSH (Thyroid-stimulating hormone).

    • Thyroid: T3 (triiodothyronine) and T4 (thyroxine).

  • Physiological effects: Regulates metabolism, growth, and development.

  • Organ hypertrophy or atrophy: If TSH is chronically elevated, the anterior pituitary may hypertrophy (enlarge), while the thyroid may hypertrophy in response to constant stimulation.

  • Castration effects: Decreased levels of sex hormones will reduce gonadal size and function.

• HPA Axis (Hypothalamic-Pituitary-Adrenal):

  • Hormones released:

    • Hypothalamus: CRH (Corticotropin-releasing hormone).

    • Anterior Pituitary: ACTH (Adrenocorticotropic hormone).

    • Adrenal Glands: Cortisol, aldosterone.

  • Physiological effects: Cortisol regulates stress response, immune suppression, glucose metabolism, and inflammation.

  • Organ hypertrophy or atrophy: Chronic cortisol release can lead to adrenal hypertrophy; prolonged cortisol excess (e.g., in Cushing’s disease) can suppress the thymus gland, leading to immune suppression.

  • Castration effects: Castrated rats will have reduced gonadal hormone production, affecting stress regulation.

• HPG Axis (Hypothalamic-Pituitary-Gonadal):

  • Hormones released:

    • Hypothalamus: GnRH (Gonadotropin-releasing hormone).

    • Anterior Pituitary: LH (Luteinizing hormone) and FSH (Follicle-stimulating hormone).

    • Gonads: Testosterone (males), estrogen, and progesterone (females).

  • Physiological effects: Regulates reproductive function, secondary sexual characteristics, and gamete production.

  • Organ hypertrophy or atrophy: In castrated rats, gonads atrophy due to lack of stimulation by LH and FSH.

  • Castration effects: Loss of sex hormones, resulting in reduced reproductive and secondary sexual characteristics.

6. Role of Comparing Intact vs. Castrated Rats

• Intact rats have normal hormonal production and feedback regulation.

• Castrated rats are useful for studying the role of gonadal hormones in the HPG axis and understanding how the absence of these hormones affects physiology (e.g., behavior, secondary sexual characteristics, organ size).

• Comparison: Castration removes gonadal feedback and can result in hypertrophy of the pituitary or changes in other endocrine glands due to loss of negative feedback from sex hormones.

7. Mrs. Campbell’s Case Study: Molecular Mechanism of Symptoms

• Symptoms:

  • Weight loss: Likely due to hyperthyroidism (e.g., in Graves’ disease) or cortisol excess (e.g., in Cushing’s syndrome), both of which increase metabolism.

  • Hyperthermia: Excess thyroid hormone (T3/T4) increases metabolic rate, leading to heat intolerance.

  • Anxiety: May be linked to excess cortisol or thyroid hormones affecting the central nervous system.

  • Increased heart rate: Typically associated with hyperthyroidism, which increases the body's basal metabolic rate and heart rate.

• Molecular mechanism: Increased levels of thyroid hormones (T3/T4) or cortisol affect the hypothalamic-pituitary-thyroid axis or the HPA axis, leading to increased metabolism, heart rate, and nervous system activation.

Key Terms to Remember:

• Endocrine system: Glands and organs that secrete hormones.

• Negative feedback: Mechanism that maintains homeostasis by inhibiting further hormone release.

• Positive feedback: Amplifies hormone release in a cycle (e.g., childbirth, oxytocin).

• Addison's Disease: Adrenal insufficiency leading to low cortisol production.

• Graves’ Disease: Autoimmune disorder causing hyperthyroidism.

• HGT, HPA, and HPG Axes: Hormonal pathways controlling metabolism, stress response, and reproduction, respectively.

• Castration: Removal of gonads, affecting hormonal feedback and organ size.

• Symptoms of Mrs. Campbell’s case: Weight loss, hyperthermia, anxiety, and increased heart rate due to thyroid or adrenal dysfunction.

Review Questions:

1. How does the HPA axis regulate the stress response and metabolism?

2. What are the symptoms and treatment options for Addison’s disease?

3. How do feedback mechanisms influence the release of hormones in the endocrine system?

4. Describe the role of the HPG axis in regulating reproductive function.

5. What molecular mechanisms could explain symptoms like weight loss, hyperthermia, and anxiety in endocrine disorders?

Use this guide to deepen your understanding of the endocrine system and its regulation of various physiological processes!