Hormones

Jim Davis

24 Hormones

Learning Objectives

After reading this section you should be able to do the following-

Describe the stimulus for release of the hormone
Identify the gland or endocrine tissue/organ and the cells within that gland/tissue/organ that produce the hormone
Name the target tissue or cells for the hormone and describe the effect(s) of the hormone on the target tissue or cells
Predict the larger effect that fluctuations in the hormone level will have on conditions (variables) within the bod

Hormonal Regulation

In the intricate dance of physiological regulation within the human body, hormones act as messengers, orchestrating a symphony of responses to maintain homeostasis. Understanding the stimulus for hormone release, their origins, target tissues, and effects is pivotal in unraveling the complexities of human physiology. In this section, we delve into the mechanisms and roles of several crucial hormones.

Growth Hormone (GH)

Stimulus for Release: Growth hormone-releasing hormone (GHRH) from the hypothalamus triggers GH release, while somatostatin inhibits its release.

Gland/Endocrine Tissue: GH is primarily produced by somatotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: GH acts on various tissues, predominantly on bones and skeletal muscles. It stimulates linear growth in children, promoting longitudinal bone growth by stimulating chondrocyte proliferation in the epiphyseal plates. In adults, GH maintains bone density and muscle mass.

Predicted Effects of Fluctuations: Increased GH levels can lead to gigantism in children and acromegaly in adults, characterized by abnormal growth of bones and tissues. Decreased levels may result in growth retardation and decreased muscle mass.

Thyroid-Stimulating Hormone (TSH)

Stimulus for Release: Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates TSH release, while thyroid hormones (T3 and T4) inhibit it via negative feedback.

Gland/Endocrine Tissue: TSH is secreted by thyrotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: TSH acts on the thyroid gland, stimulating the synthesis and secretion of thyroxine (T4) and triiodothyronine (T3). These hormones regulate metabolic rate, growth, and development.

Predicted Effects of Fluctuations: Elevated TSH levels indicate hypothyroidism, leading to symptoms like fatigue, weight gain, and cold intolerance. Conversely, decreased TSH levels suggest hyperthyroidism, characterized by symptoms such as weight loss, heat intolerance, and palpitations.

Follicle-Stimulating Hormone (FSH)

Stimulus for Release: Gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates FSH release.

Gland/Endocrine Tissue: FSH is produced by gonadotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: In females, FSH acts on ovarian follicles, stimulating follicular growth and estrogen production. In males, it targets the seminiferous tubules of the testes, promoting spermatogenesis.

Predicted Effects of Fluctuations: Elevated FSH levels may indicate ovarian failure or menopause in females and testicular failure in males. Reduced levels may lead to infertility due to impaired gametogenesis.

Luteinizing Hormone (LH)

Stimulus for Release: GnRH from the hypothalamus triggers LH release.

Gland/Endocrine Tissue: LH is synthesized by gonadotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: In females, LH acts on the ovaries, inducing ovulation and corpus luteum formation. In males, it stimulates Leydig cells in the testes to produce testosterone.

Predicted Effects of Fluctuations: High LH levels in females can indicate polycystic ovary syndrome (PCOS), while low levels may signify hypothalamic dysfunction. In males, elevated LH levels may suggest primary testicular failure, whereas low levels may indicate hypogonadism.

Adrenocorticotropic Hormone (ACTH)

Stimulus for Release: Corticotropin-releasing hormone (CRH) from the hypothalamus stimulates ACTH release.

Gland/Endocrine Tissue: ACTH is produced by corticotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: ACTH targets the adrenal cortex, specifically the zona fasciculata, stimulating the synthesis and secretion of glucocorticoids, such as cortisol.

Predicted Effects of Fluctuations: Elevated ACTH levels may result from conditions like Addison’s disease or pituitary tumors. Decreased levels may occur due to Cushing’s syndrome or exogenous glucocorticoid therapy.

Prolactin

Stimulus for Release: Prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH, dopamine) from the hypothalamus regulate prolactin release.

Gland/Endocrine Tissue: Prolactin is synthesized by lactotroph cells in the anterior pituitary gland.

Target Tissue/Cells and Effects: Prolactin primarily acts on the mammary glands, stimulating milk production (lactation) in females.

Predicted Effects of Fluctuations: Elevated prolactin levels may indicate conditions like prolactinoma or hypothyroidism. Decreased levels are rare but may be associated with severe stress or hypothalamic dysfunction.

Oxytocin:

Stimulus for Release: Oxytocin release is stimulated by various factors, including cervical and uterine dilation during childbirth, nipple stimulation during breastfeeding, and emotional cues like touch and intimacy.

Gland/Endocrine Tissue: Oxytocin is synthesized in the hypothalamus and stored in the posterior pituitary gland until release.

Target Tissue/Cells and Effects: Oxytocin primarily acts on the smooth muscles of the uterus and mammary glands. During childbirth, it stimulates uterine contractions, facilitating labor and delivery. In lactating females, oxytocin promotes milk ejection (letdown) by causing contraction of myoepithelial cells surrounding mammary alveoli, aiding in breastfeeding.

Predicted Effects of Fluctuations: Elevated oxytocin levels during labor and breastfeeding are physiologically normal and facilitate these processes. Decreased oxytocin levels may impair uterine contractions during labor or hinder milk ejection during breastfeeding.

Antidiuretic Hormone (ADH)/Vasopressin:

Stimulus for Release: ADH release is primarily stimulated by factors such as increased plasma osmolality (high solute concentration) or decreased blood volume, sensed by osmoreceptors in the hypothalamus and baroreceptors in the cardiovascular system, respectively. Stress and certain drugs can also trigger ADH release.

Gland/Endocrine Tissue: ADH is synthesized in the hypothalamus and stored in and released from the posterior pituitary gland.

Target Tissue/Cells and Effects: ADH primarily acts on the kidneys to regulate water reabsorption. It increases the permeability of the renal collecting ducts to water, allowing for its reabsorption back into the bloodstream. Additionally, ADH can cause vasoconstriction at higher concentrations, thereby increasing blood pressure (hence its alternate name, vasopressin).

Predicted Effects of Fluctuations: Elevated ADH levels, such as in response to dehydration or high blood osmolality, promote water reabsorption, leading to concentrated urine and fluid retention. Conversely, decreased ADH levels, as seen in conditions like diabetes insipidus or excessive fluid intake, result in decreased water reabsorption, leading to dilute urine and increased urine output.

Calcium regulation

Parathyroid hormone (PTH) and calcitonin play vital roles in maintaining calcium homeostasis, a cornerstone of physiological balance.

Parathyroid Hormone (PTH)

Stimulus for Release: PTH secretion is primarily triggered by low blood calcium levels, detected by calcium-sensing receptors in the parathyroid glands. Additionally, low magnesium levels and high phosphate levels can also stimulate PTH release.

Gland/Endocrine Tissue: PTH is produced by the parathyroid glands, small endocrine glands located on the posterior surface of the thyroid gland.

Target Tissue/Cells and Effects: PTH acts on several target tissues, primarily the bones, kidneys, and intestines. In bones, PTH stimulates osteoclast activity, leading to bone resorption and release of calcium into the bloodstream. In the kidneys, PTH enhances calcium reabsorption while promoting phosphate excretion. Moreover, PTH stimulates the production of active vitamin D (calcitriol) in the kidneys, which enhances intestinal calcium absorption.

Predicted Effects of Fluctuations: Elevated PTH levels, as seen in conditions like primary hyperparathyroidism, lead to increased bone resorption, hypercalcemia, and potentially kidney stones. Conversely, decreased PTH levels, as in hypoparathyroidism, result in hypocalcemia, muscle cramps, and neuromuscular irritability.

Calcitonin

Stimulus for Release: Calcitonin secretion is primarily triggered by high blood calcium levels, detected by calcium-sensing receptors in the thyroid gland’s C cells (parafollicular cells).

Gland/Endocrine Tissue: Calcitonin is synthesized and secreted by the C cells (parafollicular cells) of the thyroid gland.

Target Tissue/Cells and Effects: Calcitonin primarily acts on bones, inhibiting osteoclast activity and promoting calcium deposition into bone matrix, thus lowering blood calcium levels. However, its physiological significance in humans is debated, as its role in calcium homeostasis appears to be secondary to that of PTH.

Predicted Effects of Fluctuations: Elevated calcitonin levels are typically associated with medullary thyroid carcinoma, a rare cancer of the thyroid gland. However, the clinical significance of elevated calcitonin levels in this context is mainly related to tumor diagnosis rather than calcium homeostasis regulation. Decreased calcitonin levels are not typically associated with specific pathological conditions.

Aldosterone

Stimulus for Release: Aldosterone secretion is primarily stimulated by low blood sodium levels, high blood potassium levels, and the renin-angiotensin-aldosterone system (RAAS), activated in response to low blood pressure or decreased blood volume.

Gland/Endocrine Tissue: Aldosterone is produced by the zona glomerulosa of the adrenal cortex.

Target Tissue/Cells and Effects: Aldosterone primarily acts on the distal tubules and collecting ducts of the kidneys, enhancing sodium reabsorption and potassium secretion. This leads to increased blood volume, blood pressure, and electrolyte balance maintenance.

Predicted Effects of Fluctuations: Elevated aldosterone levels, as seen in conditions like primary hyperaldosteronism or secondary aldosteronism, lead to sodium retention, potassium excretion, and hypertension. Conversely, decreased aldosterone levels, such as in Addison’s disease, result in sodium loss, potassium retention, and hypotension.

Cortisol

Stimulus for Release: Cortisol secretion is primarily stimulated by adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, which, in turn, is stimulated by corticotropin-releasing hormone (CRH) from the hypothalamus. Stress and diurnal rhythms also influence cortisol secretion.

Gland/Endocrine Tissue: Cortisol is synthesized by the zona fasciculata of the adrenal cortex.

Target Tissue/Cells and Effects: Cortisol acts on various tissues throughout the body, exerting widespread metabolic, anti-inflammatory, and stress response effects. It promotes gluconeogenesis, inhibits glucose uptake by peripheral tissues, suppresses the immune system, and modulates cardiovascular function.

Predicted Effects of Fluctuations: Elevated cortisol levels, as seen in conditions like Cushing’s syndrome or chronic stress, lead to symptoms such as hyperglycemia, muscle wasting, immune suppression, and hypertension. Conversely, decreased cortisol levels, as in Addison’s disease or adrenal insufficiency, result in symptoms like hypoglycemia, fatigue, and impaired stress response.

Epinephrine

Stimulus for Release: Epinephrine secretion is primarily stimulated by the sympathetic nervous system in response to stress, fear, or physical exertion.

Gland/Endocrine Tissue: Epinephrine is produced by the adrenal medulla.

Target Tissue/Cells and Effects: Epinephrine acts on various target tissues throughout the body, exerting rapid and profound effects to prepare the body for “fight or flight” responses. It increases heart rate, contractility, and cardiac output, dilates airways, mobilizes glucose and fatty acids for energy, and redirects blood flow to vital organs.

Predicted Effects of Fluctuations: Elevated epinephrine levels, as seen in acute stress responses or conditions like pheochromocytoma, lead to increased heart rate, blood pressure, and metabolic rate. However, prolonged elevation can contribute to cardiovascular complications. Conversely, decreased epinephrine levels are rare but may occur in conditions like adrenal insufficiency.

Sex hormones

Several hormones orchestrate the development and function of the male and female reproductive systems. Testosterone, estrogen, progesterone, human chorionic gonadotropin (hCG), and inhibin are key players, each contributing unique roles essential for fertility and reproduction.

Testosterone

Stimulus for Release: Testosterone secretion is primarily stimulated by luteinizing hormone (LH) from the anterior pituitary gland, which is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. Testosterone levels also fluctuate in response to diurnal rhythms and feedback mechanisms.

Gland/Endocrine Tissue: Testosterone is produced by Leydig cells in the testes in males and in smaller amounts by the ovaries and adrenal glands in females.

Target Tissue/Cells and Effects: Testosterone acts on various tissues throughout the body, promoting the development and maintenance of male reproductive organs (e.g., testes, prostate) and secondary sexual characteristics (e.g., facial hair, deep voice). It also influences libido, bone density, muscle mass, and mood.

Predicted Effects of Fluctuations: Elevated testosterone levels, as seen in conditions like polycystic ovary syndrome (PCOS) in females or anabolic steroid use, may lead to symptoms such as hirsutism, acne, and virilization. Conversely, decreased testosterone levels, as in hypogonadism, result in symptoms like erectile dysfunction, decreased libido, and loss of muscle mass.

Estrogen

Stimulus for Release: Estrogen secretion is primarily stimulated by follicle-stimulating hormone (FSH) and LH from the anterior pituitary gland, which are regulated by GnRH from the hypothalamus. Estrogen levels also fluctuate throughout the menstrual cycle and pregnancy.

Gland/Endocrine Tissue: Estrogen is primarily produced by the ovaries, with smaller amounts synthesized by the adrenal glands and adipose tissue.

Target Tissue/Cells and Effects: Estrogen acts on various tissues throughout the body, promoting the development and maintenance of female reproductive organs (e.g., ovaries, uterus) and secondary sexual characteristics (e.g., breast development, widening of hips). It also influences bone density, cardiovascular health, and mood.

Predicted Effects of Fluctuations: Elevated estrogen levels, as seen in conditions like estrogen-producing tumors or hormone replacement therapy, may lead to symptoms such as breast tenderness, fluid retention, and increased risk of thrombosis. Conversely, decreased estrogen levels, as in menopause or hypothalamic amenorrhea, result in symptoms like hot flashes, vaginal dryness, and osteoporosis.

Progesterone

Stimulus for Release: Progesterone secretion is primarily stimulated by LH from the anterior pituitary gland, particularly during the luteal phase of the menstrual cycle and pregnancy.

Gland/Endocrine Tissue: Progesterone is primarily produced by the corpus luteum in the ovaries during the luteal phase of the menstrual cycle and by the placenta during pregnancy.

Target Tissue/Cells and Effects: Progesterone primarily acts on the uterus, preparing it for implantation and supporting early pregnancy. It also influences the menstrual cycle, promoting the development of the endometrium and inhibiting uterine contractions.

Predicted Effects of Fluctuations: Elevated progesterone levels, as seen in pregnancy or luteal phase of the menstrual cycle, may lead to symptoms such as breast tenderness, mood swings, and fatigue. Conversely, decreased progesterone levels, as in anovulatory cycles or luteal phase defect, may result in irregular menstruation or difficulty maintaining pregnancy.

Human Chorionic Gonadotropin (hCG)

Stimulus for Release: hCG secretion is primarily stimulated by the developing embryo after implantation in the uterus. It is produced by trophoblast cells and is a key indicator of pregnancy.

Gland/Endocrine Tissue: hCG is produced by trophoblast cells of the developing placenta.

Target Tissue/Cells and Effects: hCG primarily acts on the corpus luteum in the ovaries, maintaining its function and promoting the production of estrogen and progesterone during early pregnancy. It also plays a role in fetal development and maternal adaptations to pregnancy.

Predicted Effects of Fluctuations: Elevated hCG levels are a hallmark of pregnancy and are detected in urine and blood tests used for pregnancy diagnosis. Decreased hCG levels may indicate pregnancy loss or ectopic pregnancy.

Inhibin

Stimulus for Release: Inhibin secretion is primarily stimulated by FSH from the anterior pituitary gland. Its release is regulated by negative feedback mechanisms to maintain follicular development and regulate FSH secretion.

Gland/Endocrine Tissue: Inhibin is produced by granulosa cells in the ovaries (in females) and Sertoli cells in the testes (in males).

Target Tissue/Cells and Effects: Inhibin acts on the anterior pituitary gland to selectively inhibit FSH secretion, thereby regulating follicular development and ovarian function in females and spermatogenesis in males.

Predicted Effects of Fluctuations: Elevated inhibin levels, particularly inhibin B, are associated with increased ovarian reserve and may be used as a marker of ovarian function in fertility assessment. Decreased inhibin levels may indicate diminished ovarian reserve or impaired testicular function.

In summary, testosterone, estrogen, progesterone, hCG, and inhibin are integral to the regulation of reproductive function and fertility in both males and females. Their coordinated actions govern the menstrual cycle, ovulation, pregnancy, and sexual development, highlighting their significance in reproductive physiology and human health.

Glucose regulation and the pancreas

Insulin and glucagon stand as essential antagonists, working together to maintain glucose homeostasis and energy balance within the body. Let’s explore the mechanisms of action, stimuli for release, target tissues, effects, and predicted outcomes of fluctuations for these pivotal hormones.

Insulin

Stimulus for Release: Insulin secretion is primarily stimulated by elevated blood glucose levels, sensed by pancreatic beta cells. Additionally, other factors such as amino acids, fatty acids, incretin hormones (e.g., GLP-1), and sympathetic activity also influence insulin secretion.

Gland/Endocrine Tissue: Insulin is synthesized and secreted by beta cells in the pancreatic islets of Langerhans.

Target Tissue/Cells and Effects: Insulin primarily acts on target tissues such as the liver, adipose tissue, and skeletal muscle. Its main effects include promoting glucose uptake by cells, stimulating glycogen synthesis in the liver and muscles, inhibiting gluconeogenesis and glycogenolysis, and facilitating lipid synthesis and storage.

Predicted Effects of Fluctuations: Elevated insulin levels, as seen in conditions like type 2 diabetes or insulinoma, lead to increased glucose uptake, hypoglycemia, and potential weight gain. Conversely, decreased insulin levels, as in type 1 diabetes or insulin resistance, result in impaired glucose uptake, hyperglycemia, and increased lipolysis.

Glucagon

Stimulus for Release: Glucagon secretion is primarily stimulated by low blood glucose levels, sensed by pancreatic alpha cells. Additionally, amino acids, sympathetic activity, and cortisol can also stimulate glucagon release.

Gland/Endocrine Tissue: Glucagon is synthesized and secreted by alpha cells in the pancreatic islets of Langerhans.

Target Tissue/Cells and Effects: Glucagon primarily acts on the liver to stimulate glycogenolysis (breakdown of glycogen into glucose) and gluconeogenesis (synthesis of glucose from non-carbohydrate sources). It also promotes lipolysis in adipose tissue, releasing fatty acids as additional energy substrates.

Predicted Effects of Fluctuations: Elevated glucagon levels, as seen in conditions like glucagonoma or prolonged fasting, lead to increased hepatic glucose production, hyperglycemia, and ketogenesis. Conversely, decreased glucagon levels, as in insulinoma or hyperinsulinemia, result in decreased hepatic glucose production and hypoglycemia.

In summary, insulin and glucagon form a finely tuned regulatory system, maintaining glucose homeostasis and energy balance within the body. Their coordinated actions ensure that cells receive an adequate supply of glucose for energy metabolism while also preventing excessive fluctuations in blood glucose levels. Understanding the roles of insulin and glucagon in metabolic regulation provides insights into the pathophysiology of diabetes mellitus and other metabolic disorders, highlighting the importance of maintaining their balance for overall health and well-being.

Hormones released from the kidney

Erythropoietin (EPO), calcitriol (active form of Vitamin D), and renin play critical roles in maintaining blood pressure, red blood cell production, and calcium balance within the body. Let’s explore the mechanisms of action, stimuli for release, target tissues, effects, and predicted outcomes of fluctuations for these essential hormones.

Erythropoietin (EPO)

Stimulus for Release: EPO secretion is primarily stimulated by low oxygen levels in the blood, detected by specialized cells in the kidneys called peritubular fibroblasts. Hypoxia-inducible factors (HIFs) play a key role in regulating EPO production in response to tissue hypoxia.

Gland/Endocrine Tissue: EPO is primarily synthesized and secreted by the peritubular fibroblasts in the kidneys, although small amounts can also be produced by the liver in response to severe hypoxia.

Target Tissue/Cells and Effects: EPO primarily acts on hematopoietic stem cells in the bone marrow, stimulating their proliferation, differentiation, and maturation into red blood cells (erythropoiesis). It also enhances the release of reticulocytes (immature red blood cells) into the bloodstream.

Predicted Effects of Fluctuations: Elevated EPO levels, as seen in conditions like chronic hypoxia (e.g., high altitude, chronic lung disease) or renal cell carcinoma, lead to increased erythropoiesis and polycythemia. Conversely, decreased EPO levels, as in chronic kidney disease or bone marrow disorders, result in anemia due to impaired red blood cell production.

Calcitriol (Vitamin D)

Stimulus for Release: Calcitriol synthesis is primarily stimulated by parathyroid hormone (PTH) and low blood calcium levels, which activate the conversion of inactive Vitamin D precursors into calcitriol in the kidneys.

Gland/Endocrine Tissue: Calcitriol is synthesized in the kidneys from its inactive precursors, primarily 25-hydroxyvitamin D3 (calcidiol), which is produced in the liver from Vitamin D obtained through diet or sunlight exposure.

Target Tissue/Cells and Effects: Calcitriol primarily acts on the intestines, kidneys, and bones. It enhances intestinal absorption of calcium and phosphate, promotes renal reabsorption of calcium, and stimulates osteoclast activity in bone resorption, thereby maintaining calcium and phosphate homeostasis.

Predicted Effects of Fluctuations: Elevated calcitriol levels, as seen in conditions like hyperparathyroidism or hypervitaminosis D, lead to hypercalcemia, hypercalciuria, and potential soft tissue calcifications. Conversely, decreased calcitriol levels, as in Vitamin D deficiency or chronic kidney disease, result in hypocalcemia, hypophosphatemia, and impaired bone mineralization.

Renin

Stimulus for Release: Renin secretion is primarily stimulated by decreased blood pressure or blood volume, sensed by specialized cells in the kidneys called juxtaglomerular cells. Sympathetic nervous system activity and reduced sodium delivery to the distal tubules also stimulate renin release.

Gland/Endocrine Tissue: Renin is primarily synthesized and secreted by the juxtaglomerular cells of the renal nephrons.

Target Tissue/Cells and Effects: Renin acts on angiotensinogen, a precursor protein produced by the liver, to convert it into angiotensin I. This, in turn, is converted into angiotensin II by angiotensin-converting enzyme (ACE) primarily in the lungs. Angiotensin II then acts on blood vessels to induce vasoconstriction and stimulate aldosterone release from the adrenal glands, leading to increased blood pressure and sodium retention.

Predicted Effects of Fluctuations: Elevated renin levels, as seen in conditions like renal artery stenosis or renal hypoperfusion, lead to increased angiotensin II production, hypertension, and sodium retention. Conversely, decreased renin levels, as in primary hyperaldosteronism or excess fluid intake, result in decreased angiotensin II production and potential hypotension.

In summary, erythropoietin, calcitriol, and renin are integral to the regulation of red blood cell production, calcium balance, and blood pressure within the body. Their coordinated actions ensure optimal oxygen delivery to tissues, maintenance of bone health, and regulation of vascular tone, highlighting their significance in overall physiological function and health.

Digestive system

A trio of hormones – gastrin, secretin, and cholecystokinin (CCK) – play crucial roles in regulating various digestive processes.

Gastrin

Stimulus for Release: Gastrin secretion is primarily stimulated by the presence of food in the stomach, particularly the presence of peptides and amino acids. Gastrin release is also influenced by vagal stimulation and the presence of gastrin-releasing peptide.

Gland/Endocrine Tissue: Gastrin is produced by G cells (Gastric cells) located in the gastric mucosa of the stomach.

Target Tissue/Cells and Effects: Gastrin primarily acts on parietal cells in the stomach, stimulating gastric acid secretion (hydrochloric acid) and promoting gastric motility. It also induces the release of histamine from enterochromaffin-like cells, further enhancing acid secretion.

Predicted Effects of Fluctuations: Elevated gastrin levels, as seen in conditions like Zollinger-Ellison syndrome or chronic gastritis, may lead to excessive gastric acid secretion, gastric ulcers, and increased risk of gastric cancer. Conversely, decreased gastrin levels may result in hypochlorhydria or achlorhydria, leading to impaired digestion and malabsorption.

Secretin

Stimulus for Release: Secretin secretion is primarily stimulated by the presence of acidic chyme in the duodenum, which activates duodenal S cells.

Gland/Endocrine Tissue: Secretin is produced by S cells (S enterocytes) located in the duodenal mucosa of the small intestine.

Target Tissue/Cells and Effects: Secretin primarily acts on the pancreas and liver. It stimulates pancreatic ductal cells to secrete bicarbonate-rich pancreatic juice, which neutralizes acidic chyme entering the duodenum. Secretin also inhibits gastric acid secretion and promotes bile secretion from the liver.

Predicted Effects of Fluctuations: Elevated secretin levels may indicate conditions like duodenal ulcers or pancreatic inflammation. Conversely, decreased secretin levels may result in impaired bicarbonate secretion and alkaline tide, leading to duodenal acidity and malabsorption.

Cholecystokinin (CCK)

Stimulus for Release: Cholecystokinin (CCK) secretion is primarily stimulated by the presence of fat and protein in the duodenum, which activates duodenal I cells.

Gland/Endocrine Tissue: Cholecystokinin (CCK) is produced by I cells (duodenal and jejunal cells) located in the mucosa of the small intestine.

Target Tissue/Cells and Effects: Cholecystokinin (CCK) primarily acts on the gallbladder, pancreas, and stomach. It stimulates gallbladder contraction, leading to the release of bile into the duodenum, which aids in fat digestion and absorption. CCK also stimulates pancreatic acinar cells to secrete digestive enzymes (lipase, amylase, proteases) and inhibits gastric emptying, promoting nutrient digestion and absorption.

Predicted Effects of Fluctuations: Elevated CCK levels, as seen in conditions like cholecystitis or fatty meal ingestion, may lead to increased gallbladder contractility, gallstone formation, and potential bile duct obstruction. Conversely, decreased CCK levels may result in impaired fat digestion and malabsorption.

In summary, gastrin, secretin, and cholecystokinin (CCK) are essential gastrointestinal hormones that regulate digestive processes, including gastric acid secretion, pancreatic enzyme secretion, bile release, and gastric motility. Their coordinated actions ensure efficient digestion and absorption of nutrients, highlighting their significance in maintaining gastrointestinal health and function.

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