Topic 6: Hormones and Steroids
1. Polypeptide hormones.
2. Steroid hormones.
3. Growth hormone.
Learning Outcomes
By the end of this topic, you should be able to:
1. Describe growth hormone and growth factors;
2. Describe the vitamin D hormone, thyroid hormone and sex hormones;
and
3. Explain membrane and types of membrane transport.
Topic Overview
This topic provides an overview of polypeptide hormones, steroid hormones, and growth hormones. You will learn about growth hormone, thyroid stimulating hormone (TSH), thyrotropin, gastro intestinal hormone, sex hormone, and stress hormone. Next, you will discuss the types of membrane transport such as exocytosis, passive diffusion (osmosis), facilitated diffusion, and active transport requiring energy. Subsequently, you will learn about Proton (H1) transport, citrate transporters in mitochondria, plasma membrane amino acid transporters, and fatty acid transport proteins.
Focus Areas and Assigned Readings
Focus Areas Assigned Readings
Polypeptide Hormones, Steroid Hormones and Growth Hormone
6.1 Panhypopituitarism: Malfunction of the Hypothalamus-Pituitary- End Organ Axis
Chapter 15, pages 427–439
6.2 Growth Hormone Chapter 15, pages 439–442 6.3 Thyroid Stimulating Hormone
(TSH), Thyrotropin Chapter 15, pages 442–452 6.4 Hormones of the Gastrointestinal
(GI) Tract Chapter 15, pages 453–460
6.5 Stress, Nociceptin, Responses to
Stress Chapter 16, pages 467–473
6.6 Production of High Levels of Cortisol (Cushing’s Disease) and Subnormal Levels of Cortisol (Addison’s Disease)
Chapter 16, pages 473–477
6.7 Steroid Transporting Proteins in Plasma
Chapter 16, pages 487–490 6.8 Vitamin D Hormone, Thyroid
Hormone and Sex Hormones Chapter 16, pages 496–504 6.9 Growth Factors Chapter 17, pages 515–520 6.10 Membrane Transport -Types of
Membrane Transport, Exocytosis, Passive Diffusion (Osmosis), Facilitated Diffusion, Active Transport Requiring Energy,
Chapter 18, pages 557–564
6.11 Proton (H1) Transport, Citrate Transporters in Mitochondria and Plasma Membrane & Amino Acid Transporters.
Chapter 18, pages 571–578
6.12 Fatty Acid Transport Proteins Chapter 18, pages 578–579
Additional Recommended Readings
McMurry, et al., (2011). Fundamentals of general, organic, and biological chemistry (6th ed.). Pearson.
Recommended books, materials, and media:
Campbell, M. K., & Farrell, S. O., (2008). Biochemistry (6th ed.). Brooks Cole.
Garrett, R. H., & Grisham, C. H. (2010) Biochemistry (2nd ed.). Cengage Learning.
Ignatavicius, D., Workman. L. (2015). Medical-surgical nursing: Patient-centered collaborative care (8th ed.). Saunders. p. 1267. ISBN 978-1455772551 Molitch, M. E., Clemmons, D. R., Malozowski, S., Merriam, G. R., Shalet, S.M.,
Vance, M. L., Stephens, P. A. (2006). Evaluation and treatment of adult growth hormone deficiency: An endocrine society clinical practice guideline.
The Journal of Clinical Endocrinology and Metabolism, 91(5), 1621–34.
doi:10.1210/jc.2005-2227. PMID 16636129.
Smith, C., Marks, A., & Lieberman, M. (2009). Mark’s basic medical biochemistry.
Lippincott, Williams and Wilkins.
Refer to the following websites:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgidb=Books
Addison’s Disease: Causes, Symptoms, Diagnosis & Treatment https://my.clevelandclinic.org/health/diseases/15095-addisons-disease Biochemistry.Growth hormone Wikipedia the free encyclopedia https://en.wikipedia.org/wiki/Growth_hormone#Biochemistry
The Medical Biochemistry Page: (https://themedicalbiochemistrypage.org/)
Content Summary
6.1 Panhypopituitarism: Malfunction of the Hypothalamus-Pituitary- End Organ Axis
The terms “hypopituitarism” and “panhypopituitarism” vary significantly.
Hypopituitarism is a rare disorder that refers to a decrease in the function of the pituitary gland caused by two or more hormones. The term “panhypopituitarism” is used when all pituitary hormone production is deficient or decreased.
6.2 Growth Hormone
The major role of growth hormone (GH) in stimulating body growth is to stimulate the liver and other tissues to secrete insulin-like growth factor 1 (IGF-1). IGF-1 stimulates the proliferation of chondrocytes (cartilage cells), resulting in bone growth. Growth hormone is formed in the growth-stimulating somatotropic cells of the pituitary gland, which is located at the base of the brain. Growth hormone is needed for normal growth of the bones and tissues of the body.
6.2.1 Excess Growth Hormone
The most common disease of growth hormone (GH) excess is a pituitary tumour composed of somatotroph cells of the anterior pituitary. These somatotroph adenomas are benign and grow slowly, gradually producing more and more GH. For years, the principal clinical problems are those of GH excess. Eventually, the adenoma may become large enough to cause headaches, impair vision by pressure on the optic nerves, or cause deficiency of other pituitary hormones through displacement. Prolonged GH excess thickens the bones of the jaw, fingers, and toes, resulting in heaviness of the jaw and the increased size of digits, referred to as acromegaly.
Accompanying problems can include sweating, pressure on nerves (e.g., carpal tunnel syndrome), muscle weakness, excess sex hormone-binding globulin (SHBG), insulin resistance, or even a rare form of Type 2 diabetes and reduced sexual function.
GH-secreting tumours are typically recognised in the fifth decade of life. It is extremely rare for such a tumour to occur in childhood, but, if it does, the excessive GH can cause excessive growth, traditionally referred to as pituitary gigantism. Surgical removal is the usual treatment for GH-producing tumours. In some circumstances, focused radiation or a GH antagonist such as pegvisomant may be employed to shrink the tumour or block function. Other drugs like octreotide (somatostatin agonist) and bromocriptine (dopamine agonist) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.
6.2.2 Growth Hormone Deficiency
The effects of growth hormone (GH) deficiency vary depending on the age when it occurs. According to Ignatavicius and Workman (2015), alterations in somatomedin can result in growth hormone deficiency with two known mechanisms – failure of tissues to respond to somatomedin and failure of the liver to produce somatomedin. Major manifestations of GH deficiency in children are growth failure, the development of a short stature, and delayed sexual maturity. In adults, somatomedin alteration contributes to increased osteoclast activity, resulting in weaker bones that are more prone to pathologic fracture and osteoporosis (Ignatavicius and Workman, 2015). However, such deficiency is rare in adults, with the most common cause being a pituitary adenoma (Molitch, Clemmons, Malozowski, Merriam, Shalet, Vance, & Stephens, 2006). Other adult causes include a continuation of a childhood problem, other structural lesions or trauma, and very rarely, idiopathic GHD (Molitch et al. 2006). Adults with GHD tend to have a relative increase in fat mass and a relative decrease in muscle mass and, in many instances, decreased energy and quality of life (Molitch et al. 2006). Diagnosis of GH deficiency involves a multiple- step diagnostic process, usually culminating in GH stimulation tests to see whether the patient’s pituitary gland will release a pulse of GH when provoked by various stimuli.
6.3 Thyroid Stimulating Hormone
This is a hormone formed by the pituitary gland at the base of the brain in response to signals from the hypothalamus gland in the brain.
Thyroid stimulating hormone (TSH) promotes the growth of the thyroid gland in the neck and stimulates it to produce more thyroid hormones.
Once there is an excessive amount of thyroid hormones, the pituitary gland stops producing TSH, reducing thyroid hormone production. This mechanism maintains a relatively constant level of thyroid hormones circulating in the blood. The thyrotropin is also known as TSH.
6.4 Hormones of the Gastrointestinal (GI) Tract
The classical GI hormones are secreted by epithelial cells lining the lumen of the stomach and small intestine. These hormone-secreting cells – endocrinocytes – are interspersed among a much larger number of epithelial cells that secrete their products (acid, mucus, etc.) into the lumen or take up nutrients from the lumen. GI hormones are secreted into the blood, and hence, circulate systemically, affecting the functions of other parts of the digestive tube, liver, pancreas, brain and a variety of other targets.
6.5 Nociceptin
Nociceptin, also known as orphanin FQ, is a 17-amino-acid polypeptide that is structurally related to the opioid peptide dynorphin A. It is the endogenous ligand for the nociceptin opioid (NOP) receptor (formerly referred to as opioid receptor-like-1).
6.6 Cushing’s Disease
Cushing’s disease is caused by elevated hormone levels called cortisol, contributing to a wide variety of signs and symptoms. This disease usually occurs between the ages of 20 and 50 in adults.
Children may also be affected though. In general, the first symptom of this disorder is weight gain around the trunk and in the neck.
Individuals affected may potentially get stretch marks (striae) on their thighs and abdomen, and bruise easily. Individuals with Cushing’s disease can develop a hump on their upper back, due to abnormal fat deposits. People with this condition can have muscle weakness, severe tiredness, and progressively thin and brittle bones that are prone to fracture (osteoporosis). They also have a weakened immune system and are at an increased risk of infections. Cushing’s disease can cause mood disorders such as anxiety, irritability, and depression.
This condition can also affect a person’s concentration and memory.
People with Cushing’s disease have an increased chance of developing high blood pressure (hypertension) and diabetes. Women with Cushing’s disease may experience irregular menstruation and have excessive hair growth (hirsutism) on their face, abdomen, and legs. Men with Cushing’s disease may have erectile dysfunction.
Children with Cushing’s disease typically experience slow growth.
6.6.1 Addison’s Disease
Addison’s disease is a rare autoimmune disorder that occurs when adrenal glands fail to produce sufficient amounts of steroid hormones, primarily cortisol and sometimes, aldosterone. Cortisol is one of the body’s most important hormones with almost every cell containing receptors for it. It has far-reaching effects and is essential for many processes including metabolism and immune response. It helps control blood sugar levels, reduce inflammation, regulate metabolism, and assist in memory formation. Cortisol is best known for its crucial role in the “fight-or-flight” response in which the body gets a burst of energy and strength in preparation for what it perceives to be a threat or danger.
Aldosterone, on the other hand, plays an important role in cardiovascular health. It helps to regulate potassium and sodium levels in the body and balance the amount of electrolytes and fluids in the blood. It also plays a crucial role in controlling blood pressure. Low cortisol and aldosterone levels often lead to a number of unpleasant symptoms as well as psychological and physical health issues that can drastically affect a patient’s quality of life.
6.7 Steroid Hormone
Steroid hormones include any group of hormones that belong to the class of chemical complexes known as steroids. They are secreted by three steroid glands – the adrenal cortex, testes, and ovaries – and during pregnancy by the placenta. All steroid hormones are derived from cholesterol.
6.8 Fatty Acid Transport Proteins
Fatty acid transportation proteins (FTAPs) are a family of transmembrane transportation proteins that allow and enhance the absorption of long-chain fatty acids into cells. (Houten, Sander, Wanders, Ronald, 2010). This subfamily is part of the family of solute protein carriers. This family includes six rather homologous proteins within humans, which are distributed in all body tissues using the fatty acids, FATP1, FATP2, FTAP3, FATP4, FATP5 and FTAP6 (Doege, Holger; Stahl, Andreas, 2006).
Study Questions
1. State the growth hormone in the human body and its functions.
2. Describe the physiology of thyroid stimulating hormones in humans.
3. Differentiate between membrane transportation of exocytosis, passive diffusion (osmosis), facilitated diffusion, and active transport requiring energy.
4. Explain the process of proton (H1) transporters in the human body such as citrate transporter in mitochondria, plasma membrane, and amino acid.
5. Identify the mechanism of the fatty acid transporter protein.