18.2: Introduction to Regulation of Body Processes - Biology

18.2: Introduction to Regulation of Body Processes - Biology

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Describe how hormones regulate body processes

Hormones have a wide range of effects and modulate many different body processes. The key regulatory processes that will be examined here are those affecting the excretory system, the reproductive system, metabolism, blood calcium concentrations, growth, and the stress response.

What You’ll Learn to Do

  • Explain how hormones regulate the excretory system
  • Discuss the role of hormones in the reproductive system
  • Describe how hormones regulate metabolism
  • Explain the role of hormones in blood calcium levels
  • Explain the role of hormones in growth
  • Explain the role of hormones in stress

Learning Activities

The learning activities for this section include the following:

  • Hormonal Regulation of the Excretory System
  • Hormonal Regulation of the Reproductive System
  • Hormonal Regulation of Metabolism
  • Blood Calcium Levels and Growth
  • Hormonal Regulation of Stress
  • Self Check: Neurons and Glial Cells

18.2 Development and Organogenesis

The process by which an organism develops from a single-celled zygote to a multi-cellular organism is complex and well regulated. The regulation occurs through signaling between cells and tissues and responses in the form of differential gene expression.

Early Embryonic Development

Fertilization is the process in which gametes (an egg and sperm) fuse to form a zygote (Figure 18.8). To ensure that the offspring has only one complete diploid set of chromosomes, only one sperm must fuse with one egg. In mammals, a layer called the zona pellucida protects the egg. At the tip of the head of a sperm cell is a structure like a lysosome called the acrosome, which contains enzymes. When a sperm binds to the zona pellucida, a series of events, called the acrosomal reactions, take place. These reactions, involving enzymes from the acrosome, allow the sperm plasma membrane to fuse with the egg plasma membrane and permit the sperm nucleus to transfer into the ovum. The nuclear membranes of the egg and sperm break down and the two haploid nuclei fuse to form a diploid nucleus or genome.

To ensure that no more than one sperm fertilizes the egg, once the acrosomal reactions take place at one location of the egg membrane, the egg releases proteins in other locations to prevent other sperm from fusing with the egg.

The development of multi-cellular organisms begins from this single-celled zygote, which undergoes rapid cell division, called cleavage (Figure 18.9a), to form a hollow ball of cells called a blastula (Figure 18.9b).

In mammals, the blastula forms the blastocyst in the next stage of development. Here the cells in the blastula arrange themselves in two layers: the inner cell mass , and an outer layer called the trophoblast . The inner cell mass will go on to form the embryo. The trophoblast secretes enzymes that allow implantation of the blastocyst into the endometrium of the uterus. The trophoblast will contribute to the placenta and nourish the embryo.

Concepts in Action

Visit the Virtual Human Embryo project at the Endowment for Human Development site to click through an interactive of the stages of embryo development, including micrographs and rotating 3-D images.

The cells in the blastula then rearrange themselves spatially to form three layers of cells. This process is called gastrulation . During gastrulation, the blastula folds in on itself and cells migrate to form the three layers of cells (Figure 18.10) in a structure, the gastrula, with a hollow space that will become the digestive tract. Each of the layers of cells is called a germ layer and will differentiate into different organ systems.

The three germ layers are the endoderm, the ectoderm, and the mesoderm. Cells in each germ layer differentiate into tissues and embryonic organs. The ectoderm gives rise to the nervous system and the epidermis, among other tissues. The mesoderm gives rise to the muscle cells and connective tissue in the body. The endoderm gives rise to the gut and many internal organs.


Gastrulation leads to the formation of the three germ layers that give rise during further development to the different organs in the animal body. This process is called organogenesis .

Organs develop from the germ layers through the process of differentiation. During differentiation, the embryonic stem cells express specific sets of genes that will determine their ultimate cell type. For example, some cells in the ectoderm will express the genes specific to skin cells. As a result, these cells will take on the shape and characteristics of epidermal cells. The process of differentiation is regulated by location-specific chemical signals from the cell’s embryonic environment that sets in play a cascade of events that regulates gene expression.

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    The elements carbon, hydrogen, nitrogen, oxygen, sulfur, and phosphorus are the key building blocks of the chemicals found in living things. They form the carbohydrates, nucleic acids, proteins, and lipids (all of which will be defined later in this chapter) that are the fundamental molecular components of all organisms. In this chapter, we will discuss these important building blocks and learn how the unique properties of the atoms of different elements affect their interactions with other atoms to form the molecules of life. These interactions determine what atoms combine and the ultimate shape of the molecules and macromolecules, that shape will determine their function.

    Food provides an organism with nutrients—the matter it needs to survive. Many of these critical nutrients come in the form of biological macromolecules, or large molecules necessary for life. These macromolecules are built from different combinations of smaller organic molecules. What specific types of biological macromolecules do living things require? How are these molecules formed? What functions do they serve? In this chapter, we will explore these questions.

    Chapter 11: Introduction to the Body’s Systems

    Figure 11.1 An arctic fox is a complex animal, well adapted to its environment. (credit: Keith Morehouse, USFWS)

    The arctic fox, a complex animal that has adapted to its environment, illustrates the relationships between an animal’s form and function. The multicellular bodies of animals consist of tissues that make up more complex organs and organ systems. The organ systems of an animal maintain homeostasis within the multicellular body. These systems are adapted to obtain the necessary nutrients and other resources needed by the cells of the body, to remove the wastes those cells produce, to coordinate the activities of the cells, tissues, and organs throughout the body, and to coordinate the many responses of the individual organism to its environment.

    Waste products removed from the body with the formation and elimination of urine include many water-soluble metabolic products. The main waste products are urea — a by-product of protein catabolism — and uric acid , a by-product of nucleic acid catabolism. Excess water and mineral ions are also eliminated in urine.

    Besides the elimination of waste products such as these, the urinary system has several other vital functions. These include:

    • Maintaininghomeostasis of mineral ions in extracellular fluid: These ions are either excreted in urine or returned to the blood as needed to maintain the proper balance.
    • Maintaining homeostasis of blood pH: When pH is too low (blood is too acidic), for example, the kidneys excrete less bicarbonate (which is basic) in urine. When pH is too high (blood is too basic), the opposite occurs, and more bicarbonate is excreted in urine.
    • Maintaining homeostasis of extracellular fluids, including the blood volume, which helps maintainblood pressure: The kidneys control fluid volume and blood pressure by excreting more or less salt and water in urine.


    Among the pioneering zoologists, Linnaeus identified two body plans outside the vertebrates Cuvier identified three and Haeckel had four, as well as the Protista with eight more, for a total of twelve. For comparison, the number of phyla recognised by modern zoologists has risen to 36. [1]

    Linnaeus, 1735 Edit

    In his 1735 book Systema Naturæ, Swedish botanist Linnaeus grouped the animals into quadrupeds, birds, "amphibians" (including tortoises, lizards and snakes), fish, "insects" (Insecta, in which he included arachnids, crustaceans and centipedes) and "worms" (Vermes). Linnaeus's Vermes included effectively all other groups of animals, not only tapeworms, earthworms and leeches but molluscs, sea urchins and starfish, jellyfish, squid and cuttlefish. [2]

    Cuvier, 1817 Edit

    In his 1817 work, Le Règne Animal, French zoologist Georges Cuvier combined evidence from comparative anatomy and palaeontology [3] to divide the animal kingdom into four body plans. Taking the central nervous system as the main organ system which controlled all the others, such as the circulatory and digestive systems, Cuvier distinguished four body plans or embranchements: [4]

    1. with a brain and a spinal cord (surrounded by skeletal elements) [4]
    2. with organs linked by nerve fibres [4]
    3. with two longitudinal, ventral nerve cords linked by a band with two ganglia below the oesophagus [4]
    4. with a diffuse nervous system, not clearly discernible [4]

    Grouping animals with these body plans resulted in four branches: vertebrates, molluscs, articulata (including insects and annelids) and zoophytes or radiata.

    Haeckel, 1866 Edit

    Ernst Haeckel, in his 1866 Generelle Morphologie der Organismen, asserted that all living things were monophyletic (had a single evolutionary origin), being divided into plants, protista, and animals. His protista were divided into moneres, protoplasts, flagellates, diatoms, myxomycetes, myxocystodes, rhizopods, and sponges. His animals were divided into groups with distinct body plans: he named these phyla. Haeckel's animal phyla were coelenterates, echinoderms, and (following Cuvier) articulates, molluscs, and vertebrates. [5]

    Gould, 1979 Edit

    Stephen J. Gould explored the idea that the different phyla could be perceived in terms of a Bauplan, illustrating their fixity. However, he later abandoned this idea in favor of punctuated equilibrium. [6]

    20 out of the 36 body plans originated in the Cambrian period, [7] in the "Cambrian explosion", [8] However, complete body plans of many phyla emerged much later, in the Palaeozoic or beyond. [9]

    The current range of body plans is far from exhaustive of the possible patterns for life: the Precambrian Ediacaran biota includes body plans that differ from any found in currently living organisms, even though the overall arrangement of unrelated modern taxa is quite similar. [10] Thus the Cambrian explosion appears to have more or less completely replaced the earlier range of body plans. [7]

    Genes, embryos and development together determine the form of an adult organism's body, through the complex switching processes involved in morphogenesis.

    Developmental biologists seek to understand how genes control the development of structural features through a cascade of processes in which key genes produce morphogens, chemicals that diffuse through the body to produce a gradient that acts as a position indicator for cells, turning on other genes, some of which in turn produce other morphogens. A key discovery was the existence of groups of homeobox genes, which function as switches responsible for laying down the basic body plan in animals. The homeobox genes are remarkably conserved between species as diverse as the fruit fly and humans, the basic segmented pattern of the worm or fruit fly being the origin of the segmented spine in humans. The field of animal evolutionary developmental biology ('Evo Devo'), which studies the genetics of morphology in detail, is rapidly expanding [11] with many of the developmental genetic cascades, particularly in the fruit fly Drosophila, catalogued in considerable detail. [12]

    The Dangers of Synthetic Hormones

    Figure 18.8.
    Professional baseball player Jason Giambi publically admitted to, and apologized for, his use of anabolic steroids supplied by a trainer. (credit: Bryce Edwards)

    Some athletes attempt to boost their performance by using artificial hormones that enhance muscle performance. Anabolic steroids, a form of the male sex hormone testosterone, are one of the most widely known performance-enhancing drugs. Steroids are used to help build muscle mass. Other hormones that are used to enhance athletic performance include erythropoietin, which triggers the production of red blood cells, and human growth hormone, which can help in building muscle mass. Most performance enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, the Major League Baseball, and the National Football League.

    The side effects of synthetic hormones are often significant and non-reversible, and in some cases, fatal. Androgens produce several complications such as liver dysfunctions and liver tumors, prostate gland enlargement, difficulty urinating, premature closure of epiphyseal cartilages, testicular atrophy, infertility, and immune system depression. The physiological strain caused by these substances is often greater than what the body can handle, leading to unpredictable and dangerous effects and linking their use to heart attacks, strokes, and impaired cardiac function.

    Respiration Centres Of The Brain

    The neuronal signals transmitted between respiratory centres of the brain and the muscles in the chest and diaphragm modulate respiration. There are three main centres of the brain that regulate breathing. They are present in the medulla and the pons region of the brain. They regulate breathing by stimulating the contraction of the intercostal muscles and the diaphragm. Let’s take a closer look at these different centres.

    Browse more Topics under Breathing And Exchange Of Gases

    In Medulla

    Respiratory Rhythm Centre

    Inspiration is followed by expiration, thus creating a regular, oscillating cycle of breathing. This is the respiratory rhythm. A special centre in the medulla region of the brain is primarily responsible for regulating respiratory rhythms. This is the ‘Respiratory Rhythm Center’. This centre produces rhythmic nerve impulses that contract the muscles responsible for inspiration (diaphragm and external intercostal muscles).

    Normally, expiration happens when these muscles relax. However, in case of rapid breathing, this centre stimulates the muscles responsible for expiration (internal intercostal muscles and abdominal muscles).

    In The Pons

    Pneumotaxic Centre

    This centre regulates the functions of the respiratory rhythm centre. It controls both the rate and pattern of breathing. The pneumotaxic centre can send neural signals to reduce the duration of inspiration, thereby affecting the rate of respiration. The actions of this centre prevent the lungs from over-inflating.

    It also regulates the amount of air that the body takes in, in a single breath. If this centre is absent, it increases the depth of breathing and decreases the respiratory rate. It performs the opposite function of the Apneustic centre described below.

    Apneustic Centre

    This centre promotes inspiration by constantly stimulating the neurons in the medulla region. It sends signals that oppose the action of the signals from the pneumotaxic centre. It sends positive signals to the neurons that regulate inspiration, thereby controlling the intensity of breathing.

    Respiratory Centers of the Brain (Source: Wikimedia Commons)

    There also exists a chemosensitive area in the brain stem adjacent to the respiratory rhythm centre. It is highly sensitive to CO2 and hydrogen ions. Increase in CO2 and H + ions activate this centre, which in turn signals the rhythm centre to adjust the respiratory process and eliminate these substances.

    In addition to respiratory centres, there are certain receptors also that can detect changes in CO2 and H + ion concentration and send signals to regulate breathing. Some of these are chemoreceptors located in the medulla, aortic arch, and carotid artery whereas some are receptors in the walls of bronchi and bronchioles.

    Some factors that affect the rate of respiration are:

    Biosynthesis of Purine Nucleotides, Pyrimidine Nucleotides and Deoxyribonucleotides

    De novo (all over again) synthesis of purine nucleotides is synthesis of purines anew. The purine ring is synthesized along with the nucleotide i.e. attached to the ribose sugar provided from HMP pathway. This pathway supplies ribose sugar for the formation of the nucleotide. Activated form of D-ribose-5-phosphate serves as the starting material on which purine ring is build up step by step.

    Precursors of the members of purine ring are:

    i. N-1 is contributed by nitrogen of aspartate.

    ii. N-3 and N-9 arise from amide nitrogen of glutamine.

    iii. C-2 and C-8 originate from the formate.

    iv. C-6 is embedded from respiratory carbon dioxide.

    v. C-4, C-5 and N-7 are taken up from glycine.

    Regulation of purine nucleotide biosynthesis:

    Purine biosynthesis is regulated by feedback inhibition. This inhibition is in the 1 st step. It is the committed step which is generally irreversible. Once the committed step is passed over, the product has to be formed.

    The different mechanisms by which it is regulated are:

    Salvage Pathway:

    The de-novo synthesis does not occur in all the cells. Brain cells and leukocytes lack this mechanism. In these cells purine synthesis occurs by salvage pathway. Salvage pathway involves synthesis of purine nucleotides from free purine bases, which are salvaged from dietary sources and tissue breakdown. This pathway is promoted by the action of two enzymes which convert free purines into purine nucleotides for reuse.

    The enzymes are:

    (1) Adenine phosphoribosyl transferase and

    (2) Hypoxanthine guanine phosphoribosyl transferase (HGPRT).

    This is a genetic disorder caused due to the deficiency of the enzyme ‘Hypoxanthine Guanine Phospho Ribosyl Transferase (HGPRT)’. When this enzyme is deficient, guanine, xanthine and hypoxanthine are not salvaged and hence degraded to uric acid. This is especially seen in male children. In female children the gene is recessive and is a carrier. It is a male dominant gene. Such males show (1) mental retardation and (2) tendency for self-destruction.

    Biosynthesis of Pyrimidine Nucleotides:

    Pyrimidine nucleotide biosynthesis takes place in a different manner from that of purine nucleotides. The six membered pyrimidine ring is made first and then attached to ribose phosphate. The synthesis begins with carbon dioxide and ammonia combining to form carbamoyl phosphate catalysed by the cytosolic enzyme carbamoyl phosphate synthetase-II.

    Carbamoyl phosphate combines with aspartate to form carbamoyl aspartate aided by the enzyme aspartate transcarbamoylase. Dihydroorotate is formed from carbamoyl aspartate by removal of water and closure of the ring under the influence of the enzyme dihydroorotase.

    Dihydroorotase is oxidized to orotic acid by dehydrogenase which uses NAD + as the electron acceptor. Orotic acid is attached to ribose to yield orotidylic acid. Orotidylate is then decaroxylated to form uridylate. Uridylate is then converted to all the other pyrimidine nucleotides viz., CMP, UMP & TMP. The reaction steps involved in the biosynthesis of pyrimidine nucleotides are given under.

    Regulation of Pyrimidine Biosynthesis:

    Regulation of pyrimidine biosynthesis is by feed back inhibition at the committed step i.e. the reaction catalysed by the enzyme aspartate transcarbamoylase. This is negatively inhibited by the end product i.e. CTP. The second site is at carbamoyl phosphate synthase- II which is feedback inhibited by UMP.

    Orotic Aciduria:

    It is a metabolic disorder of pyrimidine biosynthesis characterized by accumulation of orotic acid in blood and its increased excretion in urine. It is caused due to the deficiency of enzyme orotidylic acid phosphorylase and orotidylic acid decarboxylase or orotic phosphoribosyl transferase. This leads to non-conversion of orotic acid to UMP. This may even affect the synthesis of other nucleotides. It is generally found in children who show retarded mental development and growth as there is no proper synthesis of DNA. They show megaloblastic anemia. This can be overcome by injection of CTP and UTP.

    Biosynthesis of Deoxyribonucleotides:

    Deoxyribonucleotides are obtained from ribonucleotides. Thioredoxin is a protein which takes part in the conversion of ribonucleotides to deoxyribonucleotides.

    Executive Function, Theory of Mind, and Adaptive Behavior

    Carina Coulacoglou , Donald H. Saklofske , in Psychometrics and Psychological Assessment , 2017

    Executive Function Among individuals With Tourette’s Syndrome, ADHD, and ASD

    Self-regulation is a central prerequisite for adaptive functioning and is commonly assessed via scales. EFs scales have solid associations with neurobiological bases of EF ( Isquith, Roth, & Gioia, 2013 ) and are often employed to assess clinical conditions associated with EF ( Barkley, 2011 ). One of the most used EF assessment scales is the Behavior Rating Inventory of Executive Function (BRIEF Gioia et al., 2000 ).

    Hovik et al. (2014) examined everyday EF behavior that may differentiate children with Tourette’s syndrome (TS) from typically developing children and children with ADHD-C, ADHD-1, or ASD. In the study, parents completed the BRIEF scale. While there was considerable overlap in reported EF problems in children with TS, ADHD-C, ADHD-I, and ASD, comparison of ratings on selected scales helped distinguish between children with TS and children with ADHD-C, ADHD-I, or ASD. This suggests that children with a range of common developmental disorders show EF difficulties in general, but that there may be more specific characteristics in everyday EF for specific groups. In particular, children with TS were shown to have more problems with executive control (EC) than cognitive flexibility (CF) compared to children with ASD, more problems with EC than inhibitory control compared to children with ADHD-C, and more problems with EC than planning/organizing compared to children with ADHD-I. Identifying the specific deficit in EF for individual children may guide treatment toward more targeted interventions versus a global omnibus EF rating or intervention.

    Poor inhibition has been conceptualized either as the core deficit or as an independent pathway to ADHD (e.g., Sonuga-Barke, Wiersema, van der Meere, & Roeyers, 2010 ). In the studies in which ADHD symptoms in children with ASD have been accounted for, the findings indicate that inhibition is related mainly to ADHD ( Bühler, Bachmann, Goyert, Heinzel-Gutenbrunner, & Kamp-Becker, 2011 Happé, Booth, Charlton, & Hughes, 2006 ).

    Whereas some scholars conceptualize WM deficits to be a core feature or endophenotype of ADHD ( Alderson, Rapport, Hudec, Sarver, & Kofler, 2010 ), others consider WM deficits as secondary. With regard to ASD, research has indicated that WM has a major role in social cognition and interpersonal interaction ( Barendse et al., 2013 ). Findings derived from studies that have investigated WM performance of children with ADHD and ASD suggest that WM deficits are best associated with ADHD ( Happé et al., 2006 van der Meer et al., 2012 Yerys et al., 2009 ).

    Somatic aneuploids

    Aneuploid cells can arise spontaneously in somatic tissue or in cell culture. In such cases, the initial result is a genetic mosaic of cell types.

    Human sexual mosaics—individuals whose bodies are a mixture of male and female tissue𠅊re good examples. One type of sexual mosaic, (XO)(XYY), can be explained by postulating an XY zygote in which the Y chromatids fail to disjoin at an early mitotic division, so both go to one pole:

    The phenotypic sex of such individuals depends on where the male and female sectors end up in the body. In the type of nondisjunction being considered, nondisjunction at a later mitotic division would produce a three-way mosaic (XY)(XO)(XYY), which contains a clone of normal male cells. Other sexual mosaics have different explanations as examples, XO/XY is probably due to early X-chromosome loss in a male zygote (Figure 18-24), and (XX)(XY) is probably the result of a double fertilization (fused twins). In general, sexual mosaics are called gynandromorphs.

    Figure 18-24

    Origin of a human sexual mosaic (XY)(XO) by Y chromosome loss at the first mitotic division of the zygote. (a) Fertilization. (b) Chromosome loss. (c) Resulting male and female cells. (d) Mosaic blastocyst. (After C. Stern, Principles of Human Genetics, (more. )

    Geneticists working with many species of experimental animals occasionally find gynandromorphs among their stocks. A classic example is the Drosophila gynandromorph shown in Figure 18-25. In this case, the zygote started out as a female heterozygous for two X-linked genes, white eye and miniature wing (w +  m + /w m). Loss of the wild-type allele�ring X chromosome at the first mitotic division resulted in the two cell lines and ultimately in a fly differing from one side to the other in sex, eye color, and size of wing. A similar gynandromorph in the Io moth is shown in Figure 18-26.

    Figure 18-25

    A bilateral gynandromorph of Drosophila. The zygote was w +  m + /w m, but loss of the w +  m + chromosome in the first mitotic division produced a fly that was 1/2 O/w m and male (left) and 1/2w +  m + /w m and female (more. )

    Figure 18-26

    A bilateral gynandromorph in the Io moth, Automeris io io. One half of the body is female and happens to carry the sex chromosome mutation 𠇋roken eye” the other half of the body is male and carries the normal allele of the broken-eye (more. )


    Mitotic nondisjunction and other types of aberrant mitotic chromosome behavior can give rise to mosaics consisting of two or more chromosomally distinct cell types, including aneuploids.

    Somatic aneuploidy and its resulting mosaics are often observed in association with cancer. People suffering from chronic myeloid leukemia (CML), a cancer of the white blood cells, frequently harbor cells containing the so-called Philadelphia chromosome. This chromosome was once thought to represent an aneuploid condition, but it is now known to be a translocation product in which part of the long arm of chromosome 22 attaches to the long arm of chromosome 9. However, CML patients often show aneuploidy in addition to the Philadelphia chromosome. In one study of 67 people with CML, 33 proved to have an extra Philadelphia chromosome and the remainder had various aneuploidies the most common aneuploidy was trisomy for the long arm of chromosome 17, which was detected in 28 people. Of 58 people with acute myeloid leukemia, 21 were shown to have aneuploidy for chromosome 8 16 for chromosome 9 and 10 for chromosome 21. In another study of 15 patients with intestinal tumors, 12 had cells with abnormal chromosomes, at least some with trisomy for chromosome 8, 13, 15, 17, or 21. Such studies merely established correlations, and it is not clear whether the abnormalities are best thought of as a cause or as an effect of cancer.


    Aneuploids are produced by nondisjunction or some other type of chromosome misdivision at either meiosis or mitosis.

    Watch the video: Introduction to Body Regulation (August 2022).