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Summary Medicine groups Endocrine System
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This summary is written in English and covers the full course and highlights from the lectures regarding the Medicine Group: Endocrine System.
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Endocrine systemThe endocrine system plays an important role in autonomic body functions e.g. breathing,
blood pressure, metabolism and maintaining homeostasis. The hormones that act in the ES
are made in the pituitary gland and in the hypothalamus. Neuroendocrine cells are the
messenger cells between the autonomic nervous system (fast) and the hormones (slow).
Autocrine signals are signals from within the cell itself -> the cell releases hormones and
act on its own receptors.
Paracrine signals are signals from other cells -> hormones are released from cell A and act
on cell B.
The hypothalamus regulates the release of releasing and inhibitory hormones.
The pituitary gland the release of TSH, SCTH, FSH, LH, HG, prolactin, MSH, ADH and
oxytocin.
The adrenal gland releases glucocorticosteroids (GCS), mineralocorticosteroids and
adrenal androgens.
The ovaries oestradiol and progesterone.
Thyroid gland: T3, T3, Calcitonin
Parathyroid glands: PTH
Pancreas (islets of Langerhans): Insulin, glucagon
Testes: testosterone
Protein hormones (from the hypothalamus, pit. gland, pancreas and (para)thyroid glands)
(acting on membrane receptors) are more stable effector hormones that can be taken in
orally.
All hormones from the hypothalamus are peptides (except for dopamine) and small.
Hormones from the pituitary are larger.
The hypothalamic-pituitary system
The pit. gland consists of 3 parts: the anterior pituitary,
posterior pituitary and the pars intermedia (not much
,present in humans). The hypothalamus releases hormones (regulated via neurons) that
regulate the secretion of hormones by the anterior pituitary.
Most hormones have a negative feedback system
The posterior pituitary releases ADH (vasopressin) and oxytocin. Oxytocin causes uterine
contraction and milk ejection from the breast upon labour.
Vasopressin regulates the reuptake of water in the kidneys. It activates the pituitary gland to
produce more ACTH, upon which more mineralocorticosteroids are produced.
Glycoproteins
- made of an alpha and beta subunit (2 chains in total)
- cycteine amino acids are connected via disulfide bridges
- LH, FSH, TSH, CG
- alpha subunits have 2 oligosaccharide chains, bound via asparagine
- beta subunits have the biological effect and 1-2 oligosaccharide chains.
Growth hormone lecture
Growth hormones cause growth in almost all body cells (chondrocytes in epiphyseal plates
of bones, skeletal muscle cells) and have a carbohydrate metabolic effect (protein
anabolic, glucose-sparing (induce glucose tolerance in the body), lipolytic (cleavage to
lipids to form FFAs (localytic)). Glucocorticosteroids are the main effectors of these
metabolic functions. Glucose-sparing is due to activation of gluconeogenesis in the liver,
protein catabolism due to increased proteolytic activity and reduced protein synthesis,
lipolytic activity due to the increased sensitivity to adrenaline, glucagon, GH and insulin.
The hypothalamus transfers information from different brain areas to other parts. GHRF
has a positive effect on the anterior pituitary and increases cAMP. Somatostatin has a
negative effect on the anterior pituitary and decreases cAMP levels and inhibits the TSH
release. Somatostatin stops the production of growth hormone. IGF1 has a negative
feedback effect on the growth hormone level, but a positive effect on the growth of the
peripheral tissue. Topical negative feedback mechanism: growth hormone itself has a
negative effect on the hypothalamus.
, t3 is the active hormone of thyroid and has a positive effect on GH. Stress has a negative
effect on growth hormone synthesis -> it reduces the release of growth hormone/protome
the release of somatostatin.
Somatostatins influence the activity of insulin and glucagon by modulating the release from
the pancreas by acting on the tyrosine kinase receptor.
Functional antagonism
Phosphorylation cascade: release of growth
hormone. GH is pre produced in the anterior
and due to the phosphorylation of Protein
kinase A (PKA), it releases growth
hormone. Somatostatin acts on GPCR. Due
to coupling, less phosphorylation, less
fusion of vesicles. Receptor for GHRH
(growth hormone releasing factor) is a G-
protein coupled receptor, coupled to GS and increases cAMP. Somatostatin blocks the
production of cAMP with the result less GH is released.
GH acts via dimerisation of 2 JAK receptors. Phosphorylated JAK receptor causes STAT
(transcription factor) to dimerize which induces gene transcription in the nucleus
The liver releases ILGF1. When the hypothalamic-pituitary gland interaction is altered, high
levels of GH will be produced. GH acts directly on adipose tissue and causes lipolysis
(cause: lower blood pressure). In other tissues in decreases glucose utilization, which leads
to gluconeogenesis. This causes a glucose intolerance and is the cause of hypophyseal
diabetes.
An overproduction of growth hormone results in gigantism (adults over 210cm/ 6”10) and
acromegaly and hypophyseal diabetes.
Octreotide and lanreotide are somatostatin analogues which can reduce GH release.
A GH deficiency leads to dwarfism, potentially due to abnormal IGF-1 receptors. Abnormal
IGF receptors have mutations in the amino acid sequence and cause inappriopriate
signalling with RAF.
Lecture calcium homeostatis and bone metabolism
The parathyroid gland is beneath the thyroid gland (releases calcitonin).
Calcitonin and PTH are antagonists
Biosynthesis of PTH
The PTH release form the parathyroid depends on the calcium levels outside the cell. At
high concentrations, the PTH stays in the parathyroid glands. At low levels of calcium
outside the cell, the PTH will be released. The low concentration of calcium causes no
inhibition to PTH release (= release). Kidneys cause the reabsorption of ca in blood, which
increases the blood ca2+ level which inhibits, via negative feedback, a decrease in blood
pressure. PTH cause the dissolution/release of CaPO4 crystals.
PTH increases blood ca2+ through:
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