PITUITARY AND HYPOTHALAMUS

 LITTLE ANATOMY
 Pituitary gland are stored in a cavity like structure called sella turcica
 Attached to the brain by a stalk called infundibulum
 Har two parts : adenohypophysis or ant pituitary and neurohypophysis or post pituitary
 Ant. Pituitary – has three parts
 Pars distalis or pars anterior
 Pars intermedia
 Pars tuberalis – attached to the infundibulum
 Post. Pituitary – has two parts
 pars nervosa
 stalk or infundibulum
 embryologically ant. Pituitary develops from rathke pouch and post. Pituitary develops from
lower extension of diencephalon called infundibulum
 6 hormones produced by ant pituitary:
 Growth hormone
 ACTH
 TSH
 Prolactin
 FSH
 LH
 2 hormones from post. Pituitary: oxytocin and ADH
 The release of the hormones from the ant pituitary mainly depends on the five cells from the
hypothalamus namely:
 Somatotropes – for growth hormone
 Corticotropes – ACTH
 Thyrotropes – TSH
 Gonadotropes – FSH AND LH
 Lactotropes – prolactin
 30-40% of the total cells are somatotropes, 20% is ACTH and 3-4% are the others
 Hormones of posterior pituitary are formed in the mega cellular neurons of paraventricular
and supraoptic neurons of hypothalamus. Later they are secreted to the post pituitary and
stored there
 Hormones are released from post pituitary by the nerve signals from the hypothalamus
while in the case of ant pituitary the hormones are released depending on the inhibitory or
stimulating hormone is released from the hypothalamus.
 Hormones reach the ant pituitary from the hypothalamus though a hypophyseal portal
system of capillaries that reside in the median eminence
 Hormones from the hypothalamus first enter the medians eminence and tuber cinereum (an
extension of the hypothalamic tissue into the pituitary stalk) and then through the
hypothalamus – hypophyseal portal system they enter the ant pituitary.
 For all ant pituitary hormones releasing hormones are there from hypothalamus except for
growth hormone which is controlled by both releasing and inhibiting hormone and prolactin
where the inhibitory hormone which is dopamine is dominant over the releasing hormone
 PHYSIOLOGICAL FUNCTIONS OF GROWTH HORMONE
 It mainly causes growth of all the tissues and bones present in our body
 But once the epiphyses of the bone unite with the shaft the bone does not grow anymore.
Even if many growth hormones are still present
 Growth increases the transport of proteins into the cells and increase the intracellular conc.
of proteins
 Even when the proteins inside the cell are not increased it increases the translation by the
RNA to produce proteins
 It also increases the transcription by DNA so more RNA is produced and hence more
proteins.
 Decreases the protein catabolism
 It also increases the fat mobilization which increase the conc of fatty acids in the body fluids
for energy.
 it also converts the fatty acid to acetyl CoA
 when excessive fatty acid is formed in the ECF it starts forming more acetoacetic acid which
starts to appear in urine. This is called ketosis.
 Excessive mobilization of fat can also cause fatty liver
 Growth hormone decreases the glucose utilization by the cells and increase blood glucose
levels and also increase gluconeogenesis.
 Growth hormone induces insulin resistance through unknown mechanisms
 Excess of GH may cause symptoms similar to diabetes type 2
 GH is diabetogenic
 For functioning of GH carbohydrate and insulin both are necessary as insulin takes amino
acid within the cell and can be used to form glucose
 Growth hormone has one very important function of bone growth. GH only acts at the
epiphysial cartilage which lies between the epiphysis and shaft. When a child enters
adulthood, the epiphyseal cartilage diminishes and epiphysis and the shaft combine
 Once these two combines and no epiphyseal cartilage is present the bone stops growing
even if excess GH are present.
 other way through GH supports bone growth is through stimulating osteoblasts. In this bone
can grow in thickness throughout the life.
 Many of the effects of growth hormone are not performed but through certain proteins
called insulin like growth factors or somatomedins. The most among them is IGF 1
 People despite having enough GH sometimes fail to grow normally due to the deficiency of
these factors
 Laron syndrome is one such disorder where the individuals are dwarf due lack IGF 1.
 As compared to GH, IGF 1 has longer half life in blood and stays there for a much longer
period of time for about 20 hrs as it firmly attaches to a carrier protein
 IGF 1 has longer effects than GH itself
 REGULATION OF GH
 Factors that stimulate GH secretion:
 Extreme protein deficiency
 Hypoglycaemia and low conc of fatty acids
 Exercise
 Trauma
 Ghrelin – hormone secreted by stomach before meals
 Arginine
 Excitement
 GH conc increases greatly in the first two hrs of deep sleep
 Under acute conditions GH conc is greatly affected by hypoglycaemia than protein deficiency
 Under chronic conditions protein deficiency affects GH conc more than glucose levels
 REGULATION THROUGH HYPOTHALAMUS
 GHRH AND GHIH (somatostatin) released from the hypothalamus control the secretion of
GH from ant. Pituitary.
 GHRH is secreted by the arcuate and ventromedial nuclei of the hypothalamus whereas the
somatostatin is secreted from the paraventricular nuclei of the hypothalamus
 More effective is GHRH rather than somatostatin.
 Growth hormone attaches to the surface of the cell surface
 Then this attachment activates the cAMP pathway which causes the Ca channels to be
operated and allow the GH to enter the cell.
 Or change in DNA transcription can cause the production of new GH
 DISEASES
 PANHYPOPITUITARISM
 Reduction in the release of all the ant. Pituitary hormones
 Can be congenital
 This disease in adults might caused due to tumours in pituitary gland or thrombosis of
pituitary gland
 Effects of panhypopituitarism in adults:
 hypothyroidism
 decreased secretion of glucocorticoids
 suppressed secretion of gonadotrophs
 this disorder during childhood causes dwarfism. The child does not even pass through the
stage of puberty
 human growth hormone formed by E.coli can be used for the treatment for dwarfs.
 GIGANTISM
 Over secretion of GHRH form the hypothalamus caused excess secretion of GH hormone as
well
 If this over secretion occurs before adolescence, before the fusion of epiphysis and shaft the
child might grow up till 8 feet.
 Child may also develop diabetes in later life due to hyperglycaemia
 In this case if the disease is not treated the individual might develop panhypopituitarism as
well.
 ACROMEGALY
 Excess GH after adolescence
 Bones cannot grow in length but can keep on increasing in thickness and the soft tissues as
well keep increasing in size
 Very fat hands, enlarged face, enlarged tongue, jaw protrudes forward, kyphosis etc
 POSTERIOR PITUITARY HORMONES
 Hormones are transported from the hypothalamus to the post pituitary by protein
neurophysin. Once the hormones are released these proteins return back to their place
 Supraoptic nuclei – produces ADH
 Paraventricular nuclei – produces oxytocin
 If the pituitary stalk is cut above the pituitary gland and the hypothalamus is intact the
hormones will be secreted from the post pituitary but at a lower conc
 ADH
 Main function is to reabsorb water from distal tubule and collecting ducts of the kidneys
 In the absence of ADH the urine is extremely dilutes resulting in a condition called diabetes
insipidus
 MECHANISM
 ADH attaches to the receptor on the tubular cells of collecting duct which activates the
adenylyl cyclase which results in the formation of cAMP, there are special vesicles in the cell
membrane of these vesicles called aquaporins.
 cAMP enters aquaporin and phosphorylates the elements there which causes many channels
for the entry of water to open
 REGULATION
 Regulation is mainly caused by the osmoreceptors present near the hypothalamus
 When the ECF becomes concentrated, the fluid from the osmoreceptor cells move out
causing it to shrink and this sends a signal to the hypothalamus causing the release of ADH.
The opposite happens when ECF volume is diluted
 These receptors are mainly located in the supraoptic nuclei of hypothalamus but might be
located in the organum vasculosum a region in third ventricle of the brain.
 ADH also causes the constriction of vessels so it’s also called vasopressin
 OXYTOCIN
 Main role is to act on the smooth muscles of uterus during child birth
 Why is it said that oxytocin helps in child birth?
 Duration of labour is longer indicating the presence of oxytocin
 Amount oxytocin in plasma increases during labour
 Stimulation of cervix send signals to hypothalamus which secretes oxytocin
 ROLE OF OXYTOCIN IN MILK EJECTION
 Baby sucks on the nipple this sends signals through sensory neurons to the hypothalamus to
secrete oxytocin
 Oxytocin reaches the breast and causes the contraction of myoepithelial tissues present
there which results in milk ejection
 This is positive feed back as the baby sucks more, more signals are sent and more oxytocin is
released.