Hypothalamus and Pituitary Gland

Supraoptic nucleus (water balance); paraventricular nucleus (stress response)

Regulation of appetite and controls releasing hormones

Rankthe's pouch

Hunger centre

Medial preoptic nucleus

Anterior hypothalamic area

Suprachiasmatic nucleus

Lateral hypothalamic area

Ventromedial nucleus

Dorsomedial nucleus

Posterior hypothalamic area

Feeding; stress response; water balance; thermoregulation

Within cells of the anterior pituitary itself

Within the hypothalamus

No

Superior and inferior hypophyseal arteries

Sella turcica

Formation of Rathke’s pouch from oral ectoderm; formation of the infundibulum from neuroectoderm; migration and growth of Rathke’s pouch towards the infundibulum; differentiation into the anterior and posterior pituitary

GH1 gene

GHRH

IGF-1

Inhibits release of growth hormone

Inhibits release of TSH

TRH

Inhibits prolactin release

TRH levels increase in response to low thyroid hormone levels; high levels of TRH stimulate prolactin release

TRH

CRH stimulates ACTH release by stimulating the production and cleavage of POMC

Kisspeptin

Lies in the gland itself

Lies in the pituitary gland

Stimulates GHRH

Stimulates growth hormone release, partly through GHRH

Increases somatostatin release as part of negative feedback

GHRH levels increase as somatostatin usually inhibits GHRH release

IGF-1

Growth hormone and IGF-1 levels are high during childhood and peak during puberty; they decline with age.

Increases GH cell number; increases GH synthesis; stimulates GH release

G protein-coupled receptor (Gs)

Cytokine receptor

Activating mutation in the GNAS gene, which encodes the alpha subunit of the Gs protein

A disorder caused by an activating mutation in the GNAS gene, leading to continuous activation of adenylyl cyclase and increased cAMP production

At least two of the following: café-au-lait skin pigmentation, fibrous dysplasia of bone, and endocrine hyperfunction such as precocious puberty

Five subtypes (SSTR1–SSTR5)

Growth hormone

AIP gene mutation

Cortisol

Cortisol, aldosterone and adrenal androgens

increased POMC production leads to increased ACTH and melanocyte-stimulating hormone activity, causing hyperpigmentation

Melanocortin 2 receptor (MC2R)

MC1R

Early morning, around waking

ACTH-dependent; ACTH-independent

Prescribed glucocorticoids; adrenal tumours

Inhibits FSH production and release; has little direct effect on LH

Inhibits FSH, indirectly reducing ovarian oestrogen production; it has little direct effect on testosterone production

Increases kisspeptin signalling, helping activate GnRH secretion

Preferentially increase LH release

Preferentially increase FSH release

Administer continuous GnRH or a GnRH agonist, which downregulates pituitary GnRH receptors and suppresses LH and FSH release

In the hypothalamus

Pulsatile secretion, with the largest pulse occurring during deep sleep; secretion is increased by exercise, stress and fasting

In the higher brain centres that regulate the hypothalamus

KAL1 (anosmin-1) in X-linked Kallmann syndrome

Can be X-linked, autosomal dominant or autosomal recessive, depending on the gene involved

A syndrome caused by impaired migration of GnRH-producing neurons to the hypothalamus, resulting in hypogonadotropic hypogonadism and anosmia

Loss of sense of smell; hypogonadism and delayed or absent puberty; renal agenesis may occur; increased arm span due to delayed epiphyseal closure

Stimulates uterine contractions during labour; causes milk ejection during breastfeeding; contributes to social bonding

ADH (vasopressin), in central diabetes insipidus

Desmopressin