ENDOCRINE SYSTEM - Coggle Diagram
HYPOTHALAMUS AND PITUITARY GLAND
Anatomy & Terms
is the area in the brain that is structurally and functionally connected to the pituitary gland.
is also called the hypophysis. It arises from two different tissue sources: posterior pituitary is nervous tissue (neurohypophysis) and anterior pituitary is glandular (adenohypophysis).
is the glandular portion derived from the mouth epithelium (Rathke’s pouch). It forms a cuff (pars tuberalis) around the infundibulum.
is the neural portion derived from an extension of the hypothalamus (median eminence) which remains connected throughout life by a stalk, called the infundibulum
peptides called releasing factors.
secreted in an episodic and pulsatile manner.
present at high concentrations at target cell.
present at very low concentration in systemic blood.
Actions of hypothalamic peptides
binding to plasma membrane receptors.
release of stored target hormones (in pituitary) via exocytosis.
increase of transcription of target hormones.
modulation of their receptor activity (up regulation; down regulation).
Regulation by Feedback Loops
Long loop feedback
: hormones from peripheral endocrine glands can exert feedback control on the hypothalamus and anterior pituitary. This feedback is usually negative.
: Negative feedback by pituitary hormones can inhibit the synthesis and/or secretion of the related hypothalamic hormones.
GH Secretion from Anterior Pituitary
Growth hormone (GH)
secretion is governed by the
in a pulsatile and episodic manner.
secretion of GH occurs
. Excess secretion of GH results in acromegaly. Acromegaly before puberty results in a giant. After puberty, acromegaly results in a thickening of the hands and feet and coarsening of facial features.
. Insufficiency of IGF-1 alone results in pygmies (found in Africa and Australia). Receptor resistance for GH results in Laron Dwarfism.
Disruption of Signalling in H-P Axis
As a general rule a partial or complete lesion at any step in the feedback loop results in
loss of hormones downstream
of the lesion and an
increase in hormones upstream
of the lesion.
ENDOCRINE PANCREAS & FUEL HOMEOSTASIS
Fed or anabolic state
occurs immediately after a meal when the energy of nutrients (carbohydrate, protein, or fat) is transferred to high energy compounds for immediate use or for storage. Peripheral tissues (predominantly skeletal muscle) buffer
ingested glucose by storing it
Fasted or catabolic state
occurs later when the level of available nutrients decreases in the blood, and
the stored reserves (initially glycogen) are mobilized to perform work or to generate heat
. During prolonged fasting, fat oxidation and ketone bodies are used to meet whole body
Low insulin to high glucagon ratio
occurs in the fasting and “fight or flight’ states resulting in increased levels of blood glucose. Glucose is released into the blood by the breakdown of glycogen (glycogenolysis) and fat (lipolysis).
Glucagon is secreted from the pancreatic islet alpha cells when blood glucose levels are lower than 80 mg/dL.
to low glucagon ratio occurs in the fed state activating anabolic pathways, such as storage of glucose and fatty acids as triglycerides (fats).
Insulin is secreted from the pancreatic islet beta cells when blood glucose levels are higher than 100 mg/dL.
Pancreas Secretes Insulin & Glucagon
Insulin is secreted from the pancreas by a process called
glucose stimulated insulin secretion (GSIS)
. Insulin is secreted in a
. Insulin secretion is regulated by factors other than glucose. Both an
increase in plasma amino acids
the feed forward signaling by glucagon like peptide from the small intestine
will lead to secretion of insulin.
is a peptide hormone secreted from the pancreatic islet alpha cells when glucose levels are less than 80 mg/dL. Glucagon circulates unbound in the plasma; it has a half- life of 6 minutes.
In the absence of insulin, glucagon is secreted
. Glucagon acts in a synergistic manner with cortisol and epinephrine to raise blood glucose levels
Inhibition of Insulin Secretion
There are several potent inhibitors of insulin secretion including
somatostatin and the catecholamines (epinephrine and norepinephrine)
Effects of Insulin
The primary targets for insulin are
liver, skeletal muscle, and fat
. Insulin has multiple actions in each of these tissues, the net result of which is fuel storage (glycogen or fat).
inside cells shifts the energy source to protein, fat, and glycogen. A first consequence is
protein deficiency and the second consequence is an increase in free fatty acids and triglycerides from increased lipolysis
(excess glucose in the blood) can lead to cellular dehydration. Once the kidney reaches its threshold for glucose reabsorption, glucose is excreted in the urine. This leads to an
increased output of urine and loss of electrolytes
. Long term hyperglycemia can lead to vascular injury resulting in blindness and end-stage renal disease.
Insulin-dependent diabetes mellitus (IDDM, type I)
- these patients do not produce sufficient amounts of insulin and therefore they must be injected with insulin daily.
Non-insulin dependent diabetes mellitus (NIDDM, type II)
- these patients are characterized by either insulin insufficiency due to beta cell dysfunction and/or by target cell receptor resistance.
HYPOTHALAMUS - PITUITARY - ADRENAL AXIS
The adrenal gland is located on
top of the kidney
. Like the pituitary, two distinct tissues merge during development to form the
adrenal cortex (glandular tissue)
medulla (modified neuronal tissue)
The major mineralocorticoid in humans is
. Aldosterone is NOT under the hypothalamus-pituitary control and does not mediate a negative feedback to this axis. Aldosterone secretion is increased by the
vasoconstrictor, angiotensin II, and by elevated plasma K+ concentration. Elevated plasma Na+ inhibits the secretion of aldosterone
In response to stress, the glucocorticoid,
cortisol, maintains blood glucose levels for “fight or flight”
mobilizes energy stores
. It changes metabolism in the body to
degrade protein and fat and to synthesize glucose
. These are catabolic actions that elevate blood glucose levels. Cortisol also suppresses the immune system.
is caused by over-secretion of ACTH leading to an excess of circulating cortisol.
is caused by the destruction of the adrenal gland. This is a life threatening condition due to the loss of aldosterone and cortisol.
Adrenal Medulla Hormones
Cells in the adrenal medulla synthesize and secrete
norepinephrine (NorEPI) and epinephrine (EPI)
. The ratio of the two catecholamines differs considerably among species but in humans roughly 80 % of the catecholamine output is epinephrine.
HYPOTHALAMUS - PITUITARY - THYROID AXIS
Synthesis, Secretion and Storage
of thyroid hormone takes place in the thyroid
absence of iodide
, thyroid hormones are
Thyroid hormones are
. They are transported by specific carriers (
thyroid binding globulin
Conversion in Peripheral Tissues
is the prohormone which can be
by an enzyme called
. During starvation or prolonged fasting, the deiodinase activity is inhibited
Sites and Mechanism of Thyroid Hormone Action
activates gene transcription
in all tissues. The thyroid hormone
binds to the thyroid hormone receptor (THR)
which resides on DNA in the nucleus. Transcription of two important genes, the
Na-K ATPase and the beta 1 adrenergic receptor
, are increased by TH action. Increased adrenergic receptor activity in turn leads to an
increase in the expression of uncoupling proteins in mitochondria which generates heat
is an autoimmune disease in which circulating antibodies (IgG) bind to and activate the TSH receptor on the thyroid gland follicular cells. This leads to increased secretion of T3 and T4.
can lead to an enlarged gland called a
Frank iodine deficiency
has been virtually eliminated by iodine supplementation of salt.
leads to muscle wasting, nervousness, weight loss due to increased metabolism and decreased tolerance for heat. A common sign of hyperthyroidism is a rapid heart rate.
leads to weight gain due to decreased metabolism, hair loss, mental sluggishness, and decreased tolerance to cold.