Download Endocrine

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Hypothalamus wikipedia , lookup

Pancreas wikipedia , lookup

Adrenal gland wikipedia , lookup

Hyperandrogenism wikipedia , lookup

Glycemic index wikipedia , lookup

Transcript
Cortisol hormone
Cortisol inhibits glucose
uptake, stimulates protein
degradation, promotes both
lipolysis & gluconeogenesis
Gluconeogenesis:
conversion of amino acids
into carbohydrates at liver
Control over cortisol
ACTH from anterior pituitary
stimulates cortisol secretion
Negative feedback from
cortisol inhibits
hypothalamus and anterior
pituitary
Cushing’s syndrome
Excessive cortisol often due to tumor at
pituitary or adrenal gl.
Excessive
gluconeogenesis
Cortisone injections:
Patients take cortisone (converts to cortisol)
for anti-inflammatory effects (allergies,
arthritis, trauma). Immune system is
suppressed.
Chronic (continual) release of stress
hormones
Stress responses:
SNS effects (vasoconstriction, anxiety)
Fat, sugar blood levels
Fluid retained, BP
(diabetes, arterioscl)
(hyperten, heart disease)
Immune system fxn, sexual fxn, digestion all
decrease (infertility, irritable bowel, ulcers,
vomiting)
Adrenal gland: sex hormones
DHEA from adrenal cortex is a source of
‘opposite’ sex hormone in men and women
ACTH controls adrenal androgen secretion
DHEA testosterone
in women
Adrenal medulla
Functions as a modified
postganglionic neuron of the
sympathetic NS.
It stores and secretes epinephrine and
norepinephrine
In addition to FOF responses,
stimulates glucagon secretion and
inhibits insulin secretion.
Pancreas: endocrine hormones
Alpha cells
release
glucagon
Islets of Langerhans
Beta cells
release insulin
Insulin:storage and anabolism
Insulin signals to fat and
other tissues to take up
glucose (GLUTs). Prevents
the mobilization of fat.
Liver takes up fatty acids,
makes glycogen
GH, cortisol, epinephrine,
and glucagon inhibit
insulin.
Metabolism
Anabolism – building
large molecules from
smaller ones, requiring
energy
Promoted by insulin, GH
Catabolism – breaking
down large molecules
into smaller ones.
Energy is released
Promoted by glucogon,
cortisol
How the body controls metabolism
Nutrients must be stored then
released between meals. The
brain needs a constant supply of
glucose
Most conversion of molecules
occurs in the liver. Nutrients
that cannot be formed this way
are “essential” nutrients and
must come from diet.
Storing energy in the body
Excess glucose
glycogen in liver and muscles (or
adipose when there is much glycogen)
Excess fatty acids
triglycerides, in adipose
Excess amino acids
triglycerides, in adipose
Glycogen (pink) in liver cells
Blood glucose levels
Glucose levels are consistent over the day,
range about 10-15%, through action of
insulin and glucagon
Blood glucose
Insulin
Between meals, body cells can burn fatty
acids to spare glucose for the brain.
Blood glucose levels and
glycemic index
With simple carbs (high glycemic index)
glucose absorbed to blood rapidly - insulin
spike that follows is large. Glucose reduced in
blood
Blood glucose levels and
glycemic index
With simple carbs (high glycemic index)
glucose absorbed to blood rapidly - insulin
spike that follows is large. Glucose reduced in
blood
With lower glucose levels, may crave food
again
What is diabetes?
Inadequate insulin action = diabetes
mellitus (hyperglycemia)
Type I “juvenile diabetes” - body cannot
produce insulin – autoimmune disease
Type II “adult diabetes” too little insulin
made, or target cells are insulin resistant
Apple vs. Pear
Adipose and insulin resistance
Diabetes, insulin resistance (IR) is associated
with obesity, lack of exercise
When storage at fat cells is exceeded, free fatty
acids (FA) in blood increase
Adipose and insulin resistance
High FA may cause muscle and adipose to
diminish their response to insulin (IR)
Insulin less able to clear glucose from blood, still
helps store fat.
Are there mutations that promote
obesity?
“Genome-wide studies have led to the discovery of nine loci
(Mendelian) and 58 loci (polygenic) associated with obesity.
These loci explain a small fraction of the heritability for
obesity and many genes remain to be discovered”
Appetite-related hormones
(just for your own interest...not for exam)
Ghrelin – released at stomach, duodenum when
absence of food. Stimulates appetite.
Peptide YY released by ileum, colon in response to
presence of food. Inhibits appetite. (eating protein
can boost PYY)
Leptin – released by adipose, inhibits appetite.
(Obese people can have decreased response to it, still have
lower levels when wt. lost)
Mouse w/ leptin
mutation
“Indifferent” ducts
of embryo
Y chromosome
present
Y chromosome
absent
Male
Female
ovary
penis
testis
uterus
vagina
Biology of gender
Sex chromosomes determine gonadal sex
(testis-determining factor)
Phenotypic sex is depends on development
of external genitalia w/hormone
Differentiation of genitalia depends on
whether testosterone is present
At 7 weeks
Undifferentiated
genitalia
Intersex individuals experience opposite sex
hormones during early development or are
insensitive to normal hormones.
Some examples:
–
–
–
Androgen insensitivity
Lack of enzyme for testosterone
production
Congenital adrenal hyperplasia
(enzyme missing to produce cortisol,
aldosterone. Steroids converted to
androgens instead.)
Male reproductive anatomy
During fetal development, testes
move from abdomen into scrotum
Inguinal area is a common spot for
hernias (intestine pokes through
abdominal wall)
The scrotum provides a cool area
optimal for spermatogenesis