Chapter 22 metabolism

- Insulin and glucagon * RQ vs diet

* Main function * role of oxygen
* Cat or anab? - Thermogenesis
* triggers * Regulated vs Unregulated
* systemic and tissue, cellular * Autonomic nervous system
,and molecular response branch
* co-secretions * cholinergic vs adrenergic
*where is it synthesize, tissue * role of brown fat and
and type of cell mitochondrial uncoupling
* diseases associated with it * energy balance
* synergism * heat stroke vs heat exhaustion
* permissiveness * hyper vs hypo thermia
*antagonistic * how to release and conserve
heat
* Inhibitors
*hypothalamus and fever
* tissues that depend on the
hormones
* independent tissues - Macromolecules
* feedback reg * fate of macromolecules
* Types of work performed by
the body
-Hypothalamus and endocrine system
* what is the nutrient pool
* feeding center
* Fat digestion
* satiety center
* Where is glycogen located
* Hormones involved
* which organs perform
* general mechanism
gluconeogenesis
* where is the good fat located
- Metabolism (cellular and systemic)
- Extra stuff
* what is BMR
* Amadori reaction
* factors affecting BMR
* Diabetes 1 vs Diabetes 2
* how is BMR measured
* metabolic syndrome and
* what is Respiratory Quotient visceral fat
 Insulin
* Main function : Pancreas
B-cells
Lowering blood sugar
* diseases associated with it
* Cat or anab?

Anabolic
Diabetes (1 and 2): low
* triggers
levels and resistance,
Low sugar levels respectively.
Amino acids * synergism
GLP-1 (feedforward
mech) * permissiveness
Parasympathetic input
*antagonistic
* systemic and tissue, and
Growth hormone and
cellular response
cortisol
Systemic and tissue : * Inhibitors
transport of glucose into
cells * Targets
Cellular and molecular:
Liver, muscle and adipose
inserts GLUT-4;
tissue
glyconeogenesis;
glycolysis; lipogenesis; * tissues that depend on the
protein synthesis hormones
Molecular: stimulates
enzymes for glucose use Directly: muscle and
and glycogen synthess. adipose
Inhibits enzymes for Indirectly: liver;
glycogen breakdown, stimulates the enzyme
glucose synthesis and fat hexokinase. Lowering the
breakdown. Inhibits b- intracellular
oxidation concentration of glucose
maintaining the gradient.
* co-secretions Exercising muscle can
Amylin release GLUT-4 without
Decreases insulin
glucagon secretio * independent tissues:
Slows down
digestion Brain, GI, Kidney
Slows absorption of
* Fed or fast state:
carbs
Fed state
*where is it synthesize, tissue
and type of cell * Feedback regulation
 Low sugar stops shuts off
release
Parasympathetic
stimulate
Sympathetic inhibits
secretion
Glucagon
* Main function * synergism

Preventing hypoglycemia Epinephrine and cortisol

* Cat or anab? * permissiveness

Catabolic *antagonistic

* triggers insulin

Low blood sugar * Inhibitors

Amino-acids ( activate
Amylin
insulin, sugar gets
absorbed, hypoglycemia
develops, glucagon * tissues that depend on the
release) hormones

liver
* systemic and tissue, cellular
,and molecular response * independent tissues

Systemic and tissue: * feedback reg

increase plasma glucose high plasma sugar
Cellular and molecular:
glycolysis,
gluconeogenesis,
Hypothalamus and endocrine
lipolysis, ketogenesis
system
Activates breakdown
enzymes, glucose * feeding center
forming enzymes, and
inhibits glycogen tonically active
synthase. inhibited by satiety
Cortex and limbic system
* co-secretions communicate
*where is it synthesize, tissue * satiety center
and type of cell
Inhibits feeding center
Pancreas
Alpha-cells * 2 theories

* diseases associated with it Glucostatic: glucose

metabolism by
 hypothalamic centers * how is BMR measured
regulate food intake
Lipotstatic: fat stores Measuring oxygen
modulate eating behavior consumption
MR= oxygen consumed
* Hormones involved: perday * calories
consumed perliter of
Incr food intake
oxygen
Ghrelin (stomach)
Units= calories per day
NPY (affect FC)
Decr food intake * what is Respiratory Quotient
CCK (Int)
GLP-1 Ratio of CO2/O2
CRH * RQ vs diet
Alpha-melanocyte
(pomc) Carbs = 1
Leptin (adipose) Proteins= 0.8
Fats= 0.7
-
* role of oxygen
Metabolism (cellular and
systemic) Final electron acceptor
* what is BMR Used to produce
metabolic water
Measure after 12-hour
Macromolecules
fast
Person must be at rest * fate of macromolecules
Amount of energy needed
to support the body most Energy
basic functions when at Synthesis
rest or non-stressful Storage
situations.
* Carbs, proteins and fats
Basic function: those
necessary to stay alive Carbs
Such as: pumping blood, Energy
breathing and producing (glycolysis
heat atp)
Synthesis
* factors affecting BMR
(excesss
Age goes to fat)
Sex Storage
Lean muscle (glycogen)
Diet (diet-induced Proteins
thermogenesis) Energy (if
Genetics glucose is
Hormones low, AA are
used)
Activity levels
 Synthesis In ER TG form again
(structural Big fatty acid form
proteins, chylomicronsand go to
liporpoteins, lymp
albumin, Small fatty acids go to
clotting hepatic portal system
factors) Chylomycrons in lymph
Storage go to vena cava
( excess Lipoprotein lipase break
converted to them down into remnants
fat) and FFA
Fat Remnants go to liver for
Energy procesing
(most
energy, but
hard to get)
* Where is glycogen located
Syntheis
(chylomicron All cells but specially liver
s, and muscle, some in
liporpoteins, kidney
vldl, ldl, hdl)
Storage (TG) * which organs perform
gluconeogenesis

liver

* where is the good fat located

* Types of work performed by
the body subcutaneous (most of
the energy is here)
Transport
Mechanical (external and Thermogenesis
intracellular) *energy balance
chemical
synthesis inputs= internal and
storage external
outputs= conductive,
* what is the nutrient pool
convective, evaporation,
Nutrients available for and radiation loss
immediate use. Mainly in *Inputs (internal)
plasma
Regulated vs Unregulated
* Fat digestion
Regulated:
Bile emulsification shivering
Lipases from pancreas and non-
breakdown Tg into MG shivering
and FFA Shiverinh:
Go to epithelium skeletal
 muscle MU= electron transport
contraction chain and oxidative
Non- phosphorylation are
shivering : uncoupled. Menaing that
brown fat atp is not produced and
Non- the energy of the proton
regulated motive force is used as
(skm pure heat.
contractions Thyroid hormone and
and sympathetic input to
metabolism) B3 receptors in adipose
tissue stimulate
mithocondrial uncoupling
* Autonomic nervous system
branch
* heat stroke , heat exhaustion,
Sympathetic and somatic
malignant hyperthermia
* cholinergic vs adrenergic
HS
Cholinergic: sweat high T
glands and dilation of skin is dry
some vessels. severe
Cholinergic activates in dehydration
response in high T low bp
Adrenergic: brown fats protein
and constriction of some denaturation
vessels begins
Adrenergic activates in No sweating
response to low T Rapid cooling is
Somatic: shivering mandatory
HE
* high vs low T response Severe
dehydration
HighT: maximize Core body
heat losst: by
temperature
evaporation and
( 37.5-39 C)
convection. And Muscle cramps
minimize heat Nausea
production LowT: Lots of sweating
conserve heat and Headache
produce heat Pale
* role of brown fat and
mitochondrial uncoupling Malignant
hyperthermia
Brown fat produces heat defective calcium
by mithocondrial channel in muscle
uncoupling
 ER. Releases too Fever is physiological
much calcium to Pyrogens
cytosol due to (interleukin,
defective interferons and
ryanodine TNF) reset
channels thermostat.
Cell tries to bring Set point is now
it back higher
Process needs atp, Body feels cold and
and this releases induces all the
heat mechanism to
Trigger by conserve heat and
anesthesia produce heat
DANTROLEN Shivering and non-
E (DRUG) shivering
Inhibit thermogenesis
s occurs
calciu Temperature rises
m
releas
e from
ER by
blocki
ng
ryano
dine
chann
el.

Hypermetab
olism
Acidosis
Genetic
disorder

* Hypothalamus and fever

Thermoregulatory center:
thermoreceptors are
located in
Peripherally in skin
Central
hypothlamus
Cutaneous blood flow
changes depending on
thermos-needs
Extra stuf
* Amadori reaction insulin
resistance.
Hemoglobin A1c or Elevated
glycated hemoglobin glucagon
HG reacts with glucose leves
and forms a Schiff base Glucose tolerant test
Measures average sugar Fasting person
consumption for the past drinks solution of
3 months 75g glucose
Why? Because RBC Glucose is
last for around 120 measured every 30
days. seconds for 2 hrs
* Diabetes 1 vs Diabetes 2 Normal people
experience an
D-1 increase in plasma
(insulin is not glucose but it soon
produced, levels
autoimmune Pre- diabetics and
diseases, b-cells diabetics levels
were destroyed) : can remain elevate
dehydration, low over 140mg/dl
bp, osmotic
diuresis, polyuria,
* metabolic syndrome
polyphagia,
polydispsia, if u have three of
metabolic acidosis, the following
tissue loss, incr high
ventilation, bp
hyperkalemia due centra
to acidity, increase l fat
ADH to conserve low
water, glycosuria. hdl
Satiety center is high
insulin dependent: ldl
therefore they high
cant metabolize plasm
sugar in the a TG
absence of insulin high
and polyphagia plasm
occurs. a
D-2: sugar
usually no apple-shaped
metabolic (widest waist)
acidosis women are more
high levels prone to develop
of insulin MS than pear-
because of
 shaped (widest CVD
hips). Atherosclerosis
Retinopathy and
*visceral fat
blindness
metabolize by liver
and turn into
cholesterol
increses risk of
developing: insulin
resitance,
metabolic
syndrome
heart disease

* Pancreas cells

alpha= glucagon
Beta= insulin and amylin
D= somatostatin (inhibits the
secretion of both insulin and
glucagon)
PP or F= pancreatic polypeptide

D2 and D1

D1 is an autoimmune disease
D2 is insulin resistamce
D1 most are ketoacidotic
D2 can become insulin deficient
in the future
D2 have usually elevated
glucagon levels
Why? Alpha cells
need require
insulin for sugar
intake, if they
become resistance
they cant use the
glucose, which
prompts them to
secrete GLUCAGON
Risks
Kidney failure