chapter 24 Flashcards
part 2
glycogenesis
glucose is converted to glycogen and stored in animal tissues
glycogen
polysaccharide stored in animal tissue (e.g muscle tissue cells)
when does glycogenesis occur
too much glucose in the body
what is most active in glycogen production and storage
skeletal muscle and liver
glycogenolysis
glycogen converted to glucose-6-phosphate for glycolysis
when does glycogenolysis occur
body short on glucose
in skeletal muscle
glucose-6-phosphate cannot be released must be used for itself
in liver
Hepatocytes can covert glucose-6-phosphate to free glucose and release it to blood
gluconeogenesis
formation of glucose molecules from non-carbohydrate sources
ex. lipids and proteins
when does gluconeogenesis occur
body is desperate for glucose
important of gluconeogenesis
protective measure: prevent glucose hogging organs from experiencing low blood sugar
lipogenesis
synthesis of trigylcerides
When and where does lipogenesis occur
cytoplasm of cells
when there is excess energy: after eating a carb-heavy meal
lipolysis
breakdown of triglycerides
when does lipolysis occur
body short on glucose
must break triglycerides for energy
amino acids can produce energy by
- degrading them into molecules that can be used for the citric acid cycle
- converted to glucose
what must be removed for body to use amino acids as energy
amine group (NH2)
3 processes that can convert amino acids into useable energy sources
transamination
oxidative deamination
modification of keto acids
transamination
the transfer of an amine group from an amino acid to a keto acid
what accepts the amine group in transamination
a-ketoglutaric acid which is then transformed into glutamic acid (glutamate)
oxidative deamination
amine group of glutamic acid is removed as ammonia
ammonia combined with CO2 to form urea and is excreted
what does oxidative deamination produce
a-ketoglutaric acid again, which can be used in the citric acid cycle
modification of keto acids
keto acids in number 1 are altered
- a ketoglutaric acid
- pyruvic acid
- acetyl CoA
can e used in citric acid cycle
absorptive state
nutrient storage is occuring
how does anabolic activity compare to catabolic activity in the absorptive state
anabolic > catabolic
how long does the absorptive state last
about 4 hours after eating a meal
nutrients enter blood stream from GI tract
hormonal controls of absoptive state
insulin: beta cells of pancreas release insulin in response to increasing blood glucose and amino acid levels
what does insulin cause
diffusion of glucose into body cell increases
hypoglycemic hormone
uptake of amino acids increases: protein synthesis
postabsorptive state
nutrients used to create energy
how does anabolic activity compare to catabolic activity in the postabsorptive state
catabolic> anabolic
when does postabsorptive state occur
when GI tract is completely empty: no absorption occurring
importance of postabosprtive state
maintains blood glucose levels at the desirable rate 90-110 g glucose/ dL blood
hormonal controls of postabsorptive state
glucagon: released by alpha cells in the pancreas in response to decreasing blood glucose levels
glycogenolysis and gluconeogenesis occur
cholesterol metabolism
structural basis of bile salts steroid hormones, vitamin D, plasma membranes
lipoproteins
transport cholesterol to and from body tissues
cholesterol is insoluble in water
low density lipoproteins
high lipid content
high density lipoproteins
high protein content
very low density lipoproteins
most come from the liver
70-80 triglycerides
transport triglycerides from liver to peripheral tissues
low density lipoproteins
what remains after triglycerides are unloaded from VLDLs
still has high lipid content: 30-35%
transport cholesterol from the liver to peripheral tissues
high density lipoproteins
low lipid content: triglycerides and cholesterol
high protein content
transport cholesterol from peripheral tissues to the liver
Cholesterol is broken down in the liver and used for bile
provides steroid-producing organs with cholestoral for hormone production
blood cholesterol should be
200 mg/dl blood
higher levels of cholesterol linked to
heart disease
atherosclerosis : hardening of blood vessels: incresse blood pressure
HDL are
healthy
60+ mg/dl is desirable
dispose of cholesterol in body tissues
keep LDLs
low
bring cholesterol to body tissues: can cake up in blood vessels
160+ mg/dl is not good
regulation of blood cholesterol
negative feedback loop between diet and liver
intake of saturated fats and unsaturated fats influence cholesterol levels
saturated fat intake stimulates
cholesterol production by liver and prevents its excretion
high saturated fat= high blood cholesterol
unsaturated fat intake stimulates
catabolism to bile salts and its excretion
high unsaturated fat intake= lower blood cholesterol
trans fat intake
increases LDLs and decreases HDLs
other influences of HDLs and LDLS
- stress and smoking: lower HDLS
- regular exercise and estrogen: lower LDLS
- body shape: apple-shaped ppl are more prone to higher LDLs compared to pear-shaped individuals
energy intake
energy liberated during food oxidation
energy output
energy used to do work, energy stored as fat or glycogen or energy lost as heat
heat cannot be used as an energy source but is useful for
- warming tissues and blood
- maintaining internal body temperature
what structure helps regulating food intake
hypothalamus: regulates and influences feeding behaviors
hunger promoting regions of hypothalamus
arcuate nucleus(ARC) : NPY/ AgRP neurons release neuropeptide Y and agouti-related peptide
what does NPY make us crave
carbohydrates: short on glucose
NPY makes hunger fast and severe
satiety promoting regions of the hypothalamus
Arcuate nucleus(ARCH): POMC and CART neurons release peptides: bind to brain no longer feel hunger
POMC
pro-opiomelanocortin
CART
cocaine and amphetamine-regulated transcript
short term regulation of intake
- neural signals from the digestive tract
- blood levels of nutrients
- GI tract hormones
neural signals of digestive tract
vagal nerve fibers carry information between the brain and gut and allows the brain to tell
1. content of ingested food (carbs, proteins and lipids)
2. suppression of appetite via activation stretch receptors
appetite suppressing hormones
insulin
Cholecystokinin (CCK): blocks affects of NPY
appetite stiulating hormones
glucagon
epinephrine
Ghrelin (GHr): released by stomach during fasting periods
long term regulation of intake
leptin: hormone released by adipose tissue in response to increasing body fat stores
allows brain to keep track of how much total energy is stored in fat tissue
rising leptin binds to ARC
NPY release inhibited
Stimulates CART
metabolic rate
the body’s rate of energy output, including the total heat produced by all the chemical reactions and mechanical work of the body
basal metabolic rate
the energy the body needs to perform only its most essential activities
breathing and resting level of organ function
total metabolic rate
the rate of calorie consumption needed to fuel all ongoing activities (involuntary and voluntary)
