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what is the dynamic state of lipids in the body
catabolism (breakdown) and anabolism (synthesis) are constantly happening
what are the 6 functions of lipids?
1) fats can be oxidized to CO2 for ATP (krebs)
2) make up glycolipids and phospholipids
3) contribute to lung alveolar integrity
4) solubilize & store fat-soluble vitamins (ADEK)
5) help synthesize prostaglandins, sex hormones, and adrenal hormones
6) provide energy
how are triglycerides stored in the body
in all tissues
adipose tissue: a special fat tissue made of adipocytes (fat cells that will synthesize fat & store it for later use)
what is the difference between fat storage and fat catabolism?
1) fat storage
occurs in energy surplus
glucose, proteins & fat → fat storage
2) fat catabolism
occurs in energy deficiency
fat storge → energy
what is the role of insulin?
increases fat storage
in adipocyte
released after a meal
what is the role of epinephrine
decrease fat storage when body is under stress
limits the ability of adipocytes to store fat
what is the role of cortisol
decreases fat storage
what is the role of glucagon
decreases fat storage
what is the role of growth hormone
decreases fat storage
so what 4 hormones decrease fat storage
cortisol, epinephrine, glucagon, growth hormone
how does triglyceride deposition vary between ruminants and monogastric animals?
1) monogastric: composition of TGs deposited in the body are similar to the ones consumed (eat saturated fats = deposit saturated fats)
2) ruminants: composition can be different because unsaturated fats are saturated in the rumen (so saturated fats are deposited when unsaturated fats are consumed)
how long are fat-soluble vitamins and cholesterol stored?
~30-90 days
how does lipid production in mammary tissue differ between ruminants and monogastrics?
1) monogastrics: milk fat is primarily derived from GLUCOSE
2) ruminants: milk fat is primarily derived from VFAs (ACETATE)
what are the 4 sources of acetyl-CoA?
1) CHOs
2) Proteins (amino acids)
3) VFAs in ruminants (glucose → pyruvate → lactic acid or A-CoA)
4) Degraded fats
what tissues does fatty acid synthesis take place
liver, kidney, brain, lungs, mammary gland
where in the cell does fatty acid synthesis take place
cytosol
how are fatty acids formed
1) fatty acid synthase adds 2 carbons at a time in the form of acetyl CoA
2) repeat until the fatty acid is 16 carbons long
what is the enzyme that performs fatty acid synthesis
fatty acid synthase
how is fatty acid synthase regulated
1) excess energy = ^^ fat synthesis
2) deficient energy = vv fat synthesis
how are fats broken down
1) 2 carbons at a time, beta oxidation
2) triglyceride + tissue lipase = glycerol + fatty acid
what tissues break down fats
muscle, connective tissue, liver, kidney, and adipose tissue
what body parts rely heavily on fatty acid oxidation
liver, heart, and resting skeletal muscle
whats the step by step of beta oxidation
1) 1 mole of acetate (2 carbons) is removed as acetyl CoA
2) process repeats until the fat is completely broken down
original fat has even number of C: breaks down into just acetyl CoAs
original has ODD number of C: breaks into mostly acetyl CoA and 1 propionyl CoA (3 C)
3) acetyl CoA enters the kreb cycle and produces energy
where does beta oxidation occur in the cell
mitochondria
how many ATP do you get from 1 acetyl-CoA in the krebs cycle
12
how much ATP is produced from one step of beta oxidation (removing 1 acetyl-coa)
5 (1 NADH and 1 FADH2)
when can ketosis occur
when an animal has a high energy demand, like a lactating ewe or high producing dairy cow
how does ketosis work
increase energy demand (milk production) → increased beta oxidation → increased acetyl CoA → acetyl CoA overloads the krebs cycle and backs it up → so acetyl CoA is converted to ketones → blood pH decreases → metabolic acidosis
what are the 3 examples of ketones
1) acetoacetic acid
2) beta-hydroxybutyric acid
3) acetone
what ketone is toxic in large amounts
acetoacetic acid
what are the symptoms of ketosis
weak, trembling, acetone breath (acidic)
what are the remedies for ketosis
calcium gluconate or sodium propionate
these are buffers that increase the pH of the blood and provide glucose to shut down beta oxidation (& thus decrease amt of acetyl CoA)