Creatine kinase is the driving enzyme in the reaction of transferring a phosphate from CrP to an ADP molecule to produce creatine and ATP. 

Low ATP and High ADP levels increase creatine kinase activity. 

CHO: glycogen stores broken down

PRO: broken down and converted to glucose to produce energy for the brain, CNS, and other cells

FAT: Fatty acids used to create ketone bodies for energy in other cells

CHO: broken down to glucose, stored in liver and muscles as glycogen, excess stored as fat.

PRO: amino acids used to replace body proteins, nitrogen lost to excretion, excess stored as fat

FAT: Fatty acids--> stored as body fat

Advantages: safe, non-invasive, quick, cost-efficient, portable, easy to operate, 

Disadvantages: Affected by hydration status and electrolye balance

Advantages: Gold standard in BMD measurment, non-invasive, safe if not pregnant, relatively portable

Disadvantages: metal rods/pins may throw off readings, table has a weight limit, expensive, radiation used, requires trained personnel

Advantages: noninvasive, relatively precise for body fat measurement

Disadvantages: High equipment costs, uncomfortable for subjects, inability to measure gas volume in GI tract, assumption that density of lean body mass is relatively constant, when in fact bone density typically changes with age. 

The high ratio elicits the following responses:

• Depletes alpha-ketoglutarate (transamination of amino acids in gluconeogenesis)
• Shifts in DHAP--> G3P, favors G3P formation (back bone for fatty acid synthesis)
• Slows TCA cycle by inhibiting dehydrogenase activity at alpha-ketog. and isocitrate
• Increases amount of citrate, increased fatty acid synthesis

• Acetaldehyde is able to attach to covalently to proteins and form protein adducts. If this adduct is involved with an enzyme, the activity of that enzyme will also be impaired.
• Acetaldehyde impedes the formation of microtubules in hepatocytes and develops of perivenular fibrosis --> cirrhosis

ETOH can induce enzymes of the MEOS, increasing the rate of metabolism of sbustrates oxidized by this system (CYP2E1). Although induction accelerates the hepatic oxidation product is not retinal but other polar, inert products of oxidation. 

The hepatic depletion of retinol can therefore be attributed to its accelerated metabolism, which is secondary to ETOH induction of a metabolizing enzyme. In effect, the alchoholi subject becomes tolerat to vitamin A, necessitating a higher dietary intake fo the vitamin to maintain normal hepatocyte concentrations.