Energy and organic matter balance

Question 1

Obesity

Answer 1

• Arises if the body fails to properly adjust the composition of fuel the body burns in relation to the composition of food ingested
• If more fat is consumed than burned obesity can occur
• Same thing for carbs

Question 2

RQ and FQ

Answer 2

• RQ is respiratory quotient, the amount of O2 it takes to burn off 1 CO2 from a compound
• For glucose RQ is 1, for fats RQ is .7 for proteins RQ is .85
• FQ is the relative amount of each that is absorbed
• An RQ=FQ means the body is balancing its composition by burning fats/glc at an equal ratio than it is ingesting
• If RQ>FQ then there is relatively less fat burned (more glc burned, higher RQ-closer to 1) compared to the amount ingested
• RQ>FQ will change the composition of the body

Question 3

The absorptive state

Answer 3

• Glucose and fructose are the major source of energy, w/ burning of fats reduced (thus RQ approaches 1)
• This state is stimulated by insulin, therefore insulin is a regulator of body composition
• Other actions in absorptive state: protein synthesis, glycogen synthesis, TAG synthesis and storage
• Glycerol-3-P is the backbone for TAG synthesis but is made via glycolysis in adipocytes, since adipocytes lack glycerol kinase they cannot utilize circulating glycerol

Question 4

Post absorptive state

Answer 4

• Glucose utilization is surpassed by fat utilization in all tissues but nervous tissue and RBCs
• Fats are broken into ketoacids
• Thus the RQ approaches .8
• Fats are released by adipose tissue
• Liver breaks down glycogen and begins GNG

Question 5

Insulin and the regulation of post absorptive state

Answer 5

• Insulin promotes burning of carbs, storage of carbs/fats/protein, and thus body composition
• Factors that cause insulin release: PsNS vagal stimulation of pancreas
• Incretins (GLP1) distinguishes a rise in blood glc from digestion vs a rise in blood glc from GNG/glycogenolysis
• GLP1 causes insulin release
• High levels of blood glc cause insulin release
• Beta-adrenergic receptors stimulate insulin release (but alpha receptors are dominant on pancreas, thus SNS activation causes inhibition of insulin release)
• Factors that inhibit insulin release: low blood glc, SNS activation via alpha-adrenergic receptors, pancreas-produced somatostatin inhibits insulin

Question 6

Ghrelin, amylin, and leptin

Answer 6

• Ghrelin is released by the stomach when it is empty and stimulates hunger (the nz GOAT is required for functional ghrelin)
• When stomach is full ghrelin release is diminished and hunger dissipates
• Amylin is found in the pancreas of T2 diabetics, and it inhibits insulin-induced muscle uptake of glc but had no effect on adipose tissue
• Leptin is released from fat cells when there is increased fat mass
• It binds to the arcuate nucleus of the hypothalamus to stimulate the sense of satiety, increase energy expenditure, reproductive function, and to stimulate thermogenesis

Question 7

Exercise on muscle glc uptake

Answer 7

• Exercise improves muscle response to insulin, allowing muscle to more effectively uptake glc
• This is b/c exercise depletes glycogen stores, increasing the muscle’s need for glc
• Insulin shifts muscle fuel source at rest towards fat, allowing muscles to store the glc for when it is needed instead of burning it at rest
• Together these make muscles more sensitive to insulin after exercise

Question 8

Glucagon, epinephrine regulation

Answer 8

• Both of these together oppose the action of insulin
• They cause the release of fat from adipose tissue, breakdown of glycogen, GNG, release of glc into the blood, inhibit the release of insulin, and blunt insulin’s effectiveness in muscle
• Glucagon released in response to both SNS and PsNS, and a decrease in blood glc levels
• Insulin inhibits glucagon release and vice versa

Question 9

Thermogenesis

Answer 9

• NEAT is all of the energy that is used not for sleeping, energy, sports-like activities
• All of the energy that normal activities and being alive requires
• Brown fat (BAT) can be a way to increase glc consumption and fight obesity since it burns glc into nothing but heat using uncoupling protein (UCP)
• Since cold temps increase glc consumption there may be a way to mimic this state to increase BAT glc consumption
• Also, there may be signals from BAT and muscle that signal to the CNS the status of their energy reservoirs (much like how leptin does from white fat)
• These pathways may be altered in people w/ obesity