fasting, starvation, and disorders of energy balance

Question 1

absortive state

Answer 1

• abundant nutrients circulating in GI
• glucose is taken up by different tissues

Question 2

short term fast

up to 12hr (or 24hr)

Answer 2

• hepatic glucogenolysis
• only hepatocytes have ability to breakdown glucose and release into circulation

Question 3

short term fast

beyond 24 hr

Answer 3

• glucose stores no longer available
• gluconeogenesis (makes glucose)
• uses amino acids - principle substrate coming from endogenous protein

Question 4

long term fast

Answer 4

• using ketones - keto absorption
• preserves endogenous tissues

Question 5

metabolic adaptations seen with a prolonged fast (starvation) are targeted to do what

Answer 5

spare endogenous proteins

Question 6

what is they key protein-sparing adaptation

Answer 6

ketogenesis

Question 7

what also spares energy reserves and endogenous proteins

Answer 7

decreases in metabolic rate (RER) and protein catabolism

Question 8

weight loss protocols

Answer 8

• programs induce 30-40% caloric restriction
• provide adequate protein and micronutrients
• create a negative energy balance to promote weight loss through utilization of adipose tissue

Question 9

why does weight loss often plateau after a period of energy restriction?

Answer 9

• animals total energy requirement is less - RER goes down - need to adjust plan
• do intermediate fasting to solve problem

Question 10

during a weight loss protocol, is there any way to spare endogenous protein?

Answer 10

• don’t restrict too aggressively
• dogs: enough CHO in diet
• feed high protein diets
• resistance training

Question 11

how do critical organs get amino acids in critically ill patients

Answer 11

get AA from skeletal muscle

Question 12

unstressed starvation

Answer 12

• mediators secreted in response to lack of food
• conservation of endogenous proteins
• resolves with feeding

Question 13

stressed starvation

Answer 13

• mediators secreted in response to tissue injury and inflammation
• no conservation of endogenous proteins
• resolves with healing

Question 14

what is type 1 diabetes mellitus

Answer 14

absolute deficiency of insulin

Question 15

what is type II diabetes mellitus

Answer 15

tissue insulin resistance

Question 16

pathogenesis of diabetes mellitus

Answer 16

• decreased insulin or tissue insulin sensitivity
• decreased tissue uptake and utilization of glucose, AA and FA
• increased hepatic glycogenolysis and gluconeogenesis
• hyperglycemia
• increased release of FFA by adipose tissue
• decreased hepatic lipogenesis and increased hepatic lipolysis and ketogenesis
• increased ketonemia overwhelms body’s buffering capacity and leads to metabolic acidosis