Integrative Physiology (Nutting) Flashcards
What are the body’s objectives during absorption and storage?
- fill glycogen stores
- don’t spill too much glu in urine
- utilize ingested carbs/fat for energy
- package whatever carbs/fats you don’t need as TAG and whatever aa’s as protein
During absorption and storage, what major processes are going on involving carbs?
increased glu uptake/utilization
increased glycolysis
decreased gluconeogenesis
decreased glycogenolysis
= increased glycogen stores
During absorption and storage, what major processes are going on involving fats?
increased lipogenesis
decreased lipolysis
=increased fat stores
decreased ketogenesis
During absorption and storage, what major processes are going on involving proteins?
increased protein synth
decreased protein degradation
=increased protein stores
What are the body’s objectives post-absorption (between meals)?
- keep glu constant
- decrease glu utilization
- keep some quick glycogen reserves
- burn fats for energy
- utilize the protein you can afford to spare
During post-absorption, what major processes are going on involving carbs?
decreased glu uptake/utilization
decreased glycolysis
increased gluconeogenesis
slightly increased glycogenolysis
slightly decreased glycogenesis
= only small decreases in glycogen stores
During post-absorption, what major processes are going on involving fats?
decreased lipogenesis
increased lipolysis (forming FFA + glycerol)
=decreased fat stores
increased ketogenesis
During post-absorption, what major processes are going on involving proteins?
decreased protein synth
increased protein degradation
=decreased protein stores
**esp in muscle, lymphoid tissue
What are the short-acting hormones involved in metabolism?
insulin
epi
NE
glucagon
What are the long-acting hormones involved in metabolism?
GH
thyroid hormone
GC
sex steroids
What is the onset and duration of short-acting hormones involved in metabolism?
rapid onset, with a brief (~mins) duration
What is the onset and duration of long-acting hormones involved in metabolism?
delayed (min-hours) onset, with prolonged (hours-days) duration
What is the primary mechanism of short-acting hormones involved in metabolism?
increase or decrease enzyme or protein activity
What is the primary mechanism of long-acting hormones involved in metabolism?
increase or decrease amount of enzymes or other proteins
How do the following levels change during prolonged fasting (up to 5 days, not between handfuls of Cheerios)? Glu: Insulin: Glucagon: Cortisol: GH: T3:
Glu: maintains steady level
Insulin: decreases (most significantly post-abs)
Glucagon: increases (but then remains steady)
Cortisol: remains constant
GH: increases
T3: steadily decreases (to decrease metabolic rate)
What hormone levels remain constant between the fasting and feeding phases?
cortisol
GH
T3
How is glucagon affected by fasting? By feeding?
decreases during/after meal
may increase between meals
How are Epi/NE affected by fasting? By feeding?
decrease during/after meal
tend to increase between meals
How is insulin affected by fasting? By feeding?
increases during/after meal,
decreases between meals
Effects of cortisol during/after meal?
Effects of cortisol between meals?
slight decrease in glu uptake and utilization (glycostatic)
- -Permissive to gluconeogenesis + lipolysis
- -Mildly decrease glu uptake and utilization
Effects of GH during/after meal?
Effects of GH between meals?
increase protein synth (residual effects)
- -mildly decrease glu utilization (residual effects)
- -increase lipolysis (residual effects)
- -slows protein loss
- -glycostatic
Effects of T3 during/after meal?
Effects of T3 between meals?
- -increase protein synth (residual effects)**
- -increase glycolysis (residual)
Permissive to increased lipolysis**
**synergizes with GH
Effects of glucagon during/after meal?
Effects of glucagon between meals?
few
- -increased glycogenolysis, ketogenesis and gluconeogenesis
- -decreased glycogen synth and glycolysis
Effects of Epi/NE during/after meal?
Effects of Epi/NE between meals?
few
- -increased glycogenolysis, glyconeogenesis and lipolysis
- -decreased insulin secretion
- -mildly decreased glucose uptake
Effects of insulin during/after meal?
increases many anabolic and anti-catabolic processes
decreased catabolic processes (aside from glycolysis and TCA cycle
Effects of insulin between meals?
decreases many anabolic and anti-catabolic processes, which allows catabolic processes to dominate (such as proteolysis, glycogenolysis, lipolysis)
Where does glucagon act?
liver only
How does high blood glu affect myocytes and adipocytes?
enters myocytes and phosphorylated to glu-6P; in adipocytes, FA are stored as TAG
How does low blood glu affect myocytes and adipocytes?
TAG in adipocytes is converted to FFA; myocytes then utilize blood FFA (and ketones) to generate energy
Epi/NE (increase/decrease) glu levels in the blood.
increase (via glu production by liver)
GH (increases/decreases) glu levels in the blood.
decrease (weakly, due to glu consumption by muscle and adipose)
Explain how cortisol, glucagon and epinepherine affect blood glu independently and in combination.
Cortisol alone has very little effect on blood glu
Epi alone and glucagon alone each have modest effects on blood sugar
When all 3 combined, hyperglycemic response is far greater than the additive response of all three given singly.
Epi/NE stimulate (what enzyme?), in order to generate FFA.
hormone-sensitive lipase
aka–epi/NE have lipolytic effects!
How does insulin block lipolysis?
Insulin antagonizes the lipolytic effects of epi/NE: 1) directly via inhibiting cAMP formation
2) indirectly via increased esterification of FFA
How do cortisol, T3 and GH affect lipolysis?
All 3 act on epi/NE, encouraging lipolysis via hormone-sensitive lipase (TAG»_space;FFA)
In the liver, GC promote gluconeogenesis via what mechanisms?
- previous induction of KEY gluconeogenic and amino acid metabolizing enzymes
- increased hepatic reponsiveness to glucagon (i.e. better aa uptake)
- additional GC = further increase in synthesis of gluconeogenic enzymes
In muscle, GC promote gluconeogenesis via what mechanisms?
provide more substrates for the liver by:
1. increased amino acid release via net protein breakdown (in muscle, esp)
In adipose, GC promote gluconeogenesis via what mechanisms?
provide more substrates for the liver by:
- increased glycerol release (which the liver then turns to glu)
- GC + T3 + GH permit spikes in Epi/NE, which increases lipolysis
(**TAG = FA + glycerol)
How does glucagon (via cAMP and PKA) affect phosphorylase?
increases activity (=breakdown of glycogen > G6P > glu)
How does glucagon (via cAMP and PKA) affect glycogen synthetase?
decreases activity (=breakdown of glycogen > G6P > glu)
How does glucagon (via cAMP and PKA) affect F-2,6-BP?
decreases formation by decreasing PFK activity and increasing F-1,6-BP activity
How does glucagon (via cAMP and PKA) affect PK?
decreases activity (which decreases PEP, ultimately decreasing ACoA)
How does glucagon (via cAMP and PKA) affect AcetylCoA carboxylase?
decreases activity
somehow? this eventually results in inhibition of beta-oxidation?
How does glucagon (via cAMP and PKA) affect PEP carboxykinase?
increases synthesis
How does glucagon (via cAMP and PKA) affect pyruvate carboxylase?
slight increase
What are the effects of decreased PFK activity?
decreased glycolysis (*increased formation of F-2,6-BP)
What are the effects of increasing F-1,6-BP activity?
increased gluconeogenesis (*decreased formation of F-2,6-BP)
With prolonged exercise, the contribution of fuel from ____ increases, while the contribution from _____ decreases.
plasma FFA
muscle glycogen
During moderate exercise, levels of what hormone(s) decline?
insulin
During moderate exercise, levels of what hormone(s) increase?
epi/NE
glucagon
cortisol
GH
As glucose drops from ~100 towards ~45, how does the body counterregulate hypoglycemia?
- levels of insulin drop
- glucagon and epi increase (SNS activation, which promotes gluconeogenesis and glycogenolysis)
- GH increases
- cortisol increases
- hypoglycemic symptoms (~55 mg/dl)
- hepatic glucose auto-regulation kicks in
- cognition declines (~45 mg/dl)
*actual levels not important, just the sequence
