CIS Biochem Review Flashcards
liver fn. during metabolism
- Maintain blood glucose
- Synthesize ketones from Acetyl-CoA when we switch to lipolysis
- Synthesize fatty acids, convert to triglycerides and release as VLDLs
Requirements:
- Absorptive state: glucose and amino acids for energy
- Post-absorptive state: lactate, glycerol and amino acids for gluconeogenesis
adipose
fn. during metabolism
Functions:
- Take up fatty acids and convert to triglycerides for long-term storage
- Release fatty acids into circulation
Requirements:
- Glucose to produce glycerol phosphate for the esterification of fatty acids
- Switch to fatty acids during post-absorptive
resting skeletal mm. fn. during metabolism
Functions:
Release amino acids into the blood
Requirements:
- Absorptive state: glucose for oxidation and glycogen stores, amino acids for protein synthesis
- Post-absorptive: Fatty acids and ketones for energy
active skeletal mm. energy needs?
Fast-twitch
- Anaerobic glycolysis from glycogen
Slow-twitch
- Oxidative metabolism of glycogen
- After several hours, switch to lipolysis
absorptive state
- occurs after a meal
- blood glucose level increases
- insulin is released:
- In liver and mm: stimulates glycogen synthesis to be increased, after glycogen stores are filled, glucose is converted to fatty acids
- protein synthesis increases in muscle
- adipose: triglycerides synthesis increases
- brain/blood cells: insensitive to insulin
Post-absorptive state
- during fasting/12 hours/ overnight
Glucagon is released
- Liver: glycogenolysis occurs, glucose released into blood, AA’s and FA’s taken in for gluconeogensis
- Epinerphrine released:
1. Muscle: AA’s released into blood
2. Adipose: FA’s released into blood
muscle contraction activates TCA cycle
- increases in Ca2+
- increase in ADP
- decrease in NADH/NAD + ratio
anaerobic mm. contraction
= High-Intensity Exercise
The need for ATP exceeds the mitochondria’s capacity for oxidative phosphorylation, thus focus on anaerobic glycolysis (glucose –> 2 pyruvate –> lactate using lactate dehydrogenase)
Lactate production
- Increased NADH/NAD+ ratio directs pyruvate into lactate
H+ production
- At intracellular pH, lactic acid dissociates to lactate and H+
- Decreases pH and causes pain and fatigue
aerobic mm. metabolism
Low-Intensity Exercise
Rate of ATP utilization is lower
- Fibers can generate ATP from oxidative phosphorylation
Increase CO2
- Complete oxidation of glucose to CO2
exercise and TCA cycle
- exercise increases ATP utilization
- increases TCA cycle: generates NADH and FADH2, which are driving force for ETC
- results in increased ETC, and generation of NAD and FAD+ (driving force for TCA cycle)
- if ETC wasn’t working, would build up NADH, which would inhibit TCA cycle
messengers of exercise feedback: 1-ATP/ADP ratio 2-NADH/NAD+ 3-Ca2+ 4-Citrate
- myosin ATPase generates ADP:
* * Increase in ADP stimulates:
- Isocitrate deyhydrogenase (rate limiting step in TCA)
- results in ETC forming NAD+ and FAD - ETC utilizes NADH:
- decrease in NADH stimulates isocitrate dehydrogenase along with malate dehydrogenase
NOTE: if not getting enough O2, results in halting of ETC - build up of NADH - results in lessening of TCA cycle
- increased Ca2+:
- stimulates isocitrate dehydrogenase
- alpha-ketoglutarate dehydrogenase - When NADH/NAD+ ratio increases:
- citrate inhibits Acetyl CoA entering the TCA (exerts negative feedback on the system)
- NAD+ is allowed to increase
Increase in ADP stimulates:
Isocitrate deyhydrogenase
ETC to form NAD+ and FAD
Decrease in NADH stimulates:
Isocitrate dehydrogenase
Malate dehydrogenase
Increase in Ca2+ stimulates
Isocitrate dehydrogenase
Alpha-ketoglutarate dehydrogenase
When NADH/NAD+ ratio increases
Citrate inhibits Acetyl CoA entering the TCA cycle
NAD+ is allowed to increase
isocitrate dehydrogenase
stimulated by ADP and Ca2+, and decreased NADH
inhibited by rising NADH
exercise increases skeletal mm. capacity and efficiency for fuel oxidation in which ways?
increased txn in myocytes lead to adaptive changes:
- increased TCA enzymes, decreased lactate production
- increased ETC components
- increased number and size of mitochondria
- increased vasodilatory capacity
- increased lymphatic drainage (decreased lactate)
what happens with prolonged fasting?
- glucagon and epinephrine are elevated, approx 2 days w/out eating
- epinephrine stimulates mm. glycogenolysis
- switch to lipolysis: in order to save proteins for essential fns, Acetyl-CoA is produced and converted to ketones
mm: utilizes FA’s
brain: utilizes ketones and FA’s
RBCs: still dependent on glucose
see decreased body temp, BP, HR, decreased blood glucose, increased serum ketones, positive urine ketones
sx of anorexia nervosa
Amenorrhea
- Develops when a woman’s body fat content falls below 22% of total body weight
- Due to reduced LH and FSH production
Death by Starvation
Occurs when
- Approx. 40% of ideal body weight is lost
- Approx. 30-50% of body protein is lost
- Approx. 70-95% of body fat stores are lost
Starvation causes:
- Depletion of muscle glycogen stores
- Depletion of adipose tissue triacylglycerols
- Depletion of blood glucose from liver glycogen
** can cause vitamin deficiency
vitamin deficiency:
Symptoms
- Fatigue, nausea and loss of appetite are general non-specific symptoms of vitamin deficiency
- Muscle pain as a result of glycolysis as the primary source of energy
Riboflavin
- Vitamin precursor of FAD and FMN (in ETC proteins)
- Major coenzyme in all tissues
- Widely distributed in foods and turnover is slow so signs of deficiency are slow to occur
Niacin
- Vitamin precursor of NAD+
- Can be synthesized from tryptophan
Thiamine
- Required for a-ketoglutarate dehydrogenase
Pantothenate
- Vitamin precursor to CoA
- Widely distributed in foods
iron deficiency anemia
iron is required for ETC: causes fatigue d/t inability to transfer electrons and generate ATP
