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Uman Hysiology: Metabolism and Energy Balance
Uman Hysiology: Metabolism and Energy Balance
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
Dee Unglaub Silverthorn, Ph.D.
Chapter 22
Metabolism and Energy Balance
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
Dee Unglaub Silverthorn, Ph.D.
In adipose cells
In blood: HDL, LDL
FFAs, cholesterol
(plaque build up)
Conversion in liver
Excreted in bile
Used for energy & synthesis
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-5: Transport and fate of dietary fats
Fasted State or Post-Absorptive Metabolism:
Catabolic
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-6: Fasted-state metabolism
Pancreatic Hormones, Insulin & Glucagon Regulate
Metabolism
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-10: Insulins cellular mechanism of action
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Insulin: Summary and Control Reflex Loop
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-13: Fed-state metabolism
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Relationship between HbA1c and
average finger blood glucose
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 21-14: Endocrine response to hypoglycemia
Diabetes Mellitus: Abnormally Elevated Blood
Glucose (Hyperglycemia)
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-15: Acute pathophysiology of type 1 diabetes mellitus
Diabetes Mellitus: Type II a Group of Diseases
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-17: Energy balance
Body Temperature Balance: Homeothermic
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-18: Heat balance
Thermoregulation:
Homeostatic Balancing of Body Temperature
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-19: Thermoregulatory reflexes
Thermoregulation: Prevention of Overheating
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22-20: Homeostatic responses to environmental extremes
Thermoregulation: Pathologies
Hyperthermia: body temperature too high
Fever: pyrogens fight pathogens
Heat exhaustion (1020F)
Heat stroke (1060F) death
Malignant hyperthermia defective Ca++
release
Hypothermia: body temperature too low
Metabolism slows loss of consciousness,
death
Surgical applications: heart surgery
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Malignant Hyperthermia
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic
disorder of skeletal muscle calcium regulation associated with
uncontrolled skeletal muscle hypermetabolism. Manifestations of
malignant hyperthermia (MH) are precipitated by certain volatile
anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane,
enflurane), either alone or in conjunction with a depolarizing muscle
relaxant (specifically, succinylcholine). The triggering substances release
calcium stores from the sarcoplasmic reticulum and may promote entry
of calcium from the myoplasm, causing contracture of skeletal muscles,
glycogenolysis, and increased cellular metabolism, resulting in
production of heat and excess lactate. Affected individuals experience:
acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity,
compartment syndrome, rhabdomyolysis with subsequent increase in
serum creatine kinase (CK) concentration, hyperkalemia with a risk for
cardiac arrhythmia or even arrest, and myoglobinuria with a risk for
renal failure. In nearly all cases, the first manifestations of MH
(tachycardia and tachypnea) occur in the operating room; however, MH
may also occur in the early postoperative period. There is mounting
evidence that some affected individuals will also develop MH with
exercise and/or on exposure to hot environments. Without proper and
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Malignant Hyperthermia: Molecular Genetic Testing
To date, only two genes in which mutation causes MHS have been
identified:
RYR 1 (MHS1 locus) encodes the type 1 ryanodine receptor of skeletal
muscle. Molecular genetic testing indicates that mutations in RYR1 are
identified in up to 70%-80% of individuals with confirmed MHS [
Sambuughin et al 2005, Galli et al 2006, Robinson et al 2006,
Kraeva et al 2011].
CACNA1S (MHS5 locus) encodes the 1-subunit of the skeletal
muscle dihydropyridine receptor L-type calcium channel. Mutations in
CACNA1S account for 1% of all MHS [Stewart et al 2001].