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48 Cards in this Set
- Front
- Back
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What is the Atkins diet? |
a high protein, high fat, low carb diet |
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What does the atkin's diet claim? |
that one can eat all the protein and fat he wants and still lose weight, so long as they avoid carbohydrates |
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What happens in the fed/absorbed phase after a mixed meal? |
the liver receives blood rich in glucose |
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What is the insulin/glucagon ratio after a mixed meal? |
high |
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what are the most active pathways after a mixed meal? |
glycolysis, TCA cycle/ETC/OP, Glycogenesis, Fatty acid and TAG synthesis |
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What is the insulin/glucagon ratio after a low carb meal? |
Low |
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What are the active pathways after a low carb meal? |
liver glycogenolysis, gluconeogenesis, protein utilization, lipolysis (HSL activity), fatty acid oxidation, TCA cycle/ETC/OP, Ketogenesis |
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what is the metabolic state after a low carb meal? |
Even though the body is in the fed state it acts like it is in the fasting state |
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Why does weight loss occur during the Atkins diet? |
liver glycogen is quickly depleted, body is in constant fat burning mode, gluconeogenesis is active all the time, enhanced thermogenic effect, slow gastric emptying, diet is unappetizing |
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Why does liver glycogen depletion contribute to weight loss? |
glycogen absorbs a lot of water weight |
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Why is the body in constant fast burning mode? |
TAG is mobilized from adipose tissue and fatty acids are oxidized constantly to meet energy needs of the body |
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How does gluconeogenesis contribute to weight loss? |
it consumes energy |
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What causes the enhanced thermogenic effect? |
protein requires more energy for digestion, absorbtion, and catabolism |
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How does slow gastric emptying contribute to weight loss? |
proteins and fats take a longer time to digest. They sit in the stomach longer and are thus more satiating, leading to lower food consumption |
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Why would individuals on a low carb/high protein diet often experience transient hyperglycemia if they resume a conventional diet containing significant amounts of carbs? |
Enzymes involved in carbohydrate metabolism are transcriptionally down-regulated for people who have been on the Atkin's diet for a while. |
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What are the potential hazards to the Atkin's diet? |
Micronutrient deficiency from low fruit and vegetable consumption, increased metabolic burden due to gluconeogenesis being ran 24/7, electrolyte imbalance, ketoacidosis |
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What is oxidative stress? |
Issues caused by reactive oxygen species |
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What are reactive oxygen species? |
they are formed by the partial reduction of molecular oxygen |
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What forms ROS and when are they formed? |
they are formed continuously as by-products of aerobic metabolism, reactions of drugs and toxins, low levels of anti-oxidants or infection |
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What kind of damage can oxidative stress caused by ROS cause? |
damage to DNA, proteins, lipids etc |
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What does oxidative stress lead to? |
cell death |
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How does the cell protect its self from oxidative stress? |
By cellular anti-oxidant systems |
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What are some of the anti-oxidant systems? |
antioxidant chemicals, enzymatic antioxidant reactions, superoxide dismutase, catalase, and glutathione peroxidase |
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What is glutathione peroxidase critical for? |
to keep H2O2 levels in check |
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What does glutathione peroxidase require? |
an adequate supply of NADPH |
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In cells with mitochondria, how is NADPH produced? |
NADP-malic enzyme, or the HMP shunt |
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How is NADPH produced in cells without mitochondria? |
HMP shunt is the only source of NADPH |
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What is an example of a cell that depends solely on HMP shunt for protection from oxidative stress? |
red blood cells |
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What enzyme catalyzes the rate limiting step of the oxidative branch? |
glucose-6-phosphate dehydrogenase |
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What up regulates G6PD? |
NADP |
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what down regulates G6PD |
NADPH in normal cells |
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Why is G6PD activity important? |
for coping with oxidative stress |
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What is the #1 enzyme defect leading to hemolytic anemia? |
G6PD deficiency |
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G6PD is encoded by an ..... |
X-linked gene |
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What leads to acute hemolytic anemia? |
an impaired ability to form NADPH and dispose of H2O2 |
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What can cause oxidative stress in a patient with less than %60 of normal G6PD activity? |
exposure to pathogens, ionizing radiation and chemicals; oxidant drugs such as primaquine, bacterium etc.; consumption of broad beans (rich in oxidants) |
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what does oxidative stress induced hemolytic anemia lead to? |
accumulation of H2O2 and ROS in red blood cells, oxidation of sulfhydryl groups in proteins, formation of heinz bodies, acute hemolytic anemia |
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What are heinz bodies? |
precipitation of hemoglobin protein with oxidized SH groups |
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What is a clear indicator of oxidative stress in RBCs? |
presence of heinz bodies |
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How can bactrim treatment result in hemolytic anemia in a G6PD-deficient patient? |
bacterium results in increased levels of H2O2; G6PD deficient individuals cannot produce adequate amounts of NADPH, GS-SG cannot be reduced back to G-SH, Oxidative stress, Damage to RBCs |
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Why wouldn't a patient experience hemolytic anemia in the absence of bactrim treatment? |
The level of activity of G6PD is sufficient to prevent oxidative stress under non-aggravating conditions |
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Why is the pathology of G6PD deficiency restricted to red blood cells? |
The sole source of NADPH in cells without mitochondria is the HMP shunt oxidative branch. Glutathione reduction is impaired because of decreased NADPH availability |
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What do liver and muscle cells do to get around G6PD deficiency? |
they have the malic enzyme in mitochondria that can also be used to produce NADPH, which can be used in the reduction of glutathione |
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What is RBC-specific pyruvate kinase deficiency? |
2nd major cause of hemolytic anemia due to enzyme deficiency |
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Since RBCs lack mitochondria, what are they completely dependent on for ATP production? |
Glycolysis |
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What does pyruvate kinase deficiency do to RBCs |
chronic ATP deficit, membrane rigidity due to recued activity of NA-K-ATPase, accumulation of H2O2, oxidative damage, chromic hemolysis |
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How does a decrease in glutathione impact H2O2 levels? |
A decrease in glutathione will lead to an increase in H2O2 levels, just like G6PD deficiency |
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What do individuals with a pyruvate kinase deficiency suffer hemolytic anemia? |
PK deficiency leads to chronic ATP deficit in RBCs and therefore reduced activity of NA-K-ATPase and decreased production of glutathione, leads to increased H2O2 levels and membrane damage. Membrane damage leads to hemolysis |
