Carbohydrate metabolism begins in the mouth, where the enzyme salivary amylase begins to break down complex sugars into monosaccharide, which are later absorbed in the blood stream from the small intestine. Take this Endo carb meta MCQ`s below designed to assist you in passing the upcoming exam. All the best in the exam!
It causes retinopathy
It prevents glucose utilization by cells
It stimulates fructose uptake by cells
It leads to hyper-stimulation of glycolysis
It leads to a common foot infection
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Fructose is a bad sugar because it can cause fructose intolerance
Excessive dietary fructose is a leading cause of cataracts
Dietary fructose contributes to adipose tissue stores of triglycerides
Conversion of fructose to glucose requires no energy
The balance of sugars in colas are a benefit, but caffeine is bad
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Oxidative damage to erythrocytes
High levels of intracellular galactose 1-phosphate in liver
Hyperlacticacidemia
Accumulation of glycogen in lysosomes
Hypoglycemia
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Glucose-6-phosphatase and Glucose6-phosphate dehydrogenase
Phosphofructokinase-1 and Pyruvate Kinase
Fructose-1,6-bisphosphatase and Pyruvate Carboxylase
Glycogen Synthase and Glycogen Phosphorylase
Fructokinase and Galactokinase
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Insulin stimulates glycogen synthase and phosphofructokinase-1
Insulin inhibits hexokinase and GLUT 4 transport of glucose
Insulin stimulates Glycogen Synthase Kinase-3 activity
Insulin stimulates bypass enzymes of gluconeogenesis
Insulin inhibits the activity of Pyruvate Kinase
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After exercise
After meals
After prolonged fasting
Between lunch and dinner.
With anaerobic conditions
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PFK-1
Pyruvate Kinase
Isocitrate Dehydrogenase
Glucose 6-phosphate dehydrogenase
Glycogen Phosphorylase•
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Hexokinase
Alanine aminotransferase
Phosphofructokinase-1
Phosphofructokinase-2
Glycogen Phosphorylase
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High carbohydrate to fat ratio in the diet
High fat, low carbohydrate diet
Increased activity of HMG-CoA synthase in the fed state
In patients with carnitine deficiency
When omega oxidation of fatty acids is increased
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Jaundice
Anemia
Sore throat
Intestinal discomfort
Rash
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True
False
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ATP
AMP
Low pH
Carbon Dioxide
Glucose 6-phosphate
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Glycolysis and ATP generation will be limited
Gluconeogenesis will be activated
Glycogen synthase will be inhibited by GSK-3
Glycogen phosphorylase will be inhibited by Protein Phosphatase-1
ATP levels will allosterically activate Glycogen synthase
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The Alanine Cycle
The Kreb’s Cycle (TCA)
Oxidative Phosphorylation
Glycolysis
The Cori Cycle
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Increased adipose tissue GLUT 4 translocase concentration in the plasma membrane
Activation of glycogen synthase activity in liver
Activation of protein phosphatase-1 activity in liver
Activation of cAMP phosphodiesterase activity in liver
Activation of fructose1,6 bisphosphatase activity in liver
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The insulin receptor
The glycogen synthase b enzyme
The GLUT 4 transporter
The glycogen debranching enzyme
The fructose 2, 6-bisphosphatase enzyme
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Aldolase A is found in the mitochondria, while Aldolase B is not
Aldolase A is involved in carbohydrate metabolism, and Aldolase B is not
Aldolase A is "fast" and Aldolase B is not
Aldolase A is found in liver tissue and Aldolase B is not
Aldolase A is dependent on thiamine-PP and Aldolase B is not
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Phosphofructokinase
Aldolase
Glycogen phosphorylase
Fructose-1,6-bisphosphatase
Glucose-6-phosphatase
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Ascorbate causes problems with myosin-actin
Excess fructose depletes inorganic phosphate
Excess free fructose inhibits GLUT transport
Excess free fructose inhibits hexokinase and glucokinase
Fructose cannot be used to make energy*
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Glucokinase has a Km in the physiological range of blood glucose
The Vmax of glucokinase is lower than that of hexokinase
The activity of the 'reverse' enzyme, glucose-6-phosphatase is stimulated by insulin
Hexokinase is subject to product inhibition
The reaction is endergonic, generating excess free energy
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True
False
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Glycogen phosphorylase 'a'
Pyruvate carboxylase
Glucose-6-phosphate dehydrogenase
Glucose-6-phosphatase
Phosphoglucose isomerase
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The patient has limited need for glucose at her advanced age.
The patient has a blood infection stimulated by a lack of nutrition
The circulating fatty acids are insufficient to drive liver gluconeogenesis.
Insulin release from the pancreas is limiting.
Metabolism of alcohol competitively inhibits enzymes for gluconeogenesis
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The "a" form of the enzyme will be activated to break down glycogen
The "b" form of the enzyme will be inactivated to produce less glycogen
The "a" form of the enzyme will be less active and glycogen will accumulate
There will be no change in enzyme activity in the patient
The "b" form of the enzyme will be allosterically activated
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1
2
3
4
5
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