Biochemistry Quiz: Carbohydrates and Enzymes

Multiple Choice Questions

Zymogens are inactive enzyme forms activated through proteolysis.
The small intestine is primarily responsible for enzymatic food breakdown.
Glucose is a monosaccharide.
Isomaltase cleaves (1,6) glucose-glucose branches on amylopectin/glycogen.
Lactose is composed of glucose and galactose.
Facilitated diffusion is a glucose uptake mechanism in intestinal enterocytes.

Additional Questions

The only insulin-responsive glucose transporter is GLUT4.
Fructose-1,6-bisphosphate is formed from fructose-6-phosphate by phosphofructokinase 1 (PFK1).
Conditions that elevate liver gluconeogenesis: diabetes, fasting, strenuous exercise, and carbohydrate-free diets, but not high carbohydrate diets.
Glucagon regulates glycogen breakdown
The Cori cycle involves muscle lactate as a source for gluconeogenesis.
UDP-glucose is the precursor substrate for glycogen synthesis.
The kidney becomes overwhelmed and no longer filters glucose at 170 mg/dL.
Pyruvate carboxylase converts pyruvate into oxaloacetate, a crucial step in gluconeogenesis.
Linoleic acid is an essential fatty acid.
Acetyl CoA is the substrate shuttled from the mitochondria to the cytoplasm for fatty acid synthesis.
Acetyl-CoA carboxylase is the enzyme required for the conversion of Acetyl-CoA to Malonyl-CoA.
Carnitine is the molecule used to shuttle fatty acids into mitochondria for fatty acid oxidation.
Fatty acids, triglycerides, monoacylglycerides, and cholesterol can be absorbed into intestinal cells.
Triglyceride digestion in the small intestine is facilitated by pancreatic lipase.
The carboxyl end is the omega end for fatty acids.
Very Low-Density Lipoprotein (VLDL) has the largest cholesterol content.
Cholesterol Ester Transfer Protein (CETP) targets high-density lipoproteins (HDL).
Apolipoprotein B100 is a structural component of very-low-density lipoprotein (VLDL).
Lipoprotein lipase acts on triglycerides.
Apolipoprotein C2 (ApoC2) activates lipoprotein lipase.
The liver produces high-density lipoproteins (HDL), very-low-density lipoproteins (VLDL), and chylomicrons.
Familial hypercholesterolemia (FH) is a genetic mutation in the LDL receptor.
High-density lipoprotein (HDL) is crucial for reverse cholesterol transport.
PCSK9 proteins are targeted by cholesterol-lowering drugs to lower LDL cholesterol levels.
Increased fructose consumption is linked to increased prevalence of obesity.
Fructose is readily metabolized into fat through metabolism pathways, bypassing some steps in glucose metabolism.
Glucose uptake is facilitated in the intestine by sodium-glucose transporter, in the liver by Glut 2 and in adipose by Glut 4, which is regulated and located differently from Glut2.
Gluconeogenesis is crucial for maintaining blood glucose levels during fasting by starting with non-carbohydrate substrates.
PFK1 (Phosphofructokinase 1) enzyme regulation impacts both glycolysis and gluconeogenesis.
Blood triglyceride levels peak during the first four hours after consuming a large milkshake, facilitated by chylomicrons and their apolipoproteins carrying lipids to the bloodstream. During the second four hours, chylomicron components are broken down, decreasing triglycerides during the second half of the experiment.
Statins inhibit HMG-CoA reductase, a crucial enzyme in cholesterol biosynthesis.
This inhibition leads to increased LDL receptor activity, lowering blood cholesterol levels.
Carboxypeptidase A, elastase, and chymotrypsin are protein-digesting enzymes.
Glutamine is the major nitrogen carrier in the blood.
Leucine is a solely ketogenic amino acid and valine is important and essential.
Aspartate and glutamine are amino acids.
The stomach's hydrochloric acid helps to denature proteins and activate pepsinogen, which then becomes pepsin.
Valine catabolism results in acetyl-CoA.
The urea cycle is responsible for excreting nitrogen from the body in the form of urea from ammonia.
A high protein diet is characterized by high urinary urea nitrogen levels.
The post-absorptive phase lasts up to 18–48 hours.
The primary energy source for the brain during fed and fasting states is glucose.
Adipose tissue is the primary source of ketone production during starvation.
The two amino acids primarily released by muscles during starvation are alanine and glutamine.
The liver can perform glycogenesis and gluconeogenesis but not produce glucose on its own.
A ketogenic diet is high in fat, low in carbohydrates.
Important aspects of Insulin include increased glucose transportation from the blood into muscles, increased glycogen synthesis in muscle and liver, and increased glucose transport into adipose.
Glucose transport to muscles is mediated by GLUT4.
Glycogen is produced from glucose during the fed stage in liver and muscle.
Certain drugs target PCSK9, a protein affecting LDL cholesterol levels.
The liver uses ketones for energy only when other energy sources are depleted.