What is the function of lipoprotein lipase in the capillary walls of adipose tissue, which is activated by insulin?
Explanation
For fats synthesized in the liver to be stored in adipose tissue, they must first be broken down from their transport form (triglycerides in lipoproteins) into smaller fatty acids that can be absorbed by the fat cells. Insulin activates lipoprotein lipase to perform this crucial step.
Other questions
What is the primary effect of insulin on fat metabolism when carbohydrate intake exceeds the body's immediate energy needs?
In which cells does the majority of fatty acid synthesis, stimulated by insulin, take place?
What is the approximate percentage of liver mass that can be stored as glycogen before further glucose is directed towards fat synthesis?
Which enzyme, essential for the first stage of fatty acid synthesis, is activated by an excess of citrate and isocitrate ions?
How does insulin promote the storage of fat in adipose cells by affecting hormone-sensitive lipase?
What crucial substance for triglyceride formation is formed in large quantities in adipose cells due to insulin-promoted glucose transport?
In the absence of insulin, what is the most important effect that leads to the release of free fatty acids from storage?
What is the consequence of insulin deficiency on plasma concentrations of cholesterol and phospholipids?
In the absence of insulin, how much can the total concentration of plasma lipoproteins increase?
What long-term health condition is promoted by the high concentration of cholesterol resulting from insulin deficiency?
What metabolic condition, characterized by the formation of excessive acetoacetic acid in the liver, is caused by insulin deficiency?
Which transport mechanism becomes increasingly activated in the liver during insulin deficiency, leading to rapid beta oxidation of fatty acids?
What are the three substances collectively known as 'ketone bodies' that are produced during severe insulin deficiency?
In severe diabetic ketoacidosis, what concentration can acetoacetic acid reach in the blood?
Which hormone has a direct lipolytic effect on adipose cells by activating hormone-sensitive lipase, greatly enhancing the blood concentration of fatty acids during stressful states?
What is the primary signal that controls the 'switching' mechanism between using carbohydrates and using fats for energy?
What effect does glucagon have on fat metabolism when its concentration is high?
What is the initial substance from which fatty acids are synthesized in the liver when excess glucose is available?
Why is storage of fatty acids transported from the liver almost blocked when insulin is not available?
What is the normal concentration of total plasma lipids, which can increase several-fold in severe insulin deficiency?
In the context of fat metabolism, what does insulin's function as a 'fat sparer' mean?
What is the primary reason that an absence of insulin depresses the utilization of acetoacetic acid in peripheral tissues?
What happens to the plasma concentration of free fatty acids almost immediately after the removal of the pancreas (and thus insulin)?
In type 1 diabetes, the increased utilization of fats for energy and the formation of cholesterol by the liver are a direct consequence of what?
What is the primary role of insulin in protein metabolism?
How does severe insulin deficiency lead to protein wasting?
According to the text, what can be a severe consequence of the metabolic acidosis that develops from excess keto acids in diabetes mellitus?
What is the primary way that insulin inhibits gluconeogenesis in the liver?
How does insulin indirectly contribute to inhibiting gluconeogenesis?
Which of the following hormones does NOT play a role in switching between carbohydrate and lipid metabolism?
In what way does epinephrine's action on energy metabolism differ from that of growth hormone and cortisol?
What is the quantitative relationship between the enhancement of fatty acids and blood glucose by epinephrine?
What effect does glucagon have on the storage of triglycerides in the liver?
What is the primary energy source for most body tissues, except the brain, during periods of low insulin secretion?
What is the consequence of the shift from carbohydrate to fat metabolism in diabetes regarding keto acids?
The long-term effect of insulin deficiency is especially dramatic in causing which condition that often leads to heart attacks and strokes?
What is the primary source for the glycerol portion of the fat molecule stored in adipose cells?
When the quantity of glucose entering liver cells is more than can be stored as glycogen, what does insulin promote?
What is the fate of the triglycerides that are formed in the liver from excess glucose?
The condition of polyphagia (eating large amounts of food) in severe untreated diabetes mellitus occurs alongside what other symptom related to body mass?
Which amino acids are mentioned as being most strongly transported into cells by insulin?
What happens to the ribosomes in the absence of insulin, according to the 'on-off' mechanism described?
Over a longer period, what effect does insulin have on DNA and RNA to promote protein synthesis?
In what way is the body's response to excess fat utilization in the liver in diabetes self-limiting regarding arterial walls?
What are the two factors that contribute to the formation of ketosis and acidosis in insulin deficiency?
Why does insulin deficiency lead to an increased excretion of urea in the urine?
Which two hormones interact synergistically to promote growth, with each performing a specific function?
What is the primary effect of insulin on the transport of glucose into adipose cells?
In the absence of insulin, how does the body primarily compensate for energy needs, leading to the breakdown of stored triglycerides?