Question

Which of the following metabolic changes will occur in a typical human after a meal balanced...

Which of the following metabolic changes will occur in a typical human after a meal balanced in carbohydrates, protein, and fat is consumed? (Select ALL that apply!)

Liver glycogen synthesis increases

Muscle glycogenolysis (glycogen breakdown) increases

Liver gluconeogenesis decreases

Insulin levels in the blood decrease

Ketone body production in the liver is increased

.....

Which of the following metabolic changes will occur in a typical human during 12 hours of fasting? (Select ALL that apply.)

Liver glycogen synthesis decreases

Liver glycogenolysis (glycogen breakdown) decreases

Liver gluconeogenesis increases

Liver fatty acid oxidation increases

Ketone body formation increases

.....

Fatty acids in the bloodstream that are NOT part of TAGs or phospholipids: (Select ALL that apply!)

Are present at levels that are independent of epinephrine, glucagon, or insulin levels

Are carried by the protein serum albumin

Are soluble in the aqueous phase of the blood in free form

Are nonexistent; the blood only carries ketone bodies

Are carried as part of the lipid bilayer of LDLs and chylomicrons

Originate primarily from stored TAGs in adipose tissue

Originate primarily from dietary fats that have just been released into the bloodstream from intestinal endothelial cells

....

Marasmus is the medical term for the condition that results from overall calorie starvation. In developed countries like the U.S., it is relatively uncommon. However, there is a common psychological illness, anorexia nervosa, that results in the same symptoms and problems as marasmus. Both conditions result in high ratios of glucagon to insulin. Having a high ratio of glucagon to insulin would do which of the following in most healthy people? (Select ALL that apply!)

Promote mobilization and release of fatty acids from adipose tissue

Result in increased glycogen storage by the liver

Result in increased glycogen catabolism (glycogenolysis) in the liver

Lead to increased concentrations of ketone bodies in the blood

22. What single problem in metabolism best explains Jessie's condition?

Jessie suffered from hypoglycemia due to anorexia

Jessie was suffering from a deficiency of carnitine

Jessie has a genetic disorder of CAT I or CAT II

Jessie has a vitamin deficiency

Jessie has a shortage of long-chain fatty acids

Jessie has late-onset diabetes

.....

23. What are some of the expected physiological consequences of a carnitine deficiency? (Select ALL that apply!)

Depletion of stored fat in adipocytes

Inability to metabolize short-chain fatty acids

High levels of circulating fatty acids in the blood

Chronic hypoglycemia when fasted

Impaired ability to produce ketone bodies

Inability to catabolize glucose to pyruvate

..........

24. At the biochemical level, why does a carnitine deficiency lead to impaired ketone body formation?

Loss of β-oxidation in the liver results in an inability of the brain to transport fatty acids from the blood into the cells to make ketone bodies

Ketone bodies are made directly from carnitine in humans

Ketone bodies are primarily produced from the acetyl-CoA produced from β-oxidation of the long-chain fatty acids of stored triglycerides, but β-oxidation of long-chain fatty acids cannot occur without carnitine-mediated fatty acid transport

Carnitine is necessary for long-chain fatty acid transport into liver cells, so deficiency prevents β-oxidation and the absence of β-oxidation prevents ketone body formation

Carnitine deficiency does not impair ketone body formation

.......

25. At the biochemical level, why does a carnitine deficiency lead to increased fat deposition in the liver? (Hint: the answer to this question may be found within the case itself rather than the textbook.)

In the absence of carnitine, the liver stores large amounts of glycogen, which is converted into fatty acids and stored as TAGs within the liver

Carnitine is an activator of TAG lipases in the liver; as a result, in the absence of carnitine, lipase activity is turned off, favoring TAG synthesis

Because β-oxidation is blocked, fatty acids arriving to the liver from the blood cannot be oxidized and are instead stored in the liver in intracellular lipid droplets

Carnitine is an inhibitor of fatty acid synthesis; as a result, in the absence of carnitine, fatty acid synthesis is stimulated, leading to an increase in stored TAGs in the liver

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Answer #1

Which of the following metabolic changes will occur in a typical human after a meal balanced in carbohydrates, protein, and fat is consumed?

Liver glycogen synthesis increases

Stores of readily available glucose to supply the tissues with an oxidizable energy source are found solely in the liver, as glycogen.  Glycogen is a polymer of glucose deposits connected by α-(1,4)- and α-(1,6)- glycosidic bonds. In spite of the fact that the liver is the tissue for glucose stockpiling as glycogen different tissues additionally combine glycogen and discharge glucose from glycogen for vitality needs. Two essential tissues that store glucose as glycogen as a store of vitality are skeletal muscle and the mind, mainly astrocytes. Be that as it may, the glucose in muscle and mind glycogen isn't accessible to different tissues, as a result of the nearness of hexokinase which has a high proclivity for glucose, accordingly quickly phosphorylating any glucose and in addition because of the absence of glucose-6-phosphatase.

Muscle glycogenolysis (glycogen breakdown) increases

Glycogenolysis, process by which glycogen, the essential starch put away in the liver and muscle cells of creatures, is separated into glucose to give prompt vitality and to keep up blood glucose levels amid fasting. Glycogenolysis happens basically in the liver and is animated by the hormones glucagon and epinephrine (adrenaline). When blood glucose levels fall, as during fasting, there is an increase in glucagon secretion from the pancreas.  That increase is joined by an attendant lessening in insulin emission, on the grounds that the activities of insulin, which are gone for expanding the capacity of glucose as glycogen in cells, restrict the activities of glucagon. Following emission, glucagon goes to the liver, where it animates glycogenolysis.

Liver gluconeogenesis decreases

GLUT2 is the major glucose transporter of hepatocytes. In hepatocytes GLUT2 is involved in glucose uptake and release in the fed and fasted states, respectively. In any case, it is key for glucose take-up. In the present investigation we watched diminished GLUT2 articulation in the livers of diabetic rodents , recommending diminished take-up of glucose by the liver. Moreover, GK protein level was additionally brought down recommending that diminished take-up, phosphorylation and usage by the liver adds to hyperglycemia saw in diabetic pregnant rodents.

Insulin levels in the blood decrease

Insulin is a hormone that is produced and stored in the beta cells of the pancreas. It is secreted in response to elevated blood glucosefollowing a meal  what's more, is crucial for the transportation and capacity of glucose, the body's principle wellspring of vitality. Insulin helps transport glucose from the blood to inside cells, in this manner managing blood glucose levels, and has a job in lipid digestion. This test estimates the measure of low blood glucose (hypoglycemia); to help distinguish insulin opposition, or to help decide when a sort 2 diabetic may need to begin taking insulin to enhance oral drugs.

Ketone body production in the liver is increased

Ketogenesis is the biochemical process by which organisms produce a group of substances collectively known as ketone bodies by the breakdown of fatty acids and ketogenic amino acids. This procedure supplies vitality to specific organs (especially the cerebrum) under conditions, for example, fasting, yet inadequate gluconeogenesis can cause hypoglycemia and over the top generation of ketone bodies prompts a hazardous state known as ketoacidosis.

Ketone bodies are delivered by the liver in light of the current situation recorded above (i.e. fasting, starving, low sugar eats less carbs, drawn out exercise and untreated sort 1 diabetes mellitus) because of extraordinary gluconeogenesis, which is the generation of glucose from non-starch sources (excluding unsaturated fats).

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