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Free STEP1 Exam Braindumps (page: 75)

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PDF with 845 Questions

As a hypothetical approach to treating the hyperglycemia associated with Type II diabetes, a drug firm proposes to develop an inhibitor of liver glycogen phosphorylase. What is the biochemical rationale for this approach to inducing hypoglycemia?

  1. Hepatic fatty acid oxidation will decrease leading to reduced energy production needed for gluconeogenesis.
  2. Hepatocytes will have a reduced capacity to store glucose following meals.
  3. Liver glucose output will be reduced early during fasting.
  4. The resultant increase in glycogen storage will inhibit glucose uptake by the liver, leading to increased usage in skeletal muscle.
  5. There will be an increase in hepatic gluconeogenesis.

Answer(s): C

Explanation:

During early fasting, as the level of glucose in the blood falls, the pancreas releases glucagon into the circulation to counter this drop. The major site of glucagon action is the liver. There it induces the activity of the glycogen phosphorylase leading to an increase in glucose release from glycogen stores. Thus, an inhibition of glycogen phsphorylase would limit the ability of the liver to provide glucose to the blood.
Negatively affecting the activity of glycogen phosphorylase would not significantly affect the rate of hepatic fatty acid oxidation (choice A), skeletal muscle glucose usage (choice D), nor hepatic gluconeogenesis (choice E). The liver may have a reduced capacity for de novo storage of glucose following meals (choice B) due to a prior reduction in the release of glucose via the inhibition of glycogen phosphorylase; however, on fasting there would still be a reduction in glucose release.



Lipoprotein lipase (LPL) is the endothelial cellassociated enzyme necessary for release of fatty acids from circulating lipoproteins. Which of the following apolipoproteins is required to activate LPL- mediated release of fatty acids from chylomicrons?

  1. apo A
  2. apo
  3. apo
  4. apo CII
  5. apo E

Answer(s): D

Explanation:

The presence of apo CII on the surfaces of lipoprotein particles is necessary for the activation of endothelial cell LPL. Apo AI (choice A) activates LCAT. Apo (choice B) is derived via intestinal-specific RNA editing and is exclusively a component of chylomicrons. Apo (choice C) and E
(choice E) are necessary for LDL interaction with the LDL receptor.



Which of the following is the hypophyseotropic hormone that regulates the activity of the lactotrophs of the anterior pituitary?

  1. CRH
  2. GnRH
  3. growth hormone-releasing hormone (GRH)
  4. prolactin-releasing factor (PRF)
  5. thyrotropin-releasing hormone (TRH)

Answer(s): D

Explanation:

The lactotrophs of the anterior pituitary secrete prolactin in response to the action of PRF. Corticotropin- releasing hormone, CRH (choice A) regulates primarily the secretion of ACTH, but also other products of the ACTH precursor protein, pro-opiomelanocortin, POMC. GnRH (choice B) controls the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gonadotrophs. GRH (choice C) stimulates growth hormone secretion from pituitary somatotrophs. TRH (choice E) stimulates the thyrotropes to secrete thyroid-stimulating hormone, TSH (also called thyrotropin).



An individual harboring a mutation in ornithine transcarbamoylase (OTC) would be expected to exhibit which of the following measurable abnormalities?

  1. citrullinemia
  2. elevated urinary excretion of argininosuccinic acid
  3. elevation in blood orotic acid
  4. excess production of foam cells
  5. uric acid deposition in the joints

Answer(s): C

Explanation:

A deficiency in OTC results in one of the urea cycle defect diseases, which are the major causes of hyperammonemia in the newborn. Differentiation of which urea cycle enzyme is defective and causing the hyperammonemia can be accomplished by analysis of the levels of the various intermediates in the cycle (see below figure for UCD DDx).

Adefect in OTC prevents incorporation of carbamoylphosphate into ornithine (see below figure). The carbamoylphosphate will diffuse out of the mitochondria and serve as a precursor for the synthesis of the pyrimidine nucleotides in excess of need leading to an elevation of orotic acid (pyrimidine intermediate) in the blood. A deficiency of the urea cycle enzyme, ASD, will lead to citrullinemia (choice A). Elevation in excretion of argininosuccinate (choice B) will result from a deficiency in the urea cycle enzyme, arginosuccinase. Foam cells are lipidladen cells that are characteristic of disorders in lipid etabolism such as that seen in NPD, which is caused by a deficiency in sphingomyelinase. Uric acid deposition (choice E) results from excess catabolism of the purine nucleotides.






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