Help.r 23DOMetformin is often the first drug prescribed to treat high glucose levels in blood associated with diabetes type 2. We don't know the macromolecular targets of metformin, onlythat metformin reduces glucose absorption by the intestine and modestly suppresses gluconeogenesis. Other drugs, sometimes used in combination with metformin, suppressliver gluconeogenesis significantly. What side effect is likely?O Lactic acidosisO Tourette syndromeAgoraphobiaO Atrial fibrillationWhich activities in liver are enhanced by glucagon?Conversion of glycogen to Glc-1-P.Conversion of glycogen synthase b to glycogen synthase a.Conversion of Fru-6-P to Fru-2,6-P2.Conversion of Fru-6-P to Fru-1,6-P₂.DO

Diabetes is a metabolic disease characterized by excessive blood sugar levels . Causes of diabetes…

Answered: 2 DA Metformin is often the first drug…

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter22: Gluconeogenesis, Glycogen Metabolism, And The Pentose Phosphate Pathway

Section: Chapter Questions

Problem 8P

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A Deficiency on 3-Phosphogtycerate Dehydrogenase Can Affect Amino Acid Metabolism Although serine is a nonessential amino acid, serine deficiency syndrome has been observed in humans. One such form of the syndrome is traceable to a deficiency in 3-phosphoglycerate dehydrogenase (see Figure 25.31). Individuals with this syndrome not only arc serine-deficient but also arc impaired in their ability to synthesize another common ammo acid, as well as a class of lipids. Describe why.
The interconverison of DHAP and GAP greatly favors the formation of DHAP at equilibirum. Yet the conversion of DHAP by triose phosphate isomerase proceeds readily. Why?
At body temperature, L-aspartate in proteins race-mizes to D-aspartate at an appreciable rate. Most pro-teins in the body have a very low level of D-aspartate, if itcan be detected at all. Elastin, however, has a fairly highlevel of D-aspartate. Moreover, the amount of D-aspartateincreases in direct proportion to the age of the person fromwhom the sample was taken. Why do you suppose thatmost proteins have little if any D-aspartate, while elastinhas levels of D-aspartate that increase steadily with age?
Glucokinase acts as a glucose sensor in hepatocytes (livercells), a- and b-cells in the pancreas, enterocytes (intestinalwall cells), and the hypothalamus (a control center in thebrain of numerous physiological processes). Explain whyglucokinase can perform this role.
Name the molecules used for gluconeogenesis. What are the sources of these molecules? Under what conditions would gluconeogenesis occur?
What is the end product of catabolism of the pyrimidine basethymine? Unlike uric acid, the end product of purinecatabolism, excess amounts of this molecule do not causeproblems comparable to gout. What circumstances causeexcess amounts of the end product and why doesn’t a goutlike illness result?
What properties of glucokinase allow it to phosphorylate glucose in the liver when the blood glucose concentration is higher than normal?
1.a. Given what you know about glycolysis and gluconeogenesis, does it make sense that insulin activates PDH phosphatase? Why? b.How do vitamins increase to the breadth of chemical reactions available within a biological system?
One metabolic scenario that leads to insulin resistance is the elevation of the conccentration of free fatty acids in skeletal muscle cells. Would you expect increased activity of diacylglycerol acyltransferas (DGAT) to reduce or exacerbate the resistance? Explain.
Although animals cannot synthesize glucose from acetyl-CoA, if a rat is fed 14C-labeled acetate, some of the label appears in glycogen extracted from its muscles. Explain.
If glucagon binds to the liver cell, what is the expected regulation of the bifunctional enzyme phosphofructokinase-2/fructose-2,6-bisphosphatase and how would the levels of fructose-2,6-bisphosphate be impacted?
Glucocorticoids (GC) are stress hormones that modulate glucose homeostasis. One effect is to reduce glucose uptake from the bloodstream into skeletal muscle and adipose tissue, to increase the catabolism of expendable proteins in the skeletal muscle, and to increase gluconeogenesis in the liver. Why are these metabolic adaptations important during stressful situations, like fasting/starvation? Predict how the glucocorticoid cortisol will affect blood urea concentrations.

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