Chemistry 451

Lecture #21: Control of Glycolysis and the Pentose Phosphate Pathway

Read: 406-412 AND 417-424

Optional Reading: Guided Exploration 12: Glycolysis Overview; Section 14-5, Metabolism of hexoses other than glucose. Optional Listening: In Praise of E.M.P. (eg., glycolysis); The Pentose Phosphate Shunt

HW: pg. 424 (study exercises 3,4); (Problems 7, 8, 10, 11) AND one suggested question with answer for quiz #2. Optional HW: pg. 424, problem 9

Try to pick a paper and choose poster or slide format for your next presentation by Friday, Nov 3. Although time lines are officially due on Wednesday, Nov 8, I will be out of town Nov 4-11.

Objectives:

  1. Know that phsophofructokinase is the primary flux control point for glycolysis. ATP is an allosteric inhibitor. AMP and ADP are allosteric activators.
  2. Explain how the opposing reactions of the F6P/FBP (fructose-6-phosphate/fructose bisphosphate) substrate cycle allow for large changes in glycolytic flux.
  3. In the pentose phosphate pathway, glucose-6-phosphate (G6P) is oxidized and decarboxylated to produce NADPH, CO2 and ribulose-5-phosphate (Ru5P). Ribose 5 phosphate, formed from Ru5P can be diverted for nucleotide synthesis OR converted to glycolytic intermediates. Note: some ketoses are named by inserting -ul- before the suffix -ose in the name of the corresponding aldose; thus ribulose is the ketose corresponding to the aldose ribose. Epimers are sugars that differ in configuration at one C atom, excluding the anomeric C.
  4. Evidence suggests that the primary function of the pentose phosphate pathway may be to produce NADPH which maintains glutathione in its reduced state and decreases oxidative stress (Box 14-3, pg 423).

Pandolfi PP, Sonati F, Rivi R, Mason P, Grosveld F, Luzzatto L. Targeted disruption of the housekeeping gene encoding glucose 6-phosphate dehydrogenase (G6PD): G6PD is dispensable for pentose synthesis but essential for defense against oxidative stress. EMBO J. 1995 Nov 1;14(21):5209-15.

Knight JA. The biochemistry of aging. Adv Clin Chem. 2000;35:1-62. (a Review)

Leutner S, Czech C, Schindowski K, Touchet N, Eckert A, Muller WE. Reduced antioxidant enzyme activity in brains of mice transgenic for human presenilin-1 with single or multiple mutations. Neurosci Lett. 2000 Oct 6;292(2):87-90.

Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. Science. 1996 Jul 5;273(5271):59-63. Review.