By Carolyn D Berdanier

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One might also anticipate an increase in lipogenesis in hyperinsulinemic individuals, and, indeed, obese people as well as genetically obese experimental animals are characterized by both. As a corollary, one might also anticipate that the consumption of a high-glucose, lowfat diet that stimulates insulin release and also provides ample glucose for conversion to fatty acids would be characterized by high rates of lipogenesis, particularly in the liver. In rodents, this anticipation is justified.

At this point, another rate-controlling step occurs. This step is one that shuttles reducing equivalents into the mitochondria for use by the respiratory chain. This is the α-glycerophosphate shuttle. This shuttle carries reducing equivalents from the cytosol to the mitochondria. DHAP picks up reducing equivalents when it is converted to α-glycerol phosphate. These reducing equivalents are produced when glyceraldehyde-3-phosphate is oxidized in the process of being phosphorylated to 1,3-diphosphate glyceraldehyde.

This simplistic description of the citric acid cycle implies that it is free of controls and, given adequate supplies of substrates, enzymes, and molecular oxygen, proceeds unhindered. This is not true. There are numerous controls in place that regulate the cycle. 11 Krebs citric acid cycle in the mitochondria. This cycle is also called the tricarboxylate cycle (TCA). Abbreviations used: HOH, water; FAD, flavin adenine nucleotide; FADH++, flavin adenine nucleotide, reduced; NAD, niacin adenine dinucleotide; NADH++, niacin adenine dinucleotide, reduced; GTP, guanosine triphosphate; GDP, guanosine diphosphate; CoA, coenzyme A; CO2, carbon dioxide.

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