Glycosylation is the process of attaching proteins or lipids to carbohydrates.

The final digestive products of carbohydrates are glucose, galactose, and fructose.

Cellulose is a major structural constituent in plants consisting of long linear chains of glucose, and is not broken down for energy.

Lactose consists of galactose and glucose monosaccharides, connected by an endo β(1→4) linkage.

The anomeric carbon is the carbon on the monosaccharide connected to 2 oxygen atoms.

The principle sites of digestion are the stomach, duodenum, and upper/mid jejunum.

Carbohydrates are the only dietary component for which degradation begins in the mouth.

Endoglucosidases carry out random digestion of internal α(1→4) and α(1→6) bonds.

Lactose intolerance is a defect in the lactase enzymes which affects the metabolism of lactose.

GLUT-2 is a low affinity, high capacity transporter that is stimulated to transport glucose when glucose concentrations are high.

GLUT-7 is a high affinity transporter found in the endoplasmic reticulum to transport glucose into the cell.

GLUT-4 is a high affinity, low capacity transporter found in adipose and muscle tissue that is stimulated by insulin and exercise.

GLUT-2 is a bidirectional transporter that "flips" its conformation to accommodate alternate states.

SGLT-1 is a type of Na+ monosaccharide co-transport system in which the movement of Na+ is coupled with that of glucose and galactose to transport them into the epithelial cells, up their concentration gradient.

The two anaplerotic reactions that form α-keto acids are oxidative deamination of glutamate by glutamate dehydrogenase, and transamination of glutamate with oxaloacetate via aspartate transaminase.

The regulated enzymes of the TCA cycle are citrate synthase, isocitrate dehydrogenase, and α-ketoglutarate dehydrogenase.

Dihydrolipoyl dehydrase, also known as E2, forms NADH with co-enzymes FAD+ and NAD+.

The first reaction of the TCA cycle is the conversion of pyruvate to acetyl CoA via pyruvate dehydrogenase (PDH) complex.

When PDH complex is phosphorylated, it is inactive. When PDH is dephosphorylated, it is active.

When PDH complex is phosphorylated, it is inactive. When PDH is dephosphorylated, it is active.

Citrate synthase is allosterically inhibited by the products citrate and succinyl CoA.

Citrate synthase is allosterically inhibited by the products citrate and succinyl CoA.

Citrate exits the mitochondria at high concentrations to donate acetyl CoA for fatty acid synthesis.

Citrate is a direct source of acetyl CoA, the building block of fatty acids.

Internal citrate from the mitochondria is transported into the cytosol via the membrane citrate transporter, while extracellular citrate from citrus fruits is brought into the cells by the citrate transport protein.

The oxidative decarboxylation reactions of the TCA cycle are [isocitrate → α-ketoglutarate] and [α-ketoglutarate → succinyl-CoA].

The oxidative decarboxylation reactions of the TCA cycle are [isocitrate → α-ketoglutarate] and [α-ketoglutarate → succinyl-CoA].

The only major difference between PDH complex and α-ketoglutarate dehydrogenase complex is that PDH complex has regulatory enzymes.

Substrate level phosphorylation occurs in the reaction in which succinyl-CoA is cleaved to succinate.

GTP is energetically equivalent to ATP.

The anaplerotic entry points of the TCA cycle are α-ketoglutarate, succinate, fumarate, and oxaloacetate.

The major organs of gluconeogenesis are the liver, kidneys, and small intestine.

7 reactions of glycolysis are reversible, and 4 are not.

Only gluconeogenic tissues have glucose 6-phosphatase.

The major precursors of glucose in the gluconeogenesis path are lactate, pyruvate, glycerol, and glucogenic amino acids.

Adipocytes cannot phosphorylate glycerol because they lack glycerol kinase.

Ketogenic amino acids form ketones bodies, even in low energy, and have no net synthesis of glucose.

All amino acids, both glucogenic and ketogenic, are converted into fatty acids through the intermediate, acetyl CoA.

All amino acids, both glucogenic and ketogenic, are converted into fatty acids through the intermediate, acetyl CoA.

All amino acids, both glucogenic and ketogenic, are converted into fatty acids through the intermediate, acetyl CoA.

Pyruvate and oxaloacetate are examples of α-ketoacid precursors from the TCA cycle, used for gluconeogenesis.

Pyruvate → oxaloacetate may be considered the most important anaplerotic reaction.

Acetyl CoA is the most powerful inhibitor of pyruvate carboxylase.

Starvation is equivalent to a high energy state, thus favoring gluconeogenesis.

During the carboxylation of pyruvate, pyruvate carboxylase binds a CO2 via the biotin cofactor to then transfer it to pyruvate.

Carboxylation of pyruvate carboxylase requires ATP and is allosterically stimulated by acetyl CoA.

In the mitochondria, oxaloactate is converted to malate by an oxidation reaction, catalyzed by NAD+ and mitochondrial malate dehydrogenase.

Since gluconeogenesis occurs in the cytosol, oxaloacetate is converted to malate and transported out via malate/α-ketoglutarate antiporter. It is converted back into oxaloacetate in the cytosol.

Glucose 6-phosphate is an endoplasmic reticulum transmembrane enzyme.

Glucose 6-phosphate dephosphorylated by the muscle does not contribute to blood glucose.

Both gluconeogenesis and glycogenolysis pathways require glucose 6-phosphate translocase and glucose 6-phosphatase.

PC utilizes 2 ATPs for carboxylation, and PEPCK utilizes 2 GTPs for decarboxylation.

The primary allosteric inhibitor of fructose 1,6-bisphosphotate (FBP-1) is fructose 2,6-bis-phosphate.

Fatty acid oxidation and gluconeogenesis are companion pathways, as fat mobilization provides energy to the gluconeogenic pathway.

Fatty acid oxidation and gluconeogenesis are companion pathways, as fat mobilization provides energy to the gluconeogenic pathway.

Primary sources of blood glucose include diet, gluconeogenesis, and glycogenolysis.

Skeletal muscles utilize glucose 6-phosphate for its own ATP production.

Linear glycogen units are connected by α(1→4) bonds, and branched glycogen units are connected by α(1→6) bonds.

The cytoplasmic granules containing glycogen, also contain most of the necessary enzymes for its own synthesis and degradation.

Muscle glycogen does not contribute to blood glucose, however, glycogen levels are affected by fasting.

UDP-glucose is considered the activated monomer of glucose and is derived from glucose 1-phosphate.

Glycogen branches are more soluble than linear glycogen.

The "branching enzyme" breaks α(1→4) bonds and makes α(1→6).

The "branching enzyme" breaks α(1→4) bonds and makes α(1→6).

There are two different types of "debranching enzymes," one with 4:4 transferase activity, and one with 1:6 transferase activity.

Phosphoglucomutase transfers a phosphate group from the 1 position to the 6 position and vice versa depending on the direction of the reaction (synthesis vs breakdown).

Von Gierke disease results from a defect in glucose 6-phosphatase. Symptoms include severe fasting hypoglycemia and hepato-/reno- megaly (tumors).

Because glucose 6-phosphatase is defective in Von Gierke disease, glucose 6-phosphate will accumulate and redirect to other pathways.

Because glucose 6-phosphatase is defective in Von Gierke disease, glucose 6-phosphate will accumulate and redirect to other pathways.

The glycogen structure of both Von Gierke and type II Pompe disease patients are normal.

Glycogen is a homopolymer of α-D-glucose containing both α(1→4) and α(1→6) linkages.

Glycogenin is an alternate primer used for glycogen elongation when no primers are available.

Glycogenin is an alternate primer used for glycogen elongation when no primers are available.

The two products of glycogenolysis are glucose 6-phosphate and free glucose.

Glucose 6-phosphate is an allosteric modulator of glycogen breakdown.

The main products of lipid digestion are 2-monoacylglycerol and free glycerol.

Cholesterol is an amphiphilic molecule, while cholesteryl ester is a neutral molecule.

The main structural components of lipids are fatty acid chains and a backbone which can be either glycerol or cholesterol (steroid).

Lipids are insoluble in aqueous and organic solutions.

Short and medium chain TAGs are completely digested in the stomach.

TAGs and cholesterol are not present in the plasma membrane because they are too hydrophobic and must be sequestered.

Lipids are mechanically broken down into smaller globules for emulsification by peristalsis, and enzymatically broken down by lipases, cholesteryl esterases, and phospholipases from pancreatic juice.

Lipid digestion begins in the mouth, via lingual lipase.

Bile salts are derivatives of cholesterol.

The most important emulsifying agents of lipid digestion in the small intestine are phospholipids and bile salts.

Intestinal endocrine cells secrete secretin into the blood when the lipids and partially digested proteins enter the mid-lower duodenum and jejunum to slow gastric emptying, stimulate the pancreas to secrete pancreatic (digestive) enzymes, and stimulate the gallbladder to secrete bile.

The primary location of lipid absorption is the jejunum.

The primary location of lipid absorption is the jejunum.

In the resynthesis of TAGs and CEs, long chain fatty acids are turned into fatty acyl-CoA by fatty acyl-CoA synthase and ATP, an exergonic reaction that releases a pyrophosphate.

Long chain fatty acids are too hydrophobic to enter the blood directly.

Chylomicrons consist of an outer phospholipid layer containing apolipoproteins and cholesterol, and are used to transport hydrophobic fatty acids.

Chylomicrons are not secreted directly into the blood. They are first secreted into the lymphatic system.

Lipoprotein lipase (LPL) is expressed on capillary epithelial cells of adipocytes and muscle tissue.

Once lipoprotein lipase is activated by apoC-II, TAGs within the chylomicron are extracted and hydrolyzed into free fatty acids and glycerol for tissue utilization.

Chylomicron remnants are removed from the bloodstream by the kidneys, where they are endocytosed and hydrolyzed to their component parts for recycling.