Overview of metabolism Chemical and Physical Properties

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Fatty acids (FAs) consist of a carbon chain of varying lengths with a hydrocarbon tail and a carboxyl group for a head. Upon ionization of the carboxyl group, a negative charge is created. By means of an ester bond, an FA is attached to a molecule of glycerol forming a molecule of water and a monoglyceride. A triglyceride (TG) consists of three FAs attached to a molecule of glycerol by means of ester bonding. FAs can be classified according to the number of carbons they contain (chain length), their level of saturation (number of double bonds), or the orientation of their double bonds (omega 3, omega 6, or omega 9). FAs can be short-chain (SCFA), medium-chain (MCFA), or long-chain (LCFA). The chain length, number of double bonds, and location of the double bonds determine the biological activity and physical characteristics of FAs and ultimately of TGs. A TG does not have to consist of three identical FAs but may have a mixture of FAs. Medium-chain triglycerides (MCTGs) consist predominately of MCFAs, and long-chain triglycerides (LCTGs) consist predominately of LCFAs. Figure 3.1 indicates a unit of glycerol and an MCTG. Not all FAs in nature exist as TGs, but most of them do.

The naming of FAs according to the chain length is arbitrary. There is not total agreement in the literature as to the exact dividing line between classifications of FAs by chain length. Some reports indicate that SCFAs are 2, 3, 4, or 6 carbons long, while others classify caproic, a 6-carbon FA, as an MCFA. Likewise, some classify MCFAs as 6 (or 8) carbons to 12 (or 14) carbons. In most cases, MCFAs are considered to be 6 to 12 carbons long and LCFAs are from 14 to 24 carbons.5-7 In his book Nutritional Biochemistry, Brody indicates SCFAs as less than 8 carbons, MCFAs as 8 to 12 carbons, and LCFAs as 16 to 24 carbons. He mentions that some

FIGURE 3.1 Chemical structure of glycerol and the chemical structure of a medium-chain triglyceride where the R represents a medium-length fatty acid.

TABLE 3.1

Names, Characteristics, and Dietary Sources of Some Fatty Acids Found in Nature

Fatty Acid Common Name and Formula

Caproic

CH3(CH2)4CO2H Caprylic CH3(CH2)6CO2H Capric

CH3(CH2)8CO2H Lauric

CH3(CH2)!oCO2H

Myristic

CH3(CH2)12CO2H Palmitic

CH3(CH2)14CO2H Palmitoleic CH3(CH2)5CH=CH (CH2)7CO2H Stearic

CH3(CH2)16CO2H Oleic

CH3(CH2)7CH=CH (CH2)7CO2H Linoleic

Chemical or Systematic Name

Hexanoic Octanoic Decanoic Dodecanoic

Tetradecanoic Hexadecanoic 9-Hexadecenoic

Octadecanoic 9-Octadecanoic

Carbon Atoms: Double Bonds

Medium-Chain

Long-Chain

14:0

18:2

CH3(CH2)4CH=CHC Octadecadienoic H2CH=CH(CH2)7 CO H

Solubility Melting in Water, Point, g/100 g Common Food °C at 20°C Source

Linolenic

CH3CH2CH=CHCH2 CH=CHCH2CH= CH(CH2)7CO2H

9,12,15-Octadecatrienoic

18:3

44.2

69.6

16.3

  1. 9 Palm kernel, cow's milk (butter fat) 0.068 Coconut oil
  2. 015 Coconut oil
  3. 0055 Coconut, palm kernel
  4. 0020 Coconut oil 0.00072 Animal fat

Mackerel, avocado

0.00029 Animal fat, cocoa butter

  • Olive oil, avocado oil
  • Safflower oil

Rapeseed oil (flaxseed oil)

Modified from Ralston, A.W.J. and Hoerr, C.W., J. Organ. Chem, 7, 546-555, 1942;9 Westergaard, H. and Dietschy, J.M., J. Clin. Invest, 58, 97-108, 1976.13

12- and 14-carbon FAs are considered "in between" MCFAs and LCFAs.8 Most others classify 14-carbon FAs as LCFAs.

Table 3.1 lists some of the common FAs along with their main dietary source and some of their physical and chemical characteristics. Note that as the carbon chain length increases, the melting point increases and the solubility decreases.9 This is a noteworthy and striking difference between MCFAs and LCFAs. The greater the solubility, the faster the rate of digestion and absorption of the FA. The mechanism of absorption is also different. Observe that as the number of double bonds increases, the melting point decreases dramatically. For those who classify lauric acid (a 12-carbon FA) and myristic acid (a 14-carbon FA) as being between MC and LC, it may be noted that they do appear to be in a separate classification when comparing their characteristics to the SCFAs and LCFAs, particularly the solubility constants.

3.2.2 Fat Consumption

Fat consumption refers to the ingestion of all types of TGs, regardless of their size or saturation factor. In 1997 the U.S. Department of Agriculture (USDA) reported that fat consumption by humans in the U.S. can exceed 100 g/day.10 A more recent report indicates that Americans consumed an average of 65 g of fat per capita per day in 2000. This represents a 34% increase in fat consumption since the 1970 to 1974 survey.11 In 2003 another survey found the average daily intake of total fat for adults aged 19 to 64 to be 86.5 g for males and 61.4 g for females. Some individuals consumed over 140 g of fat per day.12 A fat is generally considered to be a solid at room temperature, while an oil is generally considered to be a liquid at room temperature.

3.2.3 Fat Digestion and Absorption

Most fat is consumed in the form of TGs. Digestion of TGs, both MC and LC, begins in the stomach with lingual lipase and gastric lipase,14 but most digestion of TGs takes place in the small intestines with pancreatic lipase.15 Lingual and gastric lipase become more important with infants16 and those with malabsorption syndromes secondary to conditions such as cystic fibrosis and alcoholic pancreatitis.1518 Lingual lipase activity varies with species. Lingual lipase in humans originates from the serous secretions of von Ebner glands on the tongue.19 Gastric lipase is secreted from the glands in the fundus of the stomach.8 Lingual lipase is present in humans in trace amounts, but gastric lipase dominates in preduodenal enzymatic digestion.20 In rats and newborn infants, lingual lipase hydrolyzed MCTGs five to eight times faster than LCTGs. The optimum pH for lingual lipase in humans is 3.5 to 6.0. This means it would still have some activity when in the upper small intestines. This would be particularly true during the neonatal period when the pH in the lumen of the small intestine is close to 6.5.21 Lingual and gastric lipase digests TGs by removing the sn-3 FA (third FA) from glycerol. The remaining diglyceride and the free FAs pass to the small intestines where pancreatic lipase continues the digestion process by cleaving fatty acids from the sn-1 (first FA) position, leaving a monoglyc-eride with an attached FA at the sn-2 position.2022 Pancreatic lipase, like gastric lipase, can also remove FAs from the sn-3 position. Reports vary, but it has been suggested that lingual and gastric lipases can hydrolyze FAs from 10 to 30% of the dietary TGs while in the stomach.

Lingual and gastric lipase and the remaining diglycerides pass to the small intestines where they continue to cleave FAs along with pancreatic lipase.15,21,23

The effectiveness of digestion and absorption of LCTGs is increased by the secretion of bile acids from the gall bladder. Bile acts as an emulsifying agent that forms a micelle with LCFAs and, in addition to keeping fats separated, allows for greater surface area and facilitates their passage through the unstirred water layer that surrounds the epithelial surface of the small intestines.24 A major difference occurs at this point between MCFAs and LCFAs. Since LCFAs have a low solubility, they have a difficult time penetrating this aqueous unstirred water layer. On the other hand, MCFAs with a much higher solubility can penetrate this layer and be absorbed much quicker, even with pancreatic insufficiency.25 Thus, bile salts and pancreatic lipase are absolutely essential for efficient digestion and absorption of LCTGs.

Under normal conditions, the gastrointestinal tract can absorb greater than 95% of the TGs ingested. If greater than 5% of the ingested fat is not digested, but instead lost in the feces, steatorrhea (a form of diarrhea caused by fat malabsorption) can result.26 Most of the LCFAs and MCFAs are absorbed in the proximal small intestines,27 but can be absorbed in the ileum,28 the large intestines,29 possibly the rectum,26,30 and even the stomach.18 About half of the MCFAs in human milk can be absorbed in the stomach.31

The exact method of absorption of FAs is still under investigation, but it is believed that, for the most part, LCFAs are carried across the intestinal mucosa by a protein-mediated mechanism,32 while MCFAs can be more easily absorbed through the aqueous unstirred water layer33 and enter the intestinal mucosa by diffusion.24 It is well established that once the LCFAs are absorbed, they are incorporated into chylomicrons (CMs) in the intestinal mucosa and transported via the lymphatic system to the circulatory system and eventually to the liver.8,33,34 Most of these CMs undergo some degree of hydrolysis in extrahepatic tissue before reaching the liver and release most of the attached LCFAs as a result of hydrolysis.35 This is usually not the case with MCFAs, which can bypass the lymphatic system, be absorbed directly into the portal vein, and go straight to the liver. The percentage of FAs that are incorporated into CMs and transported via the lymphatic system vs. those that are transported via the portal vein depends on the total amount of fat ingested, the chain length of the FAs ingested, and their degree of saturation. Lymph is the major means of transporting LCFAs, while the portal blood is the major transport mechanism of MCFAs. However, some LCFAs are absorbed into the portal system and some MCFAs are reassembled into TGs and thus end up in CMs and are transported via the lymphatic system.26,36-40 MCTGs do not require bile acids for absorption, and large amounts can be absorbed in patients who are even deficient in pancreatic lipase.25 For this reason, MCTGs have been used for over 50 years to provide an enteral source of kilocalories in the treatment of fat malabsorption syndromes.41

MCFAs are usually found in adipose tissue in only trace amounts, but can be found in larger amounts after supplementation in the diet.42,43 TGs deposited in adipose tissue consist predominately of LCFAs.35 The amount and kind of FAs fed will have an effect on the transit time through the small intestines. To determine the effects of transit time, eight healthy subjects participated in a study that was designed so each subject was his own control. Four treatments were used. One LCTG treatment

TABLE 3.2

Transit Time through the Small Bowel

Treatment Transit Timea

Low dose of MCTGs 56 ± 6 min High dose of MCTGs 69 ± 9 min

Normal saline 101 ± 9 min a Compiled from Ledeboer, M. et al., JPEN, 19, 58, 1995.

was administered in a dose of 15 mmol/h, which was equal to 125 kcal/h. Two MCTG treatments were administered. One was in equimolar amounts compared to the LCTG treatment at 15 mmol/h (56 kcal/h). The second treatment contained 113 kcal/h (30 mmol/h), nearly isocaloric with LCTG treatment. Since the molecular weight of MCTGs is about half that of the LCTGs, the caloric values would be different if equimolar amounts were used. Thus, the MCTG treatment was completed twice, once as equimolar and once as equicaloric with the LCTG treatment. The fourth treatment was a control and consisted of saline solution administered at 15 ml/h. Each treatment was infused into the duodenum for 360 min followed by at least 7 days of rest. Each subject that received MCTGs complained of abdominal cramps and diarrhea. The subjects on the high dose of MCTGs experienced diarrhea until the day after the experiment. The subjects receiving the low dose of MCTGs experienced abdominal cramps and diarrhea only during the day of treatment. Because of this discomfort, only five subjects were subjected to the high-dose treatment of MCTGs. None of the subjects receiving the LCTGs experienced cramps or diarrhea. The effects on transit time can be found in Table 3.2. The transit time was significantly reduced (p < 0.05) during the administration of MCTGs, compared to the control. Also, MCTGs did not stimulate cholecystokinin (CCK) release but LCTGs did.44 In a very similar experiment conducted with intraduodenal administration of MCTGs, LCTGs, and a control at similar equimolar doses, the same results were found. The MCTG treatment significantly (p < 0.05) accelerated the small bowel transit time. CCK's secretion was significantly (p < 0.05) increased with the administration of LCTGs, but no significant alterations were observed during the MCTGs treatment or control.45 Increased transit time means increased bowel movements that would take place sooner after ingestion than usual. This would be an important consideration when using MCTGs as an ergogenic aid for athletic performance.

Most MCFAs reach the liver bound to albumin without being incorporated into CMs like LCFAs, but about 8% of the MCTGs were found in CMs 3 h after consuming a meal that contained MCTGs.41 Some propose that MCTGs be consumed in greater quantities to promote weight loss without the MCTGs being incorporated into adipose tissue. Others propose increased consumption of MCTGs for a quick source of energy that may benefit athletes. These proposals are based on assumptions that MCTGs are utilized very rapidly for energy without being converted into adipose tissue. These assumptions may not be true. Studies have shown that the liver does not utilize all MCTGs for rapid oxidation into ketone bodies for energy,35,41,46 but may reesterify some MCFAs into LCFAs after elongation.47,48 This is particularly true when the percentage of MCFAs consumed in the diet is high.48 It has been demonstrated in preterm infants that octanoic acid (an 8-carbon FA), fed in a standard formula, was detected in plasma as myristic acid (a 14-carbon FA) and palmitic acid (a 16-carbon FA).47

3.2.4 Fatty Acid Utilization

CMs are synthesized in the small intestine mucosa and are transported to the circulatory system via the thoracic duct.49 They can appear in the circulatory system in a matter of minutes.50-52 The circulating CMs are enzymatically attacked by lipoprotein lipase on the luminal side of blood vessels. TGs attached to the CMs are hydrolyzed, releasing FAs. These FAs are able to be utilized by muscle for energy or can be incorporated into adipose tissue for storage.50 The fate of the hydrolyzed FAs depends on the amount of total fat ingested, total kilocalories ingested, and the energy demands on the body. If the body is at rest and consumes an excess of fat, or an excess of kilocalories that are converted to fat, then excessive amounts of FAs will be deposited in adipose tissue as TGs. If the body is at work or does not consume an excess of fat or kilocalories, more of the FAs will be utilized by the muscle for energy. During a fasting period, the energy utilized from free FAs is produced by the hybridization of TGs stored in adipose tissue. Signaling mechanisms activate hormone-sensitive lipase, an enzyme that hydrolyzes intracellular tri- and diglycer-ides, releasing FAs into circulation in the blood (usually in the form of LCFAs). The FAs are carried by albumin to muscle tissue where they are utilized for energy.53

Higher than normal intakes of MCTGs have become attractive to the athlete since the MCFAs that make them up can be absorbed faster, go into portal circulation, and enter the mitochondria without carnitine. It is well known that increased consumption of MCTGs can increase circulation of ketone bodies.1,54,55 Provided the liver has ample calories, the rapid metabolism of MCFA can result in the production of ketone bodies (P-hydroxybutyrate, acetoacetate, and acetone) or an increase in free fatty acids (FFAs) in circulation. These ketones and FFAs can then be used by the muscles for energy.56 How well this works will be discussed in Section 3.4.

FAs are in a more reduced state than glucose. The oxidation of FAs requires more oxygen than glucose, but more energy is released in the process. Fats yield 9 kcal/g, while glucose yields 4. MCTGs provide 8.2 kcal/g.57 The oxidation of FAs takes place under aerobic conditions in the mitochondria of cells. First, LCFAs must migrate through the cytoplasm and enter the mitochondria by means of a carrier, carnitine.58 Once in the mitochondria, the LCFAs undergo beta-oxidation and enter the Krebs cycle and produce ATP. This mechanism requires enzymes and transporters inside the cell that accrue carnitine. A deficiency in any of the transporters or any of the enzymes results in an increased excretion of carnitine in the urine and an inability of LCFAs to enter the mitochondria, resulting in hypoketotic hypoglycemia and hepatic encephalopathy. Another advantage to MCFA ingestion is their ability to enter into the mitochondria without carnitine. Thus, treatment for carnitine deficiency includes a low-fat diet supplemented with MCTGs.59 Since a large percentage of ingested MCTGs can bypass the lymphatic system, enter the mitochondria directly, and be oxidized, they make an attractive alternative to a quick energy source, but ingestion of large amounts of MCTGs can have drawbacks in that they may cause gas, abdominal cramps, diarrhea, and may stimulate an elongation process and cause additional fat deposition, or may contribute to cardiovascular disease. Each of these possibilities will be discussed later.

To summarize, MCTGs are hydrolyzed faster and more completely than LCTGs and are absorbed more quickly into the small intestine mucosa. A greater percentage goes directly into portal circulation to the liver, where they can enter the mitochondria without carnitine and preferentially enter into the Krebs cycle.60 However, a large intake of MCTGs can cause gas, cramps, bloating, and diarrhea,45 and the elongation of MCFAs resulting in deposits in adipose tissue, along with the possibilities of promoting cardiovascular disease, is still under investigation.

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