Breakdown of triglycerides into fatty acids and glycerol


breakdown of triglycerides into fatty acids and glycerol

Non-profit foundation providing reliable, scientifically accurate, personalized information for convenient and enjoyable healthy eating. How Does Digestion Work and How Can I Improve Mine? (Animated graphics). The primary sources of fatty acids for oxidation are dietary and mobilization from cellular stores. Fatty acids from the diet are absorbed from the gut, packaged into.

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Overview of Fatty Acid Oxidation breakdown of triglycerides into fatty acids and glycerol

Albright and Judith S. Encyclopedia of Sports Medicine and Science, T. Internet Society for Sport Science: Adipose tissue is specialized connective tissue that functions as the major storage site for fat in the form of triglycerides.

Adipose tissue is found in mammals in two different forms: The presence, amount, and distribution of each varies depending upon the species. Most adipose tissue is white, the focus of this review. White adipose tissue serves three functions: Subcutaneous adipose tissue, found directly below the skin, is an especially important heat insulator in the body, because it conducts heat only one third as readily as other tissues.

The degree of insulation is dependent upon the thickness of this fat layer. Adipose tissue also surrounds internal organs and provides some protection for these organs from jarring. As the major form of energy storage, fat provides a buffer for energy imbalances when energy intake is not equal to energy output. It is an efficient way to store excess energy, because it is stored with very little water.

Consequently, more energy can be derived per gram of fat 9 kcal. In addition, if terrestrial animals stored their excess energy as carbohydrate, the increased mass would interfere with mobility. There are some constraints on the use of fat as fuel. Most animals cannot convert lipid into carbohydrate.

Tissues that function predominantly anaerobically e. Additionally, under normal conditions the brain is dependent upon glucose for energy and does not use fatty acids. In unusual metabolic circumstances, the brain can use ketone bodies a by-product of incomplete fat metabolism when they are present in sufficiently high quantities.

Finally, a typical diet contains a high proportion of carbohydrate, and the transport of insoluble lipids through blood requires a specific mechanism, so it may be "easier" metabolically for tissues to use glucose under typical dietary conditions. In the rat, brown adipose tissue is found primarily in the interscapular region and the axillae, minor amounts are found near the thymus and in the dorsal midline region of the thorax and abdomen.

During maturation, in non-hibernating animals, brown adipose tissue is metabolically less active, although cold exposure can activate it. In hibernating animals and neonates, brown adipose tissue is important for regulating body temperature via non-shivering thermogenesis.

Instead of serving as a substrate, the lipid in brown adipose tissue releases energy directly as heat and is, therefore used in heat production for non-shivering thermogenesis and for utilization of excess caloric intake via diet-induced-thermogenesis. The mechanism of heat generation is related to the metabolism of the mitochondria.

Mitochondria from brown adipose tissue have a specific carrier called uncoupling protein that transfers protons from outside to inside without subsequent production of ATP.

Morphology and Development of Adipose Tissue. In adult mammals, the major bulk of adipose tissue is a loose association of lipid-filled cells called adipocytes, which are held in a framework of collagen fibers. In addition to adipocytes, adipose tissue contains stromal-vascular cells including fibroblastic connective tissue cells, leukocytes, macrophages, and pre-adipocytes not yet filled with lipid , which contribute to structural integrity.

White fat cell and brown fat cell. Note the single large lipid vacuole in the white fat cell and the numerous smaller lipid vacuoles in the brown fat cell. Artwork courtesy of Dr. Unilocular cells contain a single large lipid droplet which pushes the cell nucleus against the plasma membrane, giving the cell a signet-ring shape Figure 1.

Unilocular cells, characteristic of white adipose tissue, range in size from 25 to microns. Mitochondria are found predominately in the thicker portion of the cytoplasmic rim near the nucleus. The large lipid droplet does not appear to contain any intracellular organelles. Multilocular cells, typically seen in brown adipose tissue, contain many smaller lipid droplets. A cell in brown adipose tissue may reach a diameter of 60 microns and the lipid droplet within the cell may reach 25 microns in diameter.

These mitochondria vary in size and may be round, oval, or filamentous in shape. Small amounts of free fatty acids, diglyceride, cholesterol, phospholipid and minute quantities of cholesterol ester and monoglyceride are also present. Varying the composition of your diet can vary the fatty acid profile in adipose tissue. White adipose tissue is not as richly vascularized as brown adipose tissue, but each adipocyte in white adipose tissue is in contact with at least one capillary.

This blood supply provides sufficient support for the active metabolism, which occurs in the thin rim of cytoplasm surrounding the lipid droplet. Blood flow to adipose tissue varies depending upon body weight and nutritional state, with blood flow increasing during fasting. Adipocytes are considered to originate from fibroblast-like precursor cells that differentiate into adipocytes under the appropriate stimulatory conditions described below.

The precursor cells do not possess any morphological or enzymatic marker that can be used to determine whether they will become adipocytes.

The criteria used to identify adipocytes depends upon lipid accumulation within the cell after proliferation has stopped, making early identification of adipocytes difficult. The size of adipose tissue mass is a function of both adipocyte number and size. An increase in adipose tissue mass can occur by hyperplastic growth, which is an increase in the number of adipocytes. This increase in number occurs primarily by mitotic activity in precursor cells.

Adipose tissue mass can also increase by hypertrophic growth, which is an increase in the size of adipocytes. This increase in size occurs primarily by lipid accumulation within the cell. Growth of this tissue in the rat occurs in well-defined stages. From birth to 4 weeks of age, adipose tissue growth is hyperplastic. Overfeeding a rat during this period can lead to permanent increases in body weight and fat cell number.

From 4 to 14 weeks of age both adipocyte hypertrophy and hyperplasia occur. Following 14 weeks of age, adipose tissue growth occurs predominantly by adipocyte hypertrophy. The developmental sequence of adipose tissue in humans is less well defined. In contrast to most neonates, the human neonate is born relatively fat. Two periods of hyperplastic growth are probably during the third trimester of pregnancy and just prior to and during puberty.

Contrary to earlier belief, hyperplastic growth can also occur in adulthood in both humans and rats. When adipocytes fill with lipid and get to a critical size, precursor cells are stimulated to differentiate, and an increase in adipocyte number results.

This critical size probably does not occur with moderate overfeeding unless the overfeeding is of long duration. In addition, there are probably individual differences in the size that will result in new adipocyte formation.

Once new adipocytes are formed, they remain throughout life and only a reduction in size of the cell is possible.

This increased number of adipocytes has far-reaching consequences for the treatment and prevention of obesity. Lipogenesis is the deposition of fat. This process occurs in adipose tissue and in the liver at cytoplasmic and mitochondrial sites Figure 2. Diagrammatic representation of triglyceride storage lipogenesis and breakdown lipolysis in adipocytes.

Adapted from Leibel, Berry, and Hirsch, Energy ingested as fat beyond that needed for current energy demands is stored in adipose tissue. In addition, carbohydrate and protein consumed in the diet can be converted to fat.

Energy ingested as carbohydrate can be stored as glycogen in the liver and muscle. Carbohydrate can also be converted to triglycerides primarily in the liver and transferred to adipose tissue for storage. Amino acids from ingested proteins are used for new protein synthesis or they can be converted to carbohydrate and fat.

Fatty acids, in the form of triglycerides or free fatty acids bound to albumin, are ingested in the diet or synthesized by the liver described above. Very little synthesis of free fatty acids occurs in the adipocytes. Triglycerides are the most significant source of fatty acids, because this is the form in which dietary lipids are assembled by the gut and liver. Triglycerides made up of long chain fatty acids, in the form of chylomicrons from intestinal absorption or lipoproteins from hepatic synthesis , are hydrolyzed to glycerol and free fatty acids by an enzyme called lipoprotein lipase LPL.

Lipoprotein lipase is synthesized in adipocytes and secreted into adjacent endothelial cells. Chylomicrons and lipoproteins very low density lipoproteins contain C-ll apoprotein, which activates LPL.

Free fatty acids are taken up by adipocytes in a concentration-dependent manner by a transmembrane transport protein. Once inside the adipocyte, fatty acids enter a common pool made up of both incoming and outgoing fatty acids. Fatty acids that are stored in the adipose tissue must first combine with coenzyme A to form a thioester and then they are re-esterified in a stepwise manner to triglycerides. Glucose is the primary source of glycerol for this re-esterification process.

Only a small amount of glycerol released, when triglycerides are hydrolyzed by LPL, can be reused by adipocytes to form alpha glycerol phosphate to be used for trigyceride assembly. Most glycerol is returned to the circulation. Insulin, a hormone secreted by the beta cells of the pancreas, plays a predominant role in the lipogenic process.

The net effect of insulin is to enhance storage and block mobilization and oxidation of fatty acids. Insulin exerts its effect by stimulating LPL formation, so that circulating triglycerides are hydrolyzed and free fatty acids can enter the adipocyte. Insulin is also required for the transport of glucose, which is needed for re-esterification of the triglycerides once inside the adipocyte.

Lipolysis is the chemical decomposition and release of fat from adipose tissue. This process predominates over lipogenesis when additional energy is required Figure 2. The triglycerides within the adipocyte are acted upon by a multi-enzyme complex called hormone sensitive lipase HSL , which hydrolyzes the triglyceride into free fatty acids and glycerol.

These lipases act consecutively on triglycerides, diglycerides, and monoglycerides. Triglyceride lipase regulates the rate of lipolysis, because its activity is low. Once triglycerides are hydrolyzed to fatty acids and glycerol, fatty acids enter the common free fatty acid pool where they may be re-esterified, undergo beta-oxidation metabolic degradation , or be released into the circulation as substrates for skeletal muscle, cardiac muscle, and liver.

If the fatty acids are to undergo beta-oxidation for ATP production, fatty acids move from the adipocytes into the blood and are carried to the tissues that can use them as an energy source.

Fatty acid metabolism

Thompson , Harald H. The water addition is catalyzed by an enoyl-CoA hydratase activity, the second oxidation step is catalyzed by an NAD-dependent long-chain hydroxacyl-CoA dehydrogenase activity 3-hydroxyacyl-CoA dehydrogenase activity , and finally the cleavage into an acyl-CoA and an acetyl-CoA is catalyzed by a thiolase activity. Phytochemical Analysis 4 5 , This is, of course, substrate-level regulation. Nutrition Research 7 6 , breakdown of triglycerides into fatty acids and glycerol breakdown of triglycerides into fatty acids and glycerol The oxaloacetate is returned to mitochondrion as malate and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion. Nutrition Research 7 6 Phytochemistry 17 5 Comparative Biochemistry and Physiology 29 2 Planta 4 breakdown of triglycerides into fatty acids and glycerol breakdown of triglycerides into fatty acids and glycerol breakdown of triglycerides into fatty acids and glycerol



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