Triglycerides in adipose tissue

The final site of deposition of dietary fatty acids, as well as the quantitatively major source of triglyceride reserves in the body is adipose tissue. It is by now well established that this tissue is not merely an inert pool of stored fat, but is 

A considerable part of the fat ingested is deposited in adipose tissue. Using fat with labelled fatty acids, this was found to be true even when the animal is in caloric deficit and a net decrease in stored fatty acids takes place. Inflow and outflow go on continuously (Schonheimer and Rittenberg 1935 Bernhard and Steinhauser 1943). 

Not all of the chylomicron triglycerides have to pass through the liver and recycle in the blood as lipoproteins, in order to be incorporated in adipose tissue. A part of the chylomicron triglycerides may be taken up directly. This depends on the nutritional state of the animal. When fatty acid labelled chylomicra are injected into a fasting animal only small amounts can be discovered in adipose tissue, short intervals after the injection. However, if this experiment is performed with a carbohydrate fed animal, as much as 25% can be found in adipose tissue after short periods (Bragdon and Gordon 1958). 

These findings make it probable that disruption and resynthesis of the ester bonds play a role at some phase of the facilitated transport of triglycerides into the adipose tissue cells. It is, however, not yet settled where these processes take place. Lipoprotein lipase has been implicated in this process. A lipoprotein lipase, similar to that appearing in blood following heparin injection, has been extracted from adipose tissue (Korn 1955 a) and is released into the medium when adipose tissue is incubated in a solution containing heparin (Hollenberg 1959 Cherkes and Gordon 1959 Robinson 1960). 

The nutritional conditions inducing activity of the lipoprotein lipase released by the tissue coincide with those increasing triglyceride uptake (Bragdon and Gordon 1958 Havel, Felts and van Duyne 1962 Bezman, Felts and Havel 1962). However, this correlation is far from complete. Poisons which are effective lipoprotein lipase inhibitors did not interfere with the uptake of triglycerides, while others which have no effect on the enzyme caused substantial reduction of uptake (Markscheid and Shaerir 1963). 

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Glycogenolysis in liver, release of fatty adds from triglycerides in adipose tissue... 

Sarda, P, Lepage, C., Roy C. C., and Chesses, P (1987). Storage of medium-ehain triglycerides in adipose tissue of orally fed infants- A n. f. Cltn. Nutr. 45,399-405. 

The metabolism of hexoses proceeds according to the bod/s requirements. This results in (1) energy production by conversion to carbon dioxide and water, (2) storage as glycogen in the hver or triglyceride in adipose tissue, or (3) conversion to keto acids, amino acids, or protein. 

A young woman sought the advice of her physician because she was 30 pounds overweight. The excess weight was in the form of triglycerides carried in adipose tissue. Yet when the woman described her diet, it became obvious that she actually ate very moderate amounts of fatty foods. Most of her caloric intake was in the form of carbohydrates. This included candy, cake, beer, and soft drinks. Explain how the excess calories consumed in the form of carbohydrates ended up being stored as triglycerides in adipose tissue. 

The fed state is also an opportunity to lay down storage triglycerides in adipose tissue. Insulin therefore switches on lipoprotein lipase, which downloads fatty acids from chylomicrons it switches on the enzymes that resynthesise triglyceride inside the adipocytes it switches off hormone-sensitive lipase, the one that releases fatty acids into the blood when the stores are mobilised. 

There are two types of cell membrane receptor (a and jS) for adrenaline. -Receptors which are inhibited by -blockers such as propanolol are the main type of receptor in muscle, heart, adipose tissue and many other tissues. They interact with and activate adenylate cyclase in the cell membrane so that the effect of adrenaline on muscle or adipose tissue is to increase the concentration of cAMP in the cell and thus to activate protein kinase. Stimulation of glycogen breakdown by adrenaline in muscle is then mediated by a cascade mechanism similar to that involved in the stimulation of glycogenolysis in liver by glucagon (page 353). Breakdown of triglycerides in adipose tissue, as in liver, occurs as a result of activation of triglyceride lipase by phosphorylation. 

Sarda, R, Lepage, G., Roy, C.C., and Chessex, R. Storage of medium-chain triglycerides in adipose tissue of orally fed infants. Am. J. Clin. Nutr. 45, 399-405, 1987. 

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