Adipose tissue triacylglycerols

Adipose tissue triacylglycerol 12000 450 15 Several days 70 days ... 

Glycogen conversion to Blood glucose Blood fatty acids (from adipose tissue triacylglycerol)... 

Mobilisation of triacylglycerol is due to the increased rate of lipolysis. Adipose tissue triacylglycerol contains some essential fatty acids (linoleic and linolenic acids) and these are mobilised along with the non-essential fatty acids. The... 

Fuel Reserves in Adipose Tissue Triacylglycerols, with their hydrocarbon-like fatty acids, have the highest energy content of the major nutrients. 

Fatty acids, whether synthesized by the liver or taken in through the diet, must be transported through the blood, usually for storage in the adipose tissue. Triacylglycerols have relatively low solubility in the plasma, and therefore are transported as lipoproteins (Fig. 15.6). 

A) Decreased intake of total calories, because all fuels can be converted to adipose tissue triacylglycerols... 

Adipose tissue triacylglycerols also contain fatty acids synthesized in the liver, principally from excess calories ingested as glucose. The pathway of fatty acid synthesis generates palmitate, which can be elongated to form stearate, and unsaturated to form oleate. These fatty acids are assembled into triacylglycerols and transported to adipose tissue as the lipoprotein VLDL (very-low-density lipoprotein). 

During fasting and other conditions of metabolic need, long-chain fatty acids are released from adipose tissue triacylglycerols by lipases. They travel in the blood bound in the hydrophobic binding pocket of albumin, the major serum protein (see Fig. 23.1). 

Fatty acids are used as fuels principally when they are released from adipose tissue triacylglycerols in response to hormones that signal fasting or increased demand. Many tissues, such as muscle and kidney, oxidize fatty acids completely to CO2 and H2O. In these tissues, the acetyl CoA produced by p-oxidation enters the TCA cycle. The FAD(2H) and the NADH from p-oxidation and the TCA cycle are... 

Long-chain fatty acids are a major fuel for the liver during periods of fasting, when they are released from adipose tissue triacylglycerols and travel to the liver as fatty acids bound to albumin. 

The enzymes in the pathways of fatty acid activation and p-oxidation (the synthetases, the carnitine acyltransferases, and the dehydrogenases of p-oxidation) are somewhat specific for the length of the fatty acid carbon chain. The chain length specificity is divided into enzymes for long-chain fatty acids (C20 to approximately C12), medium-chain (approximately C12 to C4), and short-chain (C4-C2). The major lipids oxidized in the liver as fuels are the long-chain fatty acids (palmitic, stearic, and oleic acids), because these are the lipids that are synthesized in the liver, are the major lipids ingested from meat or dairy sources, and are the major form of fatty acids present in adipose tissue triacylglycerols. The liver, as well as many other tissues, uses fatty acids as fuels when the concentration of the fatty acid-albumin complex is increased in the blood. 

The availability of free fatty acids in the blood, which depends on their release from adipose tissue triacylglycerols by hormone-sensitive lipase. During prolonged exercise, the small decrease of insulin, and increases of glucagon, epinephrine and norepinephrine, cortisol, and possibly growth hormone all activate adipocyte tissue lipolysis. 

When food intake is in excess of requirements, a greater proportion is used for synthesis of adipose tissue triacylglycerol reserves, so there is a considerably greater diet-induced thermogenesis. Conversely, in negative energy balance there will be considerably less synthesis of adipose tissue reserves. 

A high proportion of odd chain and of various polymethyl-branched fatty acids occurs in the adipose tissue triacylglycerols of sheep and goats when they are fed diets based on cereals such as barley. Cereal starch is fermented by bacteria in the rumen to form propionate, and when the animals capacity to metabolize propionate via methylmalonyl-CoA to succinate is overloaded, propionyl- and methylmalonyl-CoA accumulate. Garton and his colleagues showed that methylmalonyl-CoA can take the place of malonyl-CoA in fatty acid synthesis and that with acetyl- or propionyl-CoA as primers, a whole range of mono-, di- and tri-methyl branched fatty acids can be produced. 

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