Movements of Fat

Starvation ( ] glucagon i insulin) Fat degradation Diabetes ( ] glucagon i insulin) Fat degradation Excitement ( epinephrine) Fat degradation 

Fat is only an energy storage form (Fig. 17-4). Fat cannot be converted to carbohydrate equivalents. This is a very important point. Remember it The reason for this is a bit subtle. The carbon skeleton of fatty acids is metabolized to acetyl-CoA only. Glucose precursors such as oxaloacetate can be synthesized from acetyl-CoA by going around the TCA cycle. However, acetyl-CoA has 2 carbon atoms. Going around the TCA cycle burns off 2 carbon atoms (as CO2). The net number of carbon atoms that ends up in oxaloacetate is then zero. No carbohydrate can be made from fat.  

The formation of a triglyceride that requires the presence of glycerol introduces a carbohydrate requirement for the storage of fat. When 

Many tissues (muscle, liver, renal cortex) prefer fat for an energy supply, at least in the resting state. The exception is red blood cells and brain. These tissues depend heavily on glycolysis for energy. Red cells cannot survive without glucose (no mitochondria), but during prolonged starvation, brain can adapt to utilize fat metabolites produced by the liver (ketone bodies). 

The regulation of fat metabolism is relatively simple. During fasting, the rising glucagon levels inactivate fatty acid synthesis at the level of acetyl-CoA carboxylase and induce the lipolysis of triglycerides in the adipose tissue by stimulation of a hormone-sensitive lipase. This hormone-sensitive lipase is activated by glucagon and epinephrine (via a cAMP mechanism). This releases fatty acids into the blood. These are transported to the various tissues, where they are used. 

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Phosphorylation Glycogen Metabolic Movements of Glycogen Fat Metabolic Movements of Fat Protein Metabolic Movements of Protein Tissue Cooperation Liver Muscle Ketone Bodies... 

An increase in the porosity of the para-casein matrix, concurrently with the age-related increase in proteolysis (Tunick and Shieh, 1995), which may reduce the impedance of the matrix structure to the movement of fat. 

Movement of fats and oils may be as the crude, partially refined, or finished oils and may be by rail tank cars, tank trucks, barges, and tanker ships. Rail tank cars are usually of the standard 60,566-L (16,000-gal 120,000-lb) or the jumbo 232,170-L (61,333-gal 460,000-lb) size. Standard cars are designed with a thermal expansion area of about 2% of the total capacity as a dome in the car. However, the rated capacity of the jumbo cars does not include any expansion space. Rather, these cars are equipped with a permanently installed bar marker located in the passageway, above which the quantity of oil should not be loaded. Heating coils can be installed for handling higher melting fats. 

A second lipothrophic factor is betaine, which is effective because the transfer of at least one of its methyl groups to homocysteine is very efficient and can replenish methionine for choline formation. In the absence of sufficient lipotrophic factors, a fatty liver develops, and there is insufficient movement of fats either ingested or synthesized in the liver to the adipose tissue. As fats enter or are synthesized in the liver, they are repackaged or packaged as VLDLs to be moved out for transport from the blood to adipose tissue. The VLDLs contain protein, triacylglycerol, cholesterol, cholesterol esters, and phospholipids, especially phosphatidylcholine (lecithin). If one has either a protein deficiency or a lipotrophic factor deficiency, the movement of triacylglycerol s from the liver to adipose is ineffective and a fatty liver can develop. Choline can be present in the diet and need not be synthesized de novo. Phospholipid synthesis has been discussed previously (Chapter 15). 

The overall movement of fats in the rats during the last 3 days of the experiment are shown in Table 4. No significant differences between the diet groups were seen for any of the variables food intake, fat intake, dried feces mass, fat excretion, fat content of dry feces, or fat absorption coefficient. To see whether dietary DAG had any effects on the lipid composition of the feces, we also analysed the fecal lipid profiles of the two groups of rats using gas chromatography. No significant differences were found. 

In stirred-slurry reactors, momentum is transferred to the liquid phase by mechanical stirring as well as by the movement of gas bubbles. Small particles are used in most cases, and the operation is usually carried out in tank reactors with low height-to-diameter ratios. The operation is in widespread use for processes involving liquid reactants, either batchwise or continuous— for example, for the batchwise hydrogenation of fats as referred to in Section II. 

From an engineering perspective, deep-fat frying can be defined as a unit operation where heat and mass transport phenomena occur simultaneously. Convective heat is transferred from the frying media to the surface of the product, which is thereafter conducted within the food. Mass transfer is characterized by the loss of water from the food as water vapor and the movement of oil into the food (Singh, 1995). 

Spleen and Stomach, transform dampness and promote digestion, particularly the metabolism of fats. If hyperlipidemia has developed and has resulted in detectable damage to the heart, brain and vascular system, herbs to strongly remove dampness and phlegm, clear heat, stimulate Qi movement and blood circulation, nourish the Yin and pacify the Liver should be added to the formula. In all conditions, herbs that tonify the Spleen and Kidney should be prescribed. 

FIG. 1 Movement of cholesterol (CHOL) and bile acids (BA) between the liver and small intestine. CHOL and BA in the liver are secreted into the gallbladder where they are stored temporarily until a fat-containing meal causes their secretion into the intestinal lumen. BA are absorbed with high efficiency (95%) and are recycled back to the liver via the hepatic portal vein. CHOL is absorbed less efficiently (50-60%) and must be incorporated into lipoproteins (chylomicrons) for transport back to the fiver via the systemic circulation. Accumulation of CHOL in the liver can promote secretion of CHOL into plasma, thus increasing LDL-CHOL concentration. Loss of CHOL and BA in feces represents the primary route of CHOL elimination from the body. 

TCDD and OCDD in the Arctic than in sub-Arctic areas is thought to be transpolar movement of aerosols from combustion-related sources originating in Eurasia (Norstrom et al. 1990). CDDs and CDFs were determined in caribou tissue samples from 7 herds across the Canadian Arctic (Hebert et al. 1996). In contrast to marine mammals, concentrations for caribou were extremely low, sub-ng/kg (lipid basis), for all congeners except OCDD and 1,2,3,7,8-PeCDD in one herd. OCDD was found in most of the samples at concentrations ranging from < 0.2 ng/kg in fat to 4.7 ng/kg in adipose tissue. The one pooled liver sample analyzed from the Yukon had an OCDD concentration of 11 ng/kg (lipid basis). 

Figure 21.1 Metabolite and fuel movements in the fed state (high insulin/glucagon). Arrows indicate net movement of metabolites. There is a net synthesis of glycogen and fat in the liver. Glucose is converted to pyruvate and lactate during muscular activity. Both the Cori and alanine cycles are shown.

In addition to growth factors, it has been shown that countless other molecules have multiple functions. Cholecystokinin, for example, is a peptide that acts as a hormone in the intestine, where it increases the bile flow during digestion, whereas in the nervous system it behaves as a neurotransmitter. Encephalins are sedatives in the brain, but in the digestive system are hormones that control the mechanical movements of food. Insulin is universally known for lowering the sugar levels in the blood, but it also controls fat metabolism and in other less known ways it affects almost every cell of the body. 

Lipids (fats) are the other important components of cell membranes. Along with cholesterol, also a component of the cell membrane, they have acquired a bad name, but they arc nonetheless essential to the function of membranes as selective barriers to the movement of molecules. 

Cholecystokinin (cholecysto = gall bladder and kinin = movement) release is stimulated by the presence of fat in the duodenum it induces contractions of the gall bladder and common bile duct, resulting in delivery of bile into the gut. 

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