Plasma free fatty acid changes

There is a small fall in plasma glucose upon starvation, then little change as starvation progresses (Table 27-2 Figure 27-2). Plasma free fatty acids increase with onset of starvation but then plateau. There is an initial delay in ketone body production, but as starvation progresses the plasma concentration of ketone bodies increases markedly. 

Glucocorticoids not only break down protein but also stimulate the catabolism of lipids in adipose tissue and enhance the actions of other lipolytic agents. This occurrence results in an increase in plasma free fatty acids and an enhanced tendency to ketosis. The mechanism of this lipolytic action is unknown. The net effect of the biochemical changes induced by the glucocorticoids is antagonism of the actions of insulin. These biochemical events promote hyperglycemia and glycosuria, which are similar to the diabetic state. 

Free thyroxine levels are affected by plasma free fatty acids which are increased in the postoperative period. Normal variations and induced increases in free fatty acids produced no change in free thyroxine levels (K4). 

McLaughlin T, Abbasi F, Lamendola C, et al. Metabolic changes following sibutramine-assisted weight loss in obese individuals role of plasma free fatty acids in the insulin resistance of obesity. Metabolism 2001 50 819-882. 

In milk, the important interfaces are those between the liquid product and air and between the milk plasma and the fat globules contained therein. Studies of the surface tension (liquid/air) have been made to ascertain the relative effectiveness of the milk components as depressants to follow changes in surface-active components as a result of processing to follow the release of free fatty acids during lipolysis and to attempt to explain the foaming phenomenon so characteristic of milk. Interfacial tensions between milk fat and solutions of milk components have been measured in studies of the stabilization of fat globules in natural and processed milks. 

Data on the proportions of different fatty acids in plasma lipid esters (cholesteryl esters, phospholipids, free fatty acids, or triacylglycerol), erythrocyte membranes, or adipose tissue may provide a more objective and accurate path to evaluating dietary fatty acid composition (Arab, 2003 Baylin and Campos, 2006). The fatty acid composition in blood and body tissues reflects the fatty acid composition of the diet at different time points after ingestion. Short and medium-term changes in the composition of dietary fatty acid intake are reflected in plasma lipids and erythrocyte membranes, weeks and months after intake, respectively. The incorporation of fatty acids in adipose tissue reflects long-term changes in the diet (years) (Baylin and Campos, 2006 Katan et al., 1997 Ma et al., 1995 Zock et al, 1997). 

In addition to the studies of clinical biological changes in lipid profile levels in patients with major depression, the mechanism of lipid metabolism should be noted and discussed [133], In past studies, the main plasma lipid transport forms have been free fatty acids, triglycerides, and cholesteryl esters. 

Free fatty acids, derived primarily from adipocyte triglycerides, are transported as a physical complex with plasma albumin. Triglycerides and cholesteryl esters are transported in the core of plasma lipoproteins [134], Deliconstantinos observed the physical state of the Na+/K+-ATPase lipid microenvironment as it changed from a liquid-crystalline form to a gel phase [135], The studies concerning the albumin-cholesterol complex, its behavior, and its role in the structure of biomembranes provided important new clues as to the role of this fascinating molecule in normal and pathological states [135]. 

Fig. 3. Time-related changes in plasma glucose, non-esterified (or free) fatty acids (NEFA), insulin and glucagon concentrations in controls (— —) and normal-weight NIDDM patients (—O—) during insulin clamp. P<0.()1. (Source Golay et al., 1988.)...

Fever accelerates lipid metabolism. The serum concentrations of cholesterol, nonesterified fatty acids, and the other lipids may decrease initially, but within a few days the free fatty acid concentration may increase. Fever is often associated with a respiratory alkalosis caused by hyperventilation. This pH increase causes a reduction of the plasma phosphate concentration, with an increased excretion of phosphate and other electrolytes. Serum iron and zinc concentrations decline with accumulation of both elements in the liver. The copper concentration increases because of increased production of ceruloplasmin by the liver. Some representative changes in serum composition induced by fever are listed in Table 17-12. 

The four major plasma lipid fractions (phospholipids, cholesteryl esters, triglycerides, and free fatty acids) exhibited similar changes in response to the fish-oil diet. In the phospholipid fraction, the n-3 fatty acids increased from 0.4% to 34% of total fatty aicds in the fish oil diet. EPA increased from 0% to 19%, accounting for 55 percent of the total increase. Linoleic acid reciprocally decreased from 36% to 5% and total n-6 fatty acids from 48% to 12% of total fatty acids. In cholesteryl esters, n-3 fatty acids increased from 0.2% to 36%. An increase in EPA from 0% to 31% accounted for 86% of the increase, a much greater proportion than in phospholipids, whereas DHA only increased from 0% to 4%. The decline in n-6 fatty acids from 77% to 23% was largely accounted for by a decrease in linoleic acid from 73 % to 17%. Similar changes were seen in the triglycerides and free fatty acid fractions. 

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