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Adipose tissue, accumulation

Several methods are available to evaluate a patient s actual body composition rather than total body mass. Skin-fold measurement may be of value in evaluating subcutaneous adiposity (adipose tissue accumulation) proper technique is required for reliable results. Other anthropomorphic measurements such as bioelectrical impedance, dual-energy x-ray absorptiometry, and total body water immersion are also available.These last techniques are often of value in research studies, but it is clinically impractical to use them routinely (Elberg et al., 2004). [Pg.247]

In some instances the result of this vicious cycle is bodybuilders who fail to ingest adequate calories during AAS protocols as a means of decreasing adipose tissue accumulation. Unless you are from another planet you realize this also limits muscular growth potential as well. [Pg.127]

Excess blood glucose will result in excess adipose tissue accumulation. [Pg.129]

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. [Pg.212]

Importantly, the mutant chicken exhibits lower levels of lutein and zeaxanthin in plasma and several other tissues in comparison with the control chicken, and that difference is already apparent in 1-day-old chickens and remains in 28-day-old chickens fed the same diet (Connor et al., 2007). In the WHAM chickens, the levels of lutein in the plasma, retina, skin, adipose tissue, liver and heart, respectively, have been found to be only 8%, 10%, 18%, 33%, 52%, and 60% of the corresponding levels in control chickens. Even though the diet in these chickens included three times more lutein than zeaxanthin and these ratios have been present in the plasma of both the control and WHAM chickens, there was a preferential accumulation of zeaxanthin over lutein in their retinas. [Pg.320]

Of the 16 POPs listed in the 1998 Aarhus Protocol [27], 11 are organochloride pesticides, which have now been banned in several countries. Most concerns regarding these products relate to their toxicity, with health effects to humans ranging from lung damage and neurological problems to death. Many organochloride pesticides are lipophilic, and they accumulate in the adipose tissues. [Pg.10]

The main depot for dioxin accumulation in mammals is the liver and adipose tissue. When dioxin is fed to rodents with fodder, about 10% of the dose comes in the liver. Should this toxic agent be applied on rat skin, 13% of the dose is absorbed in blood already in 5 hours, and 10% remains on skin surface. [Pg.87]

PCDD/PCDFs accumulate in human adipose tissue, and the level reflects the history of intake by the individual. Several factors have been shown to affect adipose tissue concentrations/body burdens, notably age, the number of children and period of breastfeeding, and dietary habits. Breast-milk represents the most useful matrix for evaluating time trends of dioxins and many other POPs. Several factors affect the PCDD/PCDFs content of human breast-milk, most notably the mothers age, the duration of breast-feeding and the fat content of the milk. Studies should therefore ideally... [Pg.405]

Although endrin is a stereoisomer of dieldrin, it does not persist in the body as dieldrin does. The half-life of endrin in humans and animals is 2-6 days (Ert and Sullivan 1992). Thus, endrin is unlikely to accumulate in adipose tissue. There are reports of ingestion of bread contaminated with endrin which caused sudden convulsions in three persons. In one person, the serum level was 0.053 ppm 30 minutes after convulsion and 0.038 ppm after 20 hours. In the other 2 cases, no endrin was detected in the blood at 8.5 or 19 hours after the convulsions occurred (Proctor et al. 1988). [Pg.87]


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