Adipose tissue alcohols

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. 

Ethanol is membrane-permeable and is quickly resorbed. The maximum blood level is already reached within 60-90 min after drinking. The resorption rate depends on various conditions, however. An empty stomach, a warm drink (e.g., mulled wine), and the presence of sugar and carbonic acid (e.g., in champagne) promote ethanol resorption, whereas a heavy meal reduces it. Ethanol is rapidly distributed throughout the body. A large amount is taken up by the muscles and brain, but comparatively little by adipose tissue and bones. Roughly 70% of the body is accessible to alcohol. Complete resorption of the ethanol contained in one bottle of beer (16 g) by a person weighing 70 kg (distribution in 70 kg 70/100 = 49 kg) leads to a blood alcohol level of 0.33 per thousand (7.2 mM). The lethal concentration of alcohol is approximately 3.5 per thousand (76 mM). 

Methoxyethanol is rapidly absorbed through the skin and lungs into the blood. Its water solubility favors distribution to all body tissues except adipose tissue. Metabolism occurs via two pathways. Methoxyethanol is a substrate for alcohol dehydrogenase, and the resultant methoxyacetaldehyde is metabolized to methoxyacetic acid by aldehyde dehydrogenase. In rats, pretreatment with phenobarbitol decreased formation of methoxyacetaldehyde but accelerated formation of methoxyacetate in liver cytosolic fractions. A minor pathway involves demethylation by undefined enzymes to ethylene glycol and CO2. 

Alcoholism affects about 10% of the drinking population and alcohol (ethanol) abuse has been implicated in at least 20% of admissions to general hospitals. This chronic disease exhibits high mortality due to a wide variety of factors. Ethanol produces effects in virtually every organ system. The biochemical effects of ethanol are due to increased production of NADH that decreases the [NAD ]/[NADH] ratio in the cytoplasm of liver cells at least tenfold from the normal value of about 1000. Increased production of lactate and inhibition of gluconeo-genesis (Chapter 15) result. The hyperuricemia associated with ethanol consumption has been attributed to accelerated turnover of adenine nucleotides and their catabolism to uric acid (Chapter 27). Alcohol increases hepatic fatty acid and triacylglycerol synthesis and mobilization of fat from adipose tissue, which can lead to fatty liver, hepatitis, and cirrhosis. These effects are complicated by a deficiency of B vitamins and protein. 

Because of the long half-life of FAEEs in adipose tissue, it was suggested that FAEE in adipose tissue could be a laboratory marker for previous alcohol intake, particularly for forensic applications where adipose tissue samples can be readily obtained. In postmortem samples from four chronically intoxicated subjects whose blood ethanol levels were zero, it was demonstrated that prior ethanol ingestion could be established by the presence of FAEEs in the adipose tissue (Laposata, 1989). In this report, a separate series of experiments determined the half-life of EAEEs to be 16.6 h in the adipose tissue of rabbits that received 10% ethanol in their drinking water for 10 mo. 

DePergola G, Kjellstrom C, Holm C. Conradi N, Pettersson P, Bjomtorp P. The metabolism of ethyl esters of fatty acids in adipose tissue of rats chronically exposed to ethanol. Alcoholism Clin Exp Res 1991 15 184-189. 

Potassium decanoate, 359 Potassium permanganate, 274 Potassium soaps, 328,359,361 Potato lipoxygenase, 458 Poultry adipose tissue, 556 Pre-pressing, 186 Premier jus, 98,124 see also Beef tallow Primary alcohol esters, 143 Primary alcohols, 146 Prins reaction, 476 Pristane, occurrence, 138,148 Pristanic acid, 16 Process control, 217 Procetofen, 540 Production control, 217 Production of oils and fats fish oils, 130 butter, 219... 

Additionally, it has been suggested that non-alcoholic fatty liver disease (NAFLD) should be added to the classical components of the metabolic syndrome given its close association to IR as a central feature (Marchesini et al., 2001). NAFLD is defined as a broad spectrum of liver pathology, ranging from fatty liver (hepatic steatosis) without inflammation, to severe inflammatory activity with significant fibrosis or even curhosis (Marchesini et al., 2001). The release of inflammatory mediators, including C-ieactive protein (CRP), tumour necrosis factor (TNF)-a, interleukin (IL)-6 and IL-8, from the liver and adipose tissue are also characteristic of NAIT.D (Hijona et al., 2010). 

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