Marbles at Midnight

Narayan, Shyamala A.; Sen, Gautam

doi:10.2307/40135589

Cited by 1 publication

(3 citation statements)

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“…2) than in control rats fed a similar diet with 35% fat (3,4). There are several reasons for the discrepancy between our low levels of liver TG in controls fed a fat-free diet and higher levels reported previously (15)(16)(17)(18)(19). The first is that our diets did not include sucrose or glycerol which were thought to have a significant influence on the development of fatty liver (15,16).…”

Section: Discussioncontrasting

confidence: 64%

“…Fatty liver has been reported to aevelop in rats fed a (nonalcoholic) fat-free diet (15)(16)(17)(18)(19)(20). However, in the present study, the amount of liver TG observed in rats fed the control, fat-free (CF) diet was not only low, but it was less ( Fig.…”

Section: Discussioncontrasting

confidence: 52%

“…LARKIN AND G.A. RAO a shorter period of time (30 days) than in studies where fatty liver developed in rats fed no fat (10-30 weeks) (15)(16)(17). Therefore, the absence of fat in the AF diet could not have alone been responsible for the high level of fatty liver observed.…”

Section: Discussionmentioning

confidence: 99%

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Severe fatty liver in rats fed a fat‐free ethanol diet, and its prevention by small amounts of dietary arachidonate

Goheen

Larkin

Rao

1983

Lipids

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Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16:1/16:0 and 18:1/18:0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet.

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