Acute ethanol intoxication was found to promote the fatty infiltration of liver in rats. The liver lipid concentrations gradually rose to peak values, then slowly returned to normal. The duration of the fatty infiltration, and the peak liver lipid values obtained, were functions of the dose of ethanol administered. Female rats showed a more severe fatty infiltration than did males, under the same conditions. The prior administration of large quantities of choline reduced the intensity of the fatty infiltration provoked by the ethanol. In contrast to intact animals, neither adrenalectomized nor hypophysectomized rats showed an accumulation of liver lipids as a result of acute ethanol intoxication. Adrenalectomized rats maintained on cortisone, and adrenal demedullated rats, however, showed the same liver lipid response to ethanol as did intact rats. Rats chronically intoxicated for a period of 30 days exhibited hypertrophy of the adrenals. Acute intoxication produced by isopropanol administration also resulted in the accumulation of liver lipid. It is suggested that ethanol intoxication may cause the mobilization of fat from the depots to the liver, and that pituitary and adrenal cortical hormones are involved in the mechanism of this mobilization.
Male albino rats were exposed to cold or kept at room temperature for 1–24 hr. Plasmas and epididymal adipose tissues were analyzed for free fatty acid (FFA) concentrations and lipolytic activities of intact sections and homogenates, as well as release of FFA by adipose tissues, determined in vitro. Plasmas of rats exposed to cold had significantly higher FFA levels than did plasmas from controls, and intact epididymal adipose tissue sections from cold-exposed rats had higher FFA concentrations, released greater quantities of FFA, and manifested higher lipase activities in the presence of activated triglyceride substrate than did sections from control rats. Exposure to cold may increase FFA mobilization from adipose tissues as a result of enhanced lipolytic activity, due to lipase activation by catecholamines released from adrenals and sympathetic nerve endings. The enzyme activated did not possess several of the properties characteristic of lipoprotein lipase. Tissue homogenates did not manifest increased activity after cold exposure, possibly as a result of activation by the homogenization process itself.
Rats were fasted for several days, placed on diets high in carbohydrate, fat, or containing iodinated casein so as to produce hyperthyroidism, or were chronically injected with epinephrine. Lipoprotein lipase (LPL) activities of homogenates of the hearts of these animals were determined. Significant increases in LPL activity occurred in thyrotoxic animals, in rats receiving epinephrine injections chronically, or after prolonged fasting, while significant lowering of cardiac LPL activity was observed in rats on the high-carbohydrate or high-fat diets. Single doses of fat or single injections of epinephrine had no effect. Addition of epinephrine or of triiodothyronine to heart slices or homogenates in vitro caused no LPL increases. It is postulated that adaptive changes in cardiac LPL activity may occur in response to altered needs for utilization of fatty acids by the heart. Microsomal fractions of heart cells had the highest specific LPL activities, suggesting synthesis of the enzyme by these cellular components, or activity of the enzyme at the endoplasmic reticulum.
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