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 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Young adult male Sprague-Dawley rats treated with a LD95 dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibited a progressive reduction in feed intake and body weight until death occurred 15 to 32 days post-treatment. The time course and magnitude of weight loss and lethality of pair-fed control rats were essentially identical to that of TCDD-treated rats with each pair-fed control animal dying within 3 days of its TCDD-treated partner. Body composition analysis of the dead animals revealed that the total amounts of protein, fat, water, and ash in the carcasses of TCDD-treated and pair-fed control rats were each reduced to a similar extent. The temporal pattern of daily feed intake in TCDD-treated and pair-fed control rats (3 meals/day) or (1 meal/day) did not influence the results. Studies conducted at LD25-62 doses of TCDD in male Sprague-Dawley rats of different ages--weanling (90 g), young adult (275 g), and mature (450 g)--showed that the severity of the wasting syndrome in all age groups was greatest for animals that died. Also, young adult rats treated with a LD25 dose of TCDD that died displayed the same degree of hypophagia and weight loss prior to death as rats administered a LD95 dose. Histopathology of the liver and gastrointestinal tract was compared in TCDD-treated (LD95 dose) and pair-fed control rats killed 1 day before they otherwise would have died. Hepatocytes of TCDD-treated rats were enlarged relative to those of pair-fed control rats and contained nuclei that varied in size and number. Pair-fed control rats exhibited atrophy of the liver cords due to a decrease in the cytoplasmic volume of their hepatocytes. The stomach and small intestine of TCDD-treated rats were histologically similar to those of ad libitum-fed controls. In contrast, the glandular mucosa of the stomach of pair-fed control rats was ulcerated and the intestinal mucosa was atrophied. Stomach ulcers were the source of clotted blood found throughout the gastrointestinal tract of pair-fed control rats but not that of TCDD-treated animals. These findings demonstrate that hypophagia-induced weight loss is one of perhaps several responses that contribute to the death of TCDD-treated rats. That other responses are also involved is suggested by differences between pair-fed control and TCDD-treated rats in the weight and histopathology of certain organs. In addition, gastrointestinal blood loss contributes to the death of pair-fed control rats but not TCDD-treated animals.
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PMID:Relationship of the wasting syndrome to lethality in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin. 394 51

Forty crossbred beef steers (243 +/- 2 kg of BW) with ruminal and abomasal infusion catheters were used to test 2 hypotheses: 1) visceral mass is responsive to energy input and site of carbohydrate (CHO) infusion and 2) rate and site of adipose accretion are dependent on site of CHO infusion and complexity. Treatments included a pelleted, forage-based, basal diet fed at 161 (LI) or 214 (HI) kcal of ME/(kg of BW(0.75) x d), LI plus ruminal (R-SH) or abomasal (A-SH) infusion of a partial starch hydrolysate (SH), and LI plus abomasal infusion of glucose (A-G). The basal diet was fed in 12 equal portions daily at 2-h intervals, with starch and glucose infused over a 22-h period at rates of 12.6 and 14.4 g/(kg of BW(0.75) x d). After 35 d of infusion, steers were slaughtered; and visceral organ and adipose mass, subcutaneous adipose thickness over the 5th and 12th rib, and LM intramuscular fat concentration were determined. Total intake energy (IE) increased (P = 0.0001) with ME intake. Dietary IE was similar between LI and CHO treatments, but total IE increased (P < 0.001) with CHO infusion. Greater dietary ME intake and CHO infusion increased or tended (P < or = 0.09) to increase final BW and HCW. As a percentage of empty BW, total stomach complex, rumen, omasum, liver, pancreas, and kidney weights were greater (P < or = 0.05) for HI vs. LI. Stomach complex, rumen, pancreas, and kidney weights as a percentage of empty BW were greater (P < or = 0.05) for R-SH vs. A-SH. Compared with ASH, A-G increased (P < or = 0.02) total and mucosal weights from the 10-cm sections of the ileum. Increases in rumen mass were associated with no change or an increase in rumen total and mucosal DNA concentrations. Greater dietary ME tended (P = 0.06) to increase subcutaneous fat thickness at the 5th rib but did not affect alimentary adipose accretion on an empty BW basis. Omental and total alimentary adipose weights were increased (P < or = 0.04) by A-G compared with A-SH. Although SH infusion did not alter adiposity, there was a consistent numerical pattern in total alimentary and subcutaneous fat depots with CHO infusion (A-G > ASH > R-SH). Our findings demonstrate that increasing ruminal CHO supply results in a disproportionate increase in rumen mass, whereas increasing small intestinal CHO supply does not alter gastrointestinal organ mass. Small intestinal energy in the form of glucose resulted in greater adipose accretion, particularly the omental depot.
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PMID:Influence of ruminal and postruminal carbohydrate infusion on visceral organ mass and adipose tissue accretion in growing beef steers. 1743 Oct 50