Relation of Age and Body Weight to the Frequency of Local Tissue Changes Suggestive of Malnutrition

1959 ◽  
Vol 7 (2) ◽  
pp. 166-174 ◽  
Author(s):  
ROBERT W. HILLMAN
Keyword(s):  
Body Weight ◽  
Local Tissue ◽  
Tissue Changes

Behavioural and physiological effects of prolactin in incubating ring doves

1985 ◽  
Vol 105 (2) ◽  
pp. 201-209 ◽  
Author(s):  
D. S. Janik ◽  
J. D. Buntin
Keyword(s):  
Body Weight ◽  
Dose Response ◽  
Body Weight Gain ◽  
Breeding Cycle ◽  
Target Tissue ◽  
Weight Changes ◽  
Incubation Behaviour ◽  
Tissue Changes ◽  
High Doses ◽  
Ring Doves

ABSTRACT The role of prolactin in the maintenance of incubation behaviour in ring doves was re-examined and the dose–response relationships for behavioural, target tissue and body weight changes induced by injections of prolactin were compared in doves tested during the incubation phase of the breeding cycle. Doves given injections of prolactin twice a day starting on day 4 of incubation, during a 10-day period of isolation from their mates and nests, showed a higher persistence of incubation behaviour than doves injected with saline vehicle. However, the prolactin treatment failed to maintain incubation behaviour to the same extent as that observed in non-isolated untreated breeding pairs. Liver and body weights were higher and testicular weights lower in birds treated with high doses of prolactin than in non-isolated birds which had been incubating for 14 days. Good dose-response relationships were established between body, liver, crop and testes weights and the dose of prolactin administered. However, only a weak dose–response relationship was observed between prolactin and the maintenance of incubation behaviour. Overall, females injected with prolactin displayed more quiet sitting behaviour, less body weight gain and more gonadal regression than males injected with prolactin. Males in untreated breeding pairs had higher liver weights and lower crop weights than females. It is concluded that prolactin plays a role in maintaining readiness to incubate in doves, but that other factors may also contribute to this response. Further, it appears that prolactin mediates several target tissue changes which are sex-specific during incubation. J. Endocr. (1985) 105, 201–209

Tissue Changes in the Development of Fatty Liver by Chronic Ingestion of Sucrose Associated with Obesity and Dyslipidemia in Rats

2018 ◽  
Vol 88 (3-4) ◽  
pp. 117-125
Author(s):  
Mildred Solano-Silva ◽  
Iván Bazán-de Santillana ◽  
Ida Soto-Rodríguez ◽  
Christian Bautista-Piña ◽  
Alfonso Alexander-Aguilera
Keyword(s):  
Body Weight ◽  
Fatty Liver ◽  
Caloric Intake ◽  
Abdominal Fat ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Tissue Changes ◽  
Food Constituent ◽  
Chronic Ingestion ◽  
Grade 3

Abstract. A diet high in sucrose, which is a common food constituent, induces obesity and non- alcoholic fatty liver (NFLD) caused by high caloric intake; however, it is important to investigate those sequential changes in the hepatic parenchyma related to sugar consumption which are associated to obesity and dyslipidemia. We analyzed the effects of long-term sucrose intake on fatty liver development, by the administration of 30% sucrose in drinking water in healthy Wistar rats during 30 weeks. Serum variables, body fat index, caloric intake and microscopic examination of liver tissue were monitored. In the first week, grade 1 steatosis was observed with ballooned hepatocytes, with a caloric intake of 125 ± 1.90 kcal / day / 100 g of body weight; together with a gain of 71% in abdominal fat with respect to the control group and dyslipidemia. During the 10 to 20 weeks period, steatosis grade 2 with noticeable inflammation (steatohepatitis), polymorphic cells and ballooned hepatocytes were evident. After 10 weeks, the caloric intake was 72.9 ± 5.99 kcal / day / 100 g of body weight with 199% of gain in abdominal fat in SUC groups with respect control group (p < 0.01) and moderate dyslipidemia; while after 20 weeks, the caloric intake was 61.6 ± 4.65 kcal / day / 100 g of body weight with 208% of gain in abdominal fat and also moderate dyslipidemia. After 30 weeks steatosis grade 3 with marked inflammation (steatohepatitis), periportal fibrosis, globose and fat-filled hepatocytes were observed, with a caloric intake of 52.3 ± 3.05 kcal / day / 100 g of body weight and 232% of gain in abdominal fat that was related to severe dyslipidemia. In conclusion, the sequential changes in the development of NAFLD were associated with the ingestion of sucrose and obesity since the first week of administration.

Tumor-Promoting, Initiating, and Hepatotoxic Effects of 3,4,3',4'-Tetrabromobiphenyl (34-TBB) in Rats

1988 ◽  
Vol 7 (5) ◽  
pp. 687-697 ◽  
Author(s):  
D. Dixon ◽  
S.D. Sleight ◽  
S.D. Aust ◽  
M.S. Rezabek
Keyword(s):  
Body Weight ◽  
Tumor Promotion ◽  
Ultrastructural Changes ◽  
Hepatic Enzyme ◽  
Sprague Dawley ◽  
Gamma Glutamyl Transpeptidase ◽  
Sprague Dawley Rats ◽  
Body Weights ◽  
Tissue Changes ◽  
Glutamyl Transpeptidase

Female, 180–200 g Sprague-Dawley rats were used to determine if 3,4,3',4'-tetrabromobi-phenyl (34-TBB) is a promoter or initiator in a two-stage hepatocarcinogenesis assay. To test for promotion, rats were partially hepatectomized (PH) 24 hr before initiation (day 1) with 10 mg of diethylnitrosamine (DEN)/kg body weight given intraperitoneally (IP). Thirty days later, promotion was with 34-TBB (0.1,1 or 5 mg/kg) or phenobarbital (PB) (500 mg/kg) in diets for 180 days. To test for initiation, rats were PH and were initiated on day 1 with 34-TBB (1, 5, or 10 mg/kg) orally or DEN (10 mg/kg) IP. On day 31, promotion was with 500 mg of PB/kg of diet for 180 days. Noninitiated and non-PH rats were used to assess the histological and ultrastructural tissue changes associated with administration of 34-TBB in the diet for 180 days. Tumor promotion-initiation were assessed by counting and measuring hepatic enzyme-altered foci (EAF) with gamma-glutamyl transpeptidase (GGT) activity. Congener 34-TBB acts as a promoter in experimental hepatocarcinogenesis in rats, as evidenced by increased numbers of GGT-positive EAF. Also, 34-TBB may have initiation potential, as suggested by increased numbers of EAF in rats initiated with 34-TBB and promoted by PB. Dietary administration of 34-TBB for 180 days is not severely toxic in rats, as evidenced by mild histological and ultrastructural changes and minimal alterations in organ and body weights. Congener 34-TBB does not accumulate in liver and adipose tissue of rats.

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