THE UTILIZATION OF ACETATE BY LIVER AND ADIPOSE TISSUE OF GROWTH HORMONE TREATED RATS OF DIFFERENT AGES

1957 ◽  
Vol 35 (9) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.

1957 ◽  
Vol 35 (1) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.


1957 ◽  
Vol 189 (3) ◽  
pp. 433-436 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The utilization of acetate and octanoate by adipose tissue from rats 1 and 2 weeks postadrenalectomy has been studied. In addition, acetate incorporation into liver fatty acids and ketogenesis by liver slices from 2-week postoperative animals has been measured. Adrenalectomy resulted in a progressive loss of fat from adipose tissue. At 1-week postadrenalectomy the incorporation of acetate into fatty acids by adipose tissue did not differ from the control preparations but was much increased 2 weeks after adrenalectomy. At this time there was no increase in utilization of added octanoic acid by the adipose tissue and neither at 1 nor at 2 weeks was the production of CO2 from either acetate or octanoic significantly different from normal. Liver slices from 2-week adrenalectomized animals had a markedly defective ability to incorporate acetate into liver fatty acids similar to that previously noted in 1-week animals. However, liver slice preparation from 2-week adrenalectomized rats showed increased ketone body formation, indicating increased fatty acid utilization by the liver. It is suggested that there is a gradual mobilization of fat from the depots to the liver in the adrenalectomized rat with increased utilization of fat by the liver.


1961 ◽  
Vol 39 (6) ◽  
pp. 1061-1065 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The in vitro utilization of non-esterified fatty acids by various tissues and the in vitro production of non-esterified fatty acids by adipose tissue have been compared in normal and adrenalectomized rats. It was found that the production of NEFA by adipose tissue was similar in both groups of animals but that the in vitro utilization of NEFA and production of carbon dioxide by heart, diaphragm, kidney, and liver tissue was greater in the adrenalectomized animal. These findings together with the depletion of fat content of the depots are interpreted as indicating that in the adrenalectomized state there is increased peripheral utilization of fatty acids.


1958 ◽  
Vol 36 (1) ◽  
pp. 237-241
Author(s):  
William F. Perry

The in vitro incorporation of 1-C14 and 2-C14 acetate into fatty acids and carbon dioxide by liver and adipose tissue was studied in rats fasted at 5 °C. for 24 hours. Compared with fed rats at room temperature, there was a marked decrease in the incorporation of the acetate carbons into fatty acids and carbon dioxide by liver tissue. A pronounced decrease in acetate incorporation into fatty acid was also noted with adipose tissue from these same animals, but only a slight decrease in incorporation into carbon dioxide. Addition of glucose to the incubation medium caused increases in fatty acid formation by liver and adipose tissue from both normal and fasted animals, but glucose supplementation, while increasing the incorporation of acetate into carbon dioxide by liver tissue from cold fasted rats, did not affect carbon dioxide production by liver tissue from normal animals. Incorporation of acetate into carbon dioxide by adipose tissue was unaffected by glucose supplementation with tissue from both normal and cold fasted rats.


1958 ◽  
Vol 36 (2) ◽  
pp. 237-241 ◽  
Author(s):  
William F. Perry

The in vitro incorporation of 1-C14 and 2-C14 acetate into fatty acids and carbon dioxide by liver and adipose tissue was studied in rats fasted at 5 °C. for 24 hours. Compared with fed rats at room temperature, there was a marked decrease in the incorporation of the acetate carbons into fatty acids and carbon dioxide by liver tissue. A pronounced decrease in acetate incorporation into fatty acid was also noted with adipose tissue from these same animals, but only a slight decrease in incorporation into carbon dioxide. Addition of glucose to the incubation medium caused increases in fatty acid formation by liver and adipose tissue from both normal and fasted animals, but glucose supplementation, while increasing the incorporation of acetate into carbon dioxide by liver tissue from cold fasted rats, did not affect carbon dioxide production by liver tissue from normal animals. Incorporation of acetate into carbon dioxide by adipose tissue was unaffected by glucose supplementation with tissue from both normal and cold fasted rats.


1995 ◽  
Vol 20 (6) ◽  
pp. 477-484 ◽  
Author(s):  
Akihiro Kuroshima ◽  
Tomie Ohno ◽  
Mitsuru Moriya ◽  
Hiroshi Ohinata ◽  
Takehiro Yahata ◽  
...  

2011 ◽  
Vol 100 (2-3) ◽  
pp. 177-183 ◽  
Author(s):  
M. Szczesna ◽  
D.A. Zieba ◽  
B. Klocek-Gorka ◽  
D.H. Keisler

1977 ◽  
Vol 232 (6) ◽  
pp. E580
Author(s):  
M P Zabinski ◽  
P Biancani

Longitudinal force-length relationship of the rat esophagus was studied in vitro in three age groups: 1 mo, 3 mo, and 12 mo. The length of maximum force development (MFD) occurs at 1.4-1.5 times the in vivo length for all age groups. The active force developed at MFD increases markedly with age. The difference in the active forces in the 3-mo and 12-mo age groups is due to differences in cross section because the active stress of the esophagus in the longitudinal direction is approximately equal for the two age groups. The active stress in the 1-mo-old rats is lower than in the 3-mo-old rats, suggesting an increased contractility of the esophagus with age in this period of development.


2000 ◽  
Vol 278 (3) ◽  
pp. R663-R668 ◽  
Author(s):  
Hershel Raff ◽  
Eric D. Bruder ◽  
Barbara M. Jankowski ◽  
Theodore L. Goodfriend

Neonatal hypoxia increases aldosterone production and plasma lipids. Because fatty acids can inhibit aldosterone synthesis, we hypothesized that increases in plasma lipids restrain aldosteronogenesis in the hypoxic neonate. We exposed rats to 7 days of hypoxia from birth to 7 days of age (suckling) or from 28 to 35 days of age (weaned at day 21). Plasma was analyzed for lipid content, and steroidogenesis was studied in dispersed whole adrenal glands untreated and treated to wash away lipids. Hypoxia increased plasma cholesterol, triglycerides, and nonesterified fatty acids in the suckling neonatal rat only. Washing away lipids increased aldosterone production in cells from 7-day-old rats exposed to hypoxia, but not in cells from normoxic 7-day-old rats or from normoxic or hypoxic 35-day-old rats. Addition of oleic or linolenic acid to washed cells inhibited both aldosterone and corticosterone production, although cells from hypoxic 7-day-old rats were less sensitive. We conclude that hypoxia induces hyperlipidemia in the suckling neonate and that elevated nonesterified fatty acids inhibit aldosteronogenesis.


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