374 



CELLS, TISSUES, AND ORGANISMS 



TABLE V 

 Oxidation of Palmitate— 1— C'"* by Rat Diaphragm in vitro 



Ci^Oo 



(C.P.M./IOO mg. wet wt.) 



Specific Activity 

 (C.P.M.//xeq. CO2) 



2 hours 



4 hours 



2 hours 



4 hours 



1866 ± 255 (9) * 5039 ± 386 (9) 22 ± 5 (4) 58 ± 13 (3) 

 2331 ±92 (11) 5777 + 342(10) 38 ± 3 (4) 78 ± 7(3) 



2135 ± 108 (12) 4928 ± 242 (12) 35 ± 4 (4) 72 ± 3 (4) 



Normal 

 Hypophysecto- 



mized 

 Hypophysecto- 



mized + bovine 



growth 



hormone 



(2mg. /rat/day 



for 4 days ) 



Incubation 



medium: glucose-free low Ca++ Krebs Ringer phosphate containing bovine 



albumin-bound palmitate— 1— C^^* (0.3 /xeg./ml., 16,700 c.p.m./ml.) 



" Means ± S.E.; number of observations in parentheses. 



TABLE VI 

 FFA and Glycogen Content of Diaphragm 



FFA 

 jLteq./gm. tissue) 



Glycogen 



(mg. glucose/gm. 



tissue ) 



5.27 ±0.45 (5)* 

 5.11 ±0.18 (10) 



Normal 



Hypophysectomized 

 Hypophysectomized + 



bovine growth hormone 4.54 ± 0.14 (10) 



(2 mg. /rat/day for 4 days) 



1.71 ±0.30 (6) 

 1.28 ± 0.17 (6) 



1.47 ± 0.28 (6) 



" Mean ± S.E.; number of observations in parentheses. 



enous fatty acids is ruled out by the finding that the FFA content of 

 the growth-hormone-treated diaphragms was, if anything, lower than 

 that in the other groups ( Table VI ) . Similarly, under the conditions of 

 these experiments the glycogen content of the diaphragms was the 

 same in all groups. 



These findings are in harmony with the prior observations of 

 others that liver slices from hypophysectomized rats oxidize acetate to 

 carbon dioxide at the normal rate (Tompkins, Chaikoff, and Bennett, 

 1952; Baruch and Chaikoff, 1955), and that growth-hormone treatment 



