scholarly journals Effects of adrenalectomy before weaning and short- or long-term glucocorticoid administration on the genetically obese Zucker rat

1986 ◽  
Vol 238 (2) ◽  
pp. 459-463 ◽  
Author(s):  
J M Fletcher

Intact obese rats were hyperinsulinaemic, had higher rates of whole-body fatty acid synthesis, higher activities of hepatic acetyl-CoA carboxylase and tyrosine aminotransferase and a higher hepatic glycogen concentration than intact lean animals. Adrenalectomy abolished all these factors of the obese phenotype. Treatment of adrenalectomized rats with corticosterone for 24 h increased the rate of whole-body fatty acid synthesis to the same extent in both phenotypes, but caused a larger increase in glycogen concentration, tyrosine aminotransferase activity and plasma insulin concentration in obese rats.

1974 ◽  
Vol 142 (3) ◽  
pp. 611-618 ◽  
Author(s):  
D. Michael W. Salmon ◽  
Neil L. Bowen ◽  
Douglas A. Hems

1. Fatty acid synthesis de novo was measured in the perfused liver of fed mice. 2. The total rate, measured by the incorporation into fatty acid of3H from3H2O (1–7μmol of fatty acid/h per g of fresh liver), resembled the rate found in the liver of intact mice. 3. Perfusions with l-[U-14C]lactic acid and [U-14C]glucose showed that circulating glucose at concentrations less than about 17mm was not a major carbon source for newly synthesized fatty acid, whereas lactate (10mm) markedly stimulated fatty acid synthesis, and contributed extensive carbon to lipogenesis. 4. The identification of 50% of the carbon converted into newly synthesized fatty acid lends further credibility to the use of3H2O to measure hepatic fatty acid synthesis. 5. The total rate of fatty acid synthesis, and the contribution of glucose carbon to lipogenesis, were directly proportional to the initial hepatic glycogen concentration. 6. The proportion of total newly synthesized lipid that was released into the perfusion medium was 12–16%. 7. The major products of lipogenesis were saturated fatty acids in triglyceride and phospholipid. 8. The rate of cholesterol synthesis, also measured with3H2O, expressed as acetyl residues consumed, was about one-fourth of the basal rate of fatty acid synthesis. 9. These results are discussed in terms of the carbon sources of hepatic newly synthesized fatty acids, and the effect of glucose, glycogen and lactate in stimulating lipogenesis, independently of their role as precursors.


1983 ◽  
Vol 3 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock ◽  
Paul Trayhurn

Fatty-acid synthesis has been measured in vivo with 3H2O in cafeteria-fed rats exhibiting diet-induced thermogenesis. Synthesis was decreased in brown adipose tissue, the liver, white adipose tissue, and the carcass of the cafeteria-fed animals compared to rats fed the normal stock diet. Whole-body synthesis was also decreased in the cafeteria-fed group. Diet-induced thermogenesis, in contrast to cold-induced non-shivering thermogenesis does not lead to increased fatty-acid synthesis and this is presumably due to the inhibitory effects on lipogenesis of the high dietary fat intake characteristic of cafeteria diets. The results also indicate that the energy cost of body fat deposition in cafeteria-fed rats is lower than in animals fed a low-fat/high-carbohydrate stock diet.


1976 ◽  
Vol 160 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D A Hems ◽  
G Y Ma

1. Fatty acid synthesis, measured in the perfused liver of genetically obese (ob/ob) mice with 3H2O or [14C]actate, did not show the inhibition by [8-arginine]vasopressin (antidiuretic hormone) that is observed in livers from normal mice. 2. Hepatic glycogen breakdown in obese mice was stimuulated by vasopressin, but not as extensively as in lean mice. 3. If obese mice received a restricted amount of food, then fatty acid synthesis still did not respond to vasopressin, but glycogen breakdown was fully stimulated. 4. Cholesterol synthesis was not inhibited by vasopressin in livers from obese mice. 5. Vasopressin inhibited fatty acid synthesis in intact lean mice, but not in obese animals. 6. These results suggest that genetic obesity could be due to an inborn error within the mechanisms (other than adenylate cyclase) which mediate responses to extracellular effectors.


Lipids ◽  
1980 ◽  
Vol 15 (12) ◽  
pp. 993-998 ◽  
Author(s):  
R. Kannan ◽  
D. B. Learn ◽  
N. Baker ◽  
J. Elovson

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Matthew Douglas Bruss ◽  
Cyrus F Khambatta ◽  
Ishita Aggarwal ◽  
Marc K Hellerstein

1989 ◽  
Vol 257 (2) ◽  
pp. R326-R336 ◽  
Author(s):  
R. B. Harris ◽  
R. C. Bruch ◽  
R. J. Martin

Involvement of a humoral agent in regulation of energy balance has been demonstrated by parabiosis experiments. Overfed obese rats produce a blood-borne factor that inhibits adipose fatty acid synthesis in their partners, resulting in loss of body fat without significant inhibition of food intake. An in vitro bioassay was developed to test small serum samples for antilipogenic activity. Epididymal adipocytes from ad libitum-fed rats were preincubated for 12 h with 2% serum. Basal adipocyte fatty acid synthesis, measured in a subsequent serum-free incubation, was inhibited by obese serum. Insulin response was not changed. Characterization studies indicated that the factor was probably a protein, larger than 30 kDa, but not a protease or a low-density lipoprotein and was not associated with serum albumin. Physiological experiments demonstrated that the agent was produced when body weight was raised substantially above "set-point." Inhibitory activity was neither species specific nor pituitary dependent. Structure, origin, and physiological significance of the factor are unknown, but it may be involved in the control of body fat content.


Sign in / Sign up

Export Citation Format

Share Document