Fatty acid synthesis in liver and adipose tissue of normal and genetically obese (ob/ob) mice during the 24-hour cycle

Abstract

1. The synthesis of long-chain fatty acids de novo was measured in the liver and in regions of adipose tissue in intact normal and genetically obses mice throughout the daily 24h cycle. 2. The total rate of synthesis, as measured by the rate of incorporation of 3H from 3H2O into fatty acid, was highest during the dark period, in liver and adipose tissue of lean or obese mice. 3. The rate of incorporation of 14C from [U-14C]glucose into fatty acid was also followed (in the same mice). The 14C/3H ratios were higher by a factor of 5-20 in parametrial and scapular fat than that in liver. This difference was less marked during the dark period (of maximum fatty acid synthesis). 4. In normal mice, the total rate of fatty acid synthesis in the liver was about twofold greater than that in all adipose tissue regions combined. 5. In obese mice, the rate of fatty acid synthesis was more rapid than in lean mice, in both liver and adipose tissue. Most of the extra lipogenesis occurred in adipose tissue. The extra hepatic fatty acids synthesized in obese mice were located in triglyceride rather than phospholipid. 6. In adipose tissue of normal mice, the rate of fatty acid synthesis was most rapid in the intra-abdominal areas and in brown fat. In obese mice, all regions exhibited rapid rates of fatty acid synthesis. 7. These results shed light on the relative significance of liver and adipose tissue (i.e. the adipose 'organ') in fatty acid synthesis in mice, on the mino importance of glucose in hepatic lipogenesis, and on the alterations in the rate of fatty acid synthesis in genetically obese mice.

Effects of hormones on the rate of the triacylglycerol/fatty acid substrate cycle in adipocytes and epididymal fat pads

“…The degree of quenching in each sample was obtained by use of internal standards; this enabled radioactivity to be calculated in dpm. It was assumed, for the calculation of triacylglycerol and fatty acid synthesis, that the specific activity of water in the adipocyte was identical to that in the incubation flask and that each glycerol incorporated into triacylglycerol con- Table 1 Effects of some hormones, B-blockers, a-blockers and adenosine deaminase on rates of release of glycerol, fatty acids and triacylglycerol/fatty acid cycling in isolated fat cells [12,13]. Hence the rate of triacylglycerol synthesis from glycerol phosphate in vivo can be calculated; at steady-state, this rate will be equal to the rate hydrolysis of triacylglycerol (i.e., the rate of triacylglycerol/fatty acid cycle) except for the rate of de novo fatty acid synthesis within the adipose tissue cell.…”

Absence of Sterol Regulatory Element-binding Protein-1 (SREBP-1) Ameliorates Fatty Livers but Not Obesity or Insulin Resistance in Lep/Lep Mice

“…5). It has been shown by enzymatic assay experiments that lipogenesis in Lep ob/ob mouse adipose tissue is elevated in the early dynamic phase until 7-8 weeks of age and thereafter suppressed in the late static phase when insulin resistance becomes evident (32,33). In contrast, hepatic lipogenesis in Lep ob/ob mice remains consistently higher than in wild-type animals.…”

Fatty acid synthesis in liver and adipose tissue

“…The role of glucose as a lipogenic substrate in the liver of mice was questioned by Hems et al (1975); these authors calculated that glucose only contributed…”

“…There are significant diurnal rhythms in fatty acid biosynthesis in both liver and adipose tissue of laboratory rodents with a marked increase in ad lib.-fed animals during the dark period (Hems et al 1975;Cawthorne & Cornish, 1979;Cornish & Cawthome, 1978;Kimura et al 1970;Godbole & York, 1978). Rodents ingest most of their food during this period and so the variations in fatty acid synthesis may be due partly to alterations in the pattern of circulating substrates and hormones in response to feeding.…”