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THE EFFECT OF MATERNAL MALNUTRITION ON THE PROGENY IN THE RAT. STUDIES IN VITRO OF LIPOGENESIS IN LIVER AND IN VIVO OF LIPOGENESIS IN LIVER AND ADIPOSE TISSUE FOLLOWING FRUCTOSE FEEDING
Author(s) -
McLeod Katrine I,
Neste PJ,
Goldrick RB
Publication year - 1973
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1973.78
Subject(s) - lipogenesis , endocrinology , medicine , fructose , biology , adipose tissue , insulin , in vivo , offspring , biochemistry , pregnancy , genetics , microbiology and biotechnology
Summary When female rats are fed a protein‐deficient diet (6% protein) for 2 weeks prior to and during gestation, the offspring (test progeny) exhibit deficits in body weight, in liver weight and in the number of hepatocytes, which cannot be corrected by adequate post‐natal feeding. The incorporation in vitro of [l‐ 14 C] acetate and [U‐ 14 C] glucose into the various liver lipid classes was studied in such progeny at the age of 10 weeks either after chow‐feeding or following 2 weeks of fructose supplementation of the diet (20% w/v in the drinking water). Fructose feeding increased the incorporation of both glucose and acetate into total liver lipids. When the results were expressed per unit weight of tissue no differences were found between chow‐fed, control and test progeny or fructose‐fed, control and test progeny. Lipogenesis in liver tissue was significantly stimulated, by the addition of insulin to the incubation medium, to a similar extent in control and test progeny. This is in contrast to our previous finding that adipocytes of test progeny were less responsive to insulin in vitro than those from control progeny following fructose feeding. The administration in vivo of [U‐ 14 C]glucose also demonstrated that lipogenesis in the livers of fructose‐fed rats was increased to a similar degree in control and test progeny. By contrast, lipogenesis in epididymal fat adipocytes was significantly less in the test than in the control progeny, following fructose feeding. We conclude that intrauterine deprivation of protein leads to a subsequent inability of adipocytes to respond normally to the lipogenic stimulus of fructose feeding. On the other hand, hepatocytes respond normally but, since the livers of test progeny are smaller, their total lipogenic capacity is diminished. Despite these findings, fructose‐induced hypertriglyceridaemia was similar in test and control progeny.