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STUDIES ON LIPID AND CARBOHYDRATE METABOLISM IN THE RAT
Author(s) -
Goldrick RB,
Hoffmann Choo C,
Reardon M
Publication year - 1972
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.1972.24
Subject(s) - adipose tissue , lipogenesis , medicine , endocrinology , glyceride , carbohydrate metabolism , glycerol , fatty acid synthesis , fatty acid , lipid metabolism , triglyceride , biology , adipocyte , white adipose tissue , carbohydrate , metabolism , chemistry , biochemistry , cholesterol
Summary Serial studies of carbohydrate metabolism in vitro in epididymal adipose tissue and hemidiaphragms were carried out at several stages of growth in Wistar rats maintained on one of four feeding programmes— ad libitum feeding with chow with or without the addition of glucose to the drinking water or meal feeding with restricted or unrestricted quantities of chow. Supplementation of the diet with glucose accelerated the rate of fat deposition and the incorporation of glucose‐U‐ 14 C into glyceride‐glycerol and glyceride‐fatty acids in adipose tissue. Meal feeding did not stimulate glucose lipogenesis, but prevented the decline in fatty acid synthesis with ageing which occurred in epididymal adipose tissue of mature ad libitum fed rats. Adipose tissue in vitro converted amounts of glucose into glyceride‐glycerol that were calculated to be sufficient to esterify all the fatty acids which accumulated during fat deposition in vivo as judged from adipocyte enlargement with age. On the other hand, only in young glucose‐supplemented rats did adipose tissue utilize sufficient glucose for fatty acid synthesis in vitro to account for the deposition of triglyceride‐fatty acids in adipose tissue in vivo . Although the rate of glyceride‐ glycerol synthesis from glucose in adipose tissue was affected by the method of feeding and the age of the rat, it was also increased in proportion to the amount of lipid in the fat cell. There was no indication that adipose tissue became resistant to insulin in vitro as its fat cells enlarged. However, there was a progressive decrease in the responsiveness of adipose tissue to insulin in ad libitum chow‐fed rats between the ages of 10 and 34 weeks. This effect of ageing was prevented by meal feeding. There was no relationship between the effects of insulin on the concentrations of glycogen and the incorporation of glucose‐U‐ 14 C into glycogen in hemidiaphragms and the responses to insulin observed in adipose tissue. Furthermore, the responsiveness of hemidiaphragms and adipose tissue to insulin bore no relationship to the hypoglycaemic effects of exogenous insulin in vivo .