Why the study?
Does tumor growth alter lipid metabolism and lipoprotein lipase activity in rats?
Does tumor growth alter lipid metabolism and lipoprotein lipase activity in rats?
Tumor growth in rats induces hypertriglyceridemia, potentially due to a deficiency in adipose tissue lipoprotein lipase activity mediated by reduced insulin levels.
Tumor-induced LPL suppression may drive hyperlipidemia in malignancy; leaves open human relevance and requires clinical validation.
The effects of tumor growth on lipid metabolism were investigated by evaluating serum lipids, lipoprotein lipase activity (LPLA), the lipogenic enzymes, urinary catecholamines along with serum insulin and glucagon levels. We injected 1.5 X 10(6) cells of rat mammary tumor, AC33, and killed the rats on the 18th day. Serum triglycerides and free fatty acids of the tumor-bearing (TB) rats increased 4 and 5 times, respectively, more than the control (C) rats. Total liver lipids were not significantly different between the two groups. Tumor growth produced a 70% decrease in total epididymal fat pad LPLA; there were no changes in soleus muscle LPLA. Serum insulin levels of the TB rats were 49% less than the C rats. The TB rats had significantly lighter epididymal fat pads and lower activities of adipose fatty acid synthetase and citrate cleavage enzyme. Urinary catecholamines of the TB rats were reduced over 30% compared with the C rats. These results show that the hypertriglyceridemia of the TB rats may be due, in part, to a deficiency of adipose tissue LPLA. The data also suggest that the effects of the tumor on lipid metabolism may be mediated through insulin.
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Lanza‐Jacoby et al. (1982) studied this question.
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