Key result
Streptozotocin-induced insulin deficiency decreased mammary gland lipoprotein lipase activity and mRNA content in both pregnant and virgin rats, correlating linearly with plasma insulin levels.
Why the study?
Does streptozotocin-induced diabetes decrease mammary gland LPL activity and mRNA expression in pregnant and nonpregnant rats?
Does streptozotocin-induced diabetes decrease mammary gland LPL activity and mRNA expression in pregnant and nonpregnant rats?
Insulin deficiency impairs the expression of LPL in mammary glands at the mRNA level in both pregnant and nonpregnant rats.
Hypothesis-generating for insulin regulation of mammary LPL; leaves open relevance to hypertriglyceridemia in human diabetic pregnancy.
Diabetes mellitus is associated with a reduction of lipoprotein lipase (LPL) activity in adipose tissue and development of hypertriglyceridemia. To determine how a condition of severe insulin deficiency affects mammary gland LPL activity and mRNA expression during late pregnancy, streptozotocin (STZ) treated (40 mg/kg) and non-treated (control) virgin and 20 day pregnant rats were studied. In control rats, both LPL activity and mRNA were higher in pregnant than in virgin rats. When compared to control rats, STZ-treated rats, either pregnant or virgin, showed decreased LPL activity and mRNA content. Furthermore, mammary gland LPL activity was linearly correlated with mRNA content, and either variable was linearly correlated with plasma insulin levels. Thus, insulin deficiency impairs the expression of LPL in mammary glands, revealing the role of insulin as a modulator of the enzyme at the mRNA expression level.
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Blanco-Dolado et al. (2001) studied Streptozotocin-induced diabetes. Streptozotocin (STZ) vs. Non-treated (control) was evaluated on Mammary gland lipoprotein lipase (LPL) activity and mRNA expression. Streptozotocin-induced insulin deficiency decreased mammary gland lipoprotein lipase activity and mRNA content in both pregnant and virgin rats, correlating linearly with plasma insulin levels.
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