Abstract
Combined lipase deficiency (cld) is a genetic abnormality in mice resulting in the production of enzymatically inactive lipoprotein lipase (LPL). After suckling, these mice have markedly elevated levels of circulating triglyceride. An alteration of LPL gene expression in cld mice may affect the amount and/or the distribution of LPL mRNA in different cell types. Therefore, we performed in situ hybridization for LPL mRNA in tissues from normal and cld pups and adult mice using an antisense 35S-labeled cRNA probe. LPL mRNA had the same pattern of distribution in both cld and normal newborn mice; the probe hybridized strongly to pyramidal neurons of the hippocampus, heart myocytes, and hepatocytes. Despite the lack of noticeable fat stores, LPL mRNA was found in the dermal layer of the skin of cld mice and normal littermates. In adult mice, the cRNA probe for LPL hybridized to the hippocampus, to the heart, and to localized areas of the kidney. We conclude that despite great variation in plasma triglyceride levels, LPL gene is similarly expressed in animals with or without LPL activity.
Highlights
Combined lipase deficiency is a genetic abnormality in mice resulting in the production of enzymatically inactive lipoprotein lipase (LPL)
I) Synthesis of LPL protein is the same in adipocytes isolated from fed or fasted animals [9]. 2) LPL activity increases with feeding, but no change in LPL protein or LPL mRNA was found in human adipose biopsies [10]
We describe thedistribution of LPL mRNA in tissues from normalneonatal, cld, andadult mice
Summary
Combined lipase deficiency (cld) is a genetic abnormality in mice resulting in the production of enzymatically inactive lipoprotein lipase (LPL). After suckling, these mice have markedly elevated levels of circulating triglyceride. We performed in situ hybridization for LPL mRNA in tissues from normal and cld pups and adult mice using an antisense 35S-labeledcRNA probe. Lipoprotein lipase mRNA in neonatal and adult mouse tissues: comparison of normal and combined lipase deficiency (cld) mice assessed by in situ hybridization. Plasma insulin levels increase in the postprandial period; the effects of insulin and feeding on LPL activity and mRNA differ. Perhaps triglycerides or fatty acids, may be involved in the response to feeding and may counter the stimulating effects of insulin on adipose LPL gene expression [14]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.