Combined lipase deficiency (cld) is a recessive mutation in mice that causes a severe lack of lipoprotein lipase (LPL) and hepatic lipase (HL) activities, hyperlipemia, and death within 3 days after birth. Earlier studies showed that inactive LPL and HL were synthesized by cld/cld tissues and that LPL synthesized by cld/cld brown adipocytes was retained in their ER. We report here a study of HL in liver, adrenal, and plasma of normal newborn and cld/cld mice.
View Article and Find Full Text PDFObjective: To measure the timing, frequency, and severity of hormone-related symptoms in oral contraceptive (OC) users, specifically to compare active-pill with hormone-free intervals.
Methods: Using daily diaries, women recorded pelvic pain, bleeding, headaches, analgesic use, nausea or vomiting, bloating or swelling, and breast tenderness during active-pill intervals and hormone-free intervals. Participants either had no prior OC use, had taken OCs and were restarting, or had been taking OCs continuously for 12 months or longer.
Lipoprotein lipase (LPL) and hepatic lipase (HL), which act on plasma lipoproteins, belong to the same gene family as pancreatic lipase. LPL is synthesized in heart, muscle and adipose tissue, while HL is synthesized primarily in liver. LPL is also synthesized in liver of newborn rodents.
View Article and Find Full Text PDFBrown adipocytes cultured from newborn combined-lipase-deficient (cld/cld) mice and castanospermine (CST)-treated 3T3-L1 adipocytes synthesize lipoprotein lipase (LPL) which is inactive and retained in the endoplasmic reticulum (ER) [Masuno, Blanchette-Mackie, Chernick and Scow (1990) J.Biol. Chem.
View Article and Find Full Text PDFpH-dependent multilamellar structures in fetal mouse bone: possible involvement of fatty acids in bone mineralization. Am. J.
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