Studies were carried out to examine the effects of dietary fat and cholesterol on cholesterol homeostasis in man. 75 12-wk studies were carried out during intake of 35% of calories as either saturated or polyunsaturated fat, first low and then high in dietary cholesterol. Dietary fat and cholesterol intakes, plasma lipid and lipoprotein levels, cholesterol absorption and sterol synthesis in isolated blood mononuclear leukocytes were measured during each diet period. In 69% of the studies the subjects compensated for the increased cholesterol intake by decreasing cholesterol fractional absorption and/or endogenous cholesterol synthesis. When an increase in plasma cholesterol levels was observed there was a failure to suppress endogenous cholesterol synthesis. Plasma cholesterol levels were more sensitive to dietary fat quality than to cholesterol quantity.The results demonstrate that the responses to dietary cholesterol and fat are highly individualized and that most individuals have effective feedback control mechanisms.
Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoproteinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.Premature atherosclerosis and its sequelae, myocardial infarction and cerebrovascular accident, have recently been recognized as complications of systemic lupus erythematosus (SLE) (1-7). Possible etiologies include dyslipoproteinemia, vasculitis, hypertension, and increased tendency for thrombosis associated with the presence of circulating anticoagulant (1-8).Dyslipoproteinemia is common in adult SLE patients (9); however, the relationships of disease activity, diet, corticosteroid therapy, and concurrent renal, liver, and pancreatic disease have not been studied well. To differentiate the roles of corticosteroids and disease activity in the dyslipoproteinemia of SLE, we studied newly diagnosed pediatric patients both before and after high-dose systemic prednisone therapy. PATIENTS AND METHODSPatients. Ten successive pediatric patients (younger than 21 years of age) newly diagnosed as having SLE were enrolled after informed consent was obtained. Nine fulfilled the requirements of the American Rheumatism Association revised diagnostic criteria (10). The other (patient 5) had anticardiolipin, high-titer speckled antinuclear, anti-Smith, and anti-double-stranded DNA antibodies, circulating lupus anticoagulant, hypocomplementemia, and recurrent pulmonary emboli. He was not treated with corticosteroids. Eight patients underwent percutaneous renal biopsy prior to therapy. Results are shown in Table 1. In all 10 patients at diagnosis, and in 8 patients at 4-8 weeks after institution of 1-2 mg/kg/day of prednisone, fasting plasma lipid profiles (see below) were obtained. Dietary intake was quantified by 3-day diet record, and this was supplemented with 24-hour recall
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.