Advances in lipid research 

About: Advances in lipid research is an academic journal. The journal publishes majorly in the area(s): Cholesterol & Lipid metabolism. It has an ISSN identifier of 0065-2849. Over the lifetime, 183 publications have been published receiving 15727 citations.

Practical methods for plasma lipoprotein analysis.

Abstract: Publisher Summary This chapter discusses the practical methods for plasma lipoprotein analysis Changes in the concentration and sometimes in the nature of the plasma lipoproteins occur in a variety of diseases The pioneering work of Gofman and his colleagues in the early 1950s was responsible for much of the knowledge of these complex proteins that is now available Their techniques of analytical ultracentrifugation were, and still remain, the primary standard for lipoprotein analysis These methods are available in very few medical centers; however, excluding access to them by most of the laboratories where the interest and availability of patients or subjects for investigation are the greatest Recent simplifications and improvements of other analytical methods have made these a partial replacement for the analytical ultracentrifuge, and newer methods have proved their value Techniques of protein chemistry and immunology have added a new dimension to lipoprotein analysis —that of specific recognition and quantitation of the protein moieties

Regulation of HMG-CoA Reductase

Abstract: Publisher Summary This chapter discusses the regulation of HMG-CoA reductase, which catalyzes the rate-limiting reaction of hepatic sterol synthesis. Both mitochondrial and extramitochondrial forms of acetoacetyl-CoA thiolase and the HMG-CoA synthase are present in liver tissue. The reductase activity of cultured mammalian cells or of bacteria is readily assayed in crude homogenates. The HMG-CoA reductase activity may be readily assayed in the post-mitochondrial supernatant fraction obtained by high-speed centrifugation of homogenates of tissues, including liver. The chapter also discusses familial hypercholesterolemia (FH), which is an autosomal, dominant genetic disorder estimated to affect 0.1–0.2% of the population. FH may involve defects in the regulation of both cholesterol synthesis and degradation. The data for adults heterozygous for FH indicate that the rate of cholesterol synthesis in vivo is subnormal. The basic defect in FH may be a low affinity of the cellular plasma membrane for cholesterol. This defect, observed in fibroblasts and leukocytes, leads to an impaired uptake of cholesterol from serum lipoproteins and an enhanced release of cellular cholesterol. If this defect is present in the liver, it could account for the relatively ineffective feedback suppression of cholesterol synthesis.

Structural and Lipid Biochemical Correlates of the Epidermal Permeability Barrier

Abstract: Publisher Summary This chapter discusses the structural and lipid biochemical correlates of the epidermal permeability barrier. A pivotal point in terrestrial adaptation is prevention of desiccation and maintenance of internal water homeostasis. The outermost integumentary tissue, the epidermis, maintains a reserve of germinal cell layers whose proliferation, stratification, and differentiation result in the production of the outermost layer, the anucleate stratum corneum. The stratum corneum has heterogeneous tissue structure possessing a selected array of enzymatic activity. The sequestration of lipids to intercellular domains and their organization into a unique multilamellar system have broad implications for permeability barrier function, water retention, desquamation, and percutaneous drug delivery. Yet, the functions and organization of specific lipid species in this membrane system are still unknown. Further, elucidation of the molecular architecture and interactions of lipid and nonlipid components of the stratum corneum intercellular domains will be a prerequisite for a comprehensive understanding of stratum corneum function.

The Metabolic Role of Lecithin: Cholesterol Acyltransferase: Perspectives from Pathology

Abstract: Publisher Summary This chapter discusses the metabolic role of enzyme lecithin called cholesterol acyltransferase (LCAT). The role of the LCAT reaction is to prevent unesterified cholesterol, derived mainly from the surfaces of chylomicrons and very low density lipoproteins, from accumulating in the plasma. This is successfully accomplished only when the LCAT reaction balances the mechanisms that increase plasma unesterified cholesterol. A balance does not occur in familial LCAT deficiency because the enzyme is absent. It does not occur in cholesterol-fed guinea pigs because unusually large amounts of dietary unesterified cholesterol enter the plasma through inadequate control in either the intestine or the liver. It does not occur in cholestasis because phospholipid bilayers are formed and promote the accumulation of unesterified cholesterol in plasma through increased hepatic biosynthesis. Unesterified cholesterol becomes associated with the surfaces of newly formed lipoproteins by physical equilibration within the cells of the intestinal mucosa and the liver. The function of the LCAT reaction is to transport unesterified cholesterol synthesized in peripheral tissues to the liver.

Carnitine and its role in fatty acid metabolism.

Abstract: Publisher Summary This chapter describes carnitine and its role in fatty acid metabolism. Carnitine (s-hydroxy-γ-trimethylammonium butyrate) is widely distributed in tissues of animals, plants, and microorganisms, with highest concentrations in muscles of vertebrates and invertebrates. It has the property of increasing oxygen consumption and catalytically stimulating long- chain fatty acid oxidation by a variety of suitable tissue preparations, of which heart responds to the greatest degree. Carnitine is unable to substitute for dietary choline in the prevention of fatty liver formation in rats or as a growth factor in several choline-requiring organisms. In two species of the order Diptera, however, carnitine can replace choline. According to Fraenkel, Drosophila melanogaster could grow almost as well on carnitine as on choline, and Hodgson demonstrated that carnitine can completely replace choline in Phormia regina .