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PubMed2007

Conditional animal models for the study of lipid metabolism and lipid disorders.

The advent of technologies that allow conditional mutagenesis has revolutionized our ability to explore gene functions and to establish animal models of human diseases. Both aspects have proven to be of particular importance in the study of lipid-related disorders. Classical approaches to gene inactivation by conventional gene targeting strategies have been successfully applied to generate animal models like the LDL receptor- and the apolipoprotein E-knockout mice, which are still widely used to study diverse aspects of atherosclerosis, lipid transport, and neurodegenerative disease. In many cases, however, simply inactivating the gene of interest has resulted in early lethal or complex phenotypes which are difficult to interpret. In recent years, additional tools have therefore been developed that allow the spatiotemporally controlled manipulation of the genome, as described in detail in Part I of this volume. Our aim is to provide an exemplary survey of the application of different conditional mutagenesis techniques in lipid research in order to illustrate their potential to unravel physiological functions of a broad range of genes involved in lipid homeostasis.

Animals↗
PubMed1978

Importance of apolipoproteins in lipid metabolism.

Lipids, which serve as a source of energy and are an important constituent of cell membrane structure, are readily stored in the body. By definition they are insoluble in water. Specific proteins called apolipoproteins interact with lipids to form soluble lipid-protein complexes called lipoproteins. It is in this form that the major lipids--cholesterol, triglyceride and phospholipid--circulate in plasma. Unesterified fatty acids, another major lipid group, are bound to albumin in the circulation. The plasma lipoproteins are complex macromolecules composed of lipids, apolipoproteins and carbohydrates. The relative proportions of these components differ markedly between lipoprotein classes. Hyperlipidemia is a term used for increased concentrations of plasma cholesterol and/or triglycerides. Any one plasma lipid is present in several types of lipoproteins. Thus, hyperlipidemia implies the presence of hyperlipoproteinemia. The latter has important therapeutic implications. Most of the recent attempts at classification have been directed at the lipoprotein level of plasma lipid organization. Decreased concentrations of lipids in plasma can be achieved by altering the rates of metabolism of lipoproteins. Decrease in lipoprotein synthesis, increased catabolism or impaired release from cells into the blood stream may all result in a decrease of plasma lipids. Drugs which affect one or more of these factors are used to treat hyperlipoproteinemia. In order to elucidate the mechanism of action of hypolipidemic drugs it is necessary to understand the lipoprotein defect at the molecular level. This requires a more detailed knowledge of lipoprotein metabolism than is presently available for most of the hyperlipoproteinemias. This paper will review some of the generally accepted properties of the plasma lipoproteins, describe some difficulties which hamper the understanding of lipoprotein metabolism, and identify possible mechanisms by which drugs may affect lipoprotein metabolism.

Apolipoproteins↗
PubMed2005

The effect of plant stanol- and sterol-enriched foods on lipid metabolism, serum lipids and coronary heart disease.

Phytosterols are plant sterols, mainly campesterol and sitosterol, and their respective stanols (5alpha-saturated derivatives), which chemically resemble cholesterol. They are present in a normal diet and are absorbed proportionally to cholesterol, but to a much lesser extent, such that less than 0.1% of serum sterols are plant sterols. Phytosterols inhibit intestinal cholesterol absorption, and fat-soluble plant stanol esters were introduced as a functional food for lowering serum cholesterol in the early 1990s; plant sterol esters entered the market at the end of the 1990s. Inhibition of the intestinal absorption of cholesterol stimulates cholesterol synthesis, a factor which limits serum cholesterol lowering to about 10% with phytosterols. Enrichment of the diet with plant stanol esters reduces absorption and serum concentrations of both cholesterol and plant sterols, whereas enrichment of the diet with plant sterol esters, especially in combination with statins, lowers serum cholesterol but increases serum plant sterol levels. Recent studies have suggested that high-serum plant sterol levels may be associated with increased coincidence of coronary heart disease. Estimates of coronary heart disease reduction by 20--25% with plant sterols/stanols is based mainly on short-term studies. Long-term cholesterol lowering, needed for the prevention of coronary heart disease, may be successful with plant stanol esters, which lower serum cholesterol in both genders over at least a year.

Coronary Artery Disease↗
PubMed2004

Hormones regulating lipid metabolism and plasma lipids in childhood obesity.

OBJECTIVE: To review the mechanisms by which leptin, insulin and adiponectin influence lipid metabolism and plasma lipids in obesity, as well as to describe the associations between these hormones in prepubertal children. METHOD: Revision of relevant papers published in the last 5 y related to the interactions of leptin, insulin and adiponectin, with special emphasis on those reporting potential mechanisms by which these hormones regulate lipid metabolism and plasma lipids. We also provide original results concerning the relationships found between plasma lipids and leptin, and insulin and adiponectin in prepubertal obese children. RESULTS: Recent data in the literature shed new light to explain the effects of both leptin and adiponectin in the regulation of lipid metabolism in peripheral tissues. Activation of the AMP-dependent kinase pathway and subsequent increased fatty acid oxidation seems to be the main mechanism of action of these hormones in the regulation of lipid metabolism. In addition, we have found that insulin plasma levels are positively associated to leptin but negatively correlated with adiponectin in obese children. Adiponectin is negatively associated to plasma lipid markers of metabolic syndrome but positively related to HDL-cholesterol, whereas insulin and leptin show opposite patterns. These results support the effect of adiponectin in increasing insulin sensitivity and decreasing plasma triglycerides. CONCLUSION: Leptin, insulin and adiponectin are associated hormones that regulate lipid metabolism in childhood. Adiponectin appears to be the missing link to explain the alterations in lipid metabolism and plasma lipids seen in obesity.

Adiponectin↗
PubMed2005

Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.

OBJECTIVES: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and beta-cell function in lipodystrophic HIV-infected patients. METHODS: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naive to antiretroviral therapy (NAIVE) respectively). beta-cell function was evaluated by an intravenous glucose tolerance test. RESULTS: Compared with NONLIPO and NAIVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; > 34%, P < 0.001), hepatic insulin sensitivity (> 40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. CONCLUSION: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and beta-cell function.

Adult↗