I Diretriz sobre o consumo de Gorduras e Saúde Cardiovascular Definição do grau dos níveis de evidência Recomendações Classe I: Condições para as quais há evidências conclusivas e, na sua falta, consenso geral de que o procedimento é seguro útil/eficaz. Classe II: Condições para as quais há evidências conflitantes e/ou divergência de opinião sobre segurança e utilidade/ eficácia do procedimento. Classe IIa: Peso ou evidência/opinião a favor do procedimento. A maioria aprova. Classe IIb: Segurança e utilidade/eficácia menos bem estabelecidas, não havendo predomínio de opniões a favor. Classe III: Condições para as quais há evidências e/ou consenso de que o procedimento não é útil/eficaz e, em alguns casos, pode ser prejudicial. Evidências Nível A: Dados obtidos a partir de múltiplos estudos randomizados de bom porte, concordantes e/ou de Metanálise robusta de estudos clínicos randomizados. Nível B: Dados obtidos a partir de Metanálise menos robusta, a partir de um único estudo randomizado ou de estudos não randomizados (observacionais). Nível C: Dados obtidos de opiniões consensuais de especialistas.

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Several factors may be responsible for the high prevalence of premature atherosclerosis in diabetes mellitus [1], including possible alterations in the reverse cholesterol transport system [2][3][4][5][6][7].Plasma lipoproteins (LP) are continually modified intravascularly and in the interstitium due to enzymatic action and interchanges of lipid fractions and apolipoproteins [2,8,9]. The role of cholesteryl ester transfer protein (CETP) in intravascular cholesteryl ester (CE) transport has been fully reviewed [2,[10][11][12]. In addition to promoting a bidirectional flux of cholesteryl ester between LP, CETP also mediates the heteromolecular exchange whereby triglyceride (TG)-rich LP gains CE and loses TG [13]. The direction of this flow is partially determined by the lipid composition of the LP involved [14,15]. Diabetologia (1997Diabetologia ( ) 40: 1085Diabetologia ( -1093 Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins Summary Alterations in the reverse cholesterol transport system have been described in diabetic mellitus patients in several but not all studies. Furthermore, recently published investigations suggest that a faster "in vitro" transfer rate of cholesteryl ester from high density lipoproteins to apoB-containing lipoproteins could be solely ascribed to variation of the plasma lipoprotein composition and concentration in the diabetic state. The present study analysed the influence of lipoprotein glycation on the cholesteryl ester transfer protein-mediated transfer of esterified cholesterol from high density lipoprotein and its subfractions to lighter density lipoproteins. For this purpose two sets of "in vitro" experiments were carried out utilizing:1) plasma lipoproteins drawn from diabetic and from normal subjects and; 2) normal lipoproteins or partially purified cholesteryl ester transfer protein submitted to "in vitro" glycation. The transfer rate of 14 C-cholesteryl ester labelled HDL subfractions to low or very low density lipoproteins was measured in all experiments. After incubations with plasma d > 1.21 g/ml or with purified cholesteryl ester transfer protein, apoB-containing lipoproteins were precipitated with a dextran sulfate/MgCl 2 solution. The "in vitro" glycation of the partially purified cholesteryl ester transfer protein markedly impaired its activity. However, greater transfer rates were observed when lipoproteins from diabetic individuals or the "in vitro" glycated lipoproteins were utilized. This effect was attributed to glycation of the protein component of HDL. In conclusion, lipoprotein glycation elicits an enrichment of the apoB-containing lipoproteins with cholesteryl ester that is likely related to the premature atherosclerosis in patients with poorly controlled diabetes. [Diabetologia (1997[Diabetologia ( ) 40: 1085[Diabetologia ( -1093

Chylomicrons transport fat and cholesterol via lymphatic vessels from the intestine into the bloodstream. The understanding of the metabolism of chylomicrons in man has been slowed by the difficulty of obtaining lymph chylomicrons for experimental studies. Acceptable methods for the study of chylomicron clearance in man are required, because the metabolism of chylomicrons may be abnormal in diseases such as diabetes mellitus. Metabolism of chylomicrons may also play a role in the development of atherosclerosis. In the present work, lipid emulsions were used as a physical model of chylomicrons. Triacylglycerol-rich lipid emulsions labelled with tracer amounts of radioactive triolein and cholesteryl oleate were prepared by sonication and purified by density gradient ultracentrifugation, then injected into unanaesthetized rats and normal human subjects. Plasma radioactivities were measured for 30 min in rats and 90 min in human subjects. Rat lymph chylomicrons were also injected into rats for comparison with the clearance of the lipid emulsions. The plasma clearance data for triacylglycerols and cholesteryl esters were fitted with a kinetic model using the SAAM/CONSAM programs. Multiple studies analysis of the individual studies in each group was used to obtain estimates of the parameter average values and variabilities. The plasma residence times of the lipid labels were obtained from the fitted clearance data. Our results suggest that information about chylomicron metabolism in man can be obtained by analysis of the plasma clearance data following the injection of suitably labelled chylomicron-like lipid emulsions. Our data provide a baseline for comparisons with individuals having abnormalities of lipid metabolism or risk factors for arteriosclerosis.

Abstract-Lipid transfer inhibitor protein (LTIP, apolipoprotein F) regulates the interaction of cholesteryl ester transfer protein (CETP) with lipoproteins and is postulated to enhance the ability of CETP to stimulate reverse cholesterol transport. The factors that regulate LTIP levels and control its biosynthesis are unknown. Here, we demonstrate that plasma LTIP is dramatically increased (3-fold) in hypercholesterolemic subjects with normal to mildly elevated plasma triglyceride (TG) levels compared with control subjects. LTIP in these subjects is not correlated with the extent of hypercholesterolemia or with low density lipoprotein (LDL), high density lipoprotein, or CETP levels. [3][4][5] However, the overall impact of CETP activity on atherogenesis has remained controversial, inasmuch as CETP can potentially facilitate processes that would appear to be proatherogenic and antiatherogenic.CETP activity is regulated by another plasma component, lipid transfer inhibitor protein (LTIP). We recently purified and cloned LTIP and demonstrated its identity with apoF. 6 Although LTIP was first identified simply by its capacity to suppress CETP activity in binary lipid transfer assays, 7 it now appears that LTIP plays a more complex role in regulating CETP. CETP has little preference for interacting with different lipoprotein classes under steady-state conditions, 8 and within a mixture of lipoproteins, CETP mediates transfer events between lipoprotein classes at rates that are largely determined by their relative concentrations. 9 This finding contrasts with that seen in plasma, in which HDL appears to be a preferred CETP substrate. 10 -12 We have recently demonstrated that LTIP activity accounts for this discrepancy. 9 This is hypothesized to occur because LTIP preferentially suppresses the interaction of CETP with LDL. 13 Because VLDL concentrations are rate limiting in normal plasma to the CE-TG exchange process, 14 the suppression of transfers with LDL results in a stimulation of lipid exchange between VLDL and HDL. 9,15 Therefore, LTIP is a regulator of CETP function in that it controls the rate of individual lipid transfer reactions. We have proposed that LTIP augments the antiatherogenic capacities of CETP by stimulating reverse cholesterol transport. 9,15 CETP synthesis is strongly upregulated by cholesterol, 16,17 and elevated CETP levels are commonly observed in hypercholesterolemic subjects. 18,19 This appears to be an adaptive response to enhance mechanisms responsible for sterol homeostasis. Because the beneficial actions of CETP are likely to be enhanced by LTIP, it seems reasonable that LTIP levels may be increased by similar stimuli. At present, nothing is