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PubMed2000

Vascular disease prevention in patients with diabetes.

Prevention is the key to reducing the vascular sequelae of diabetes. Prevention starts with good glycaemic control and continues with a comprehensive programme of risk modification, such as lipid-lowering therapy, antihypertensive treatment, and improved lifestyle. With regard to lipid modification, agents such as statins may provide additional, non-lipid effects in both the diabetic and non-diabetic patient. This review discusses recent studies supporting risk reduction, available treatments, and recommendations applicable to the diabetic patient.

Arteriosclerosis↗

PubMed2004

Outer surface lipoproteins of Borrelia burgdorferi vary in their ability to induce experimental joint injury.

OBJECTIVE: To examine the ability of bacterial lipoproteins from the spirochete Borrelia burgdorferi to cause in vivo tissue injury (arthritis). METHODS: Outer surface proteins (OSPs) from B burgdorferi were used in a rat model of antigen-induced allergic arthritis. Intraarticular challenge with recombinant OspA, OspB, and OspC in nonlipidated (peptide) and lipidated forms was performed in the left knee joint; the contralateral joint received buffer as control. Inflammation was monitored by technetium scintigraphy and histology. RESULTS: Nonlipidated (peptide) OspA, OspB, and OspC did not induce arthritis; the only exception was polymerized OspA, which was tested in preimmunized rats. Lipidated OspA from 2 different strains and lipidated OspC induced severe arthritis, whereas lipidated OspB failed to induce injury. A synthetic analog of the OSP lipid modification, lipopeptide Pam(3)Cys-Ser-Lys(4)-OH, either alone or coupled to bovine serum albumin, also failed to induce injury. Injury did not develop in control groups that were given the appropriate buffers or lipopolysaccharide. This showed that lipidated borrelial OSPs can be potent arthritogens but vary greatly with respect to their injury-inducing potential. The possession of a lipid modification is essential but is not sufficient to render an OSP arthritogenic. CONCLUSION: This is the first study to demonstrate that individual lipoproteins from B burgdorferi can induce experimental joint injury in vivo. These results may help elucidate the pathogenesis of Lyme arthritis and, above all, underline the importance of bacterial lipoproteins as major virulence factors.

Animals↗

PubMed1997

A head-to-head comparison of the cost effectiveness of HMG-CoA reductase inhibitors and fibrates in different types of primary hyperlipidemia.

The objective of this study was to compare the lifetime cost-effectiveness of HMG-CoA reductase inhibitors and fibrates for the treatment of hyperlipidemia. Estimates of lipid modification achieved due to drug therapy were based on published head-to-head comparisons of specific HMG-CoA reductase inhibitors and fibrates in randomized, double-blind studies. We used a validated coronary heart disease (CHD) prevention computer model to estimate the costs and benefits of lifelong lipid modification. The patients were middle-aged men and women who were free of CHD, with either primary type IIa or IIb hyperlipidemia. The intervention used were specific HMG-CoA reductase inhibitors and fibrates at several dosages, which reduced total cholesterol 11-34% and increased high-density lipoprotein cholesterol 1-29%. The main outcome measure was the cost per year of life saved after discounting benefits and costs by 5% annually. The lifetime cost effectiveness of HMG-CoA reductase inhibitors (fluvastatin, lovastatin, pravastatin, simvastatin) and fibrates (bezafibrate, fenofibrate, gemfibrozil) for the treatment of primary hyperlipidemia varied according to patient population, the effectiveness of each drug in modifying lipid levels, and the price of each drug. The estimates of cost per year of life saved for HMG-CoA reductase inhibitors range from $19,886 to $73,632, and $16,955 to $59,488 for fibrates according to gender and type of primary hyperlipidemia. Fluvastatin 20 mg/day was significantly more cost effective than gemfibrozil 1200 mg/day for male patients with type IIa hyperlipidemia. Simvastatin 17.3 mg/day or 20 mg/day yielded similar cost-effectiveness ratios compared with fibrates among type II hyperlipidemic patients. However, micronized fenofibrate was more cost effective than simvastatin 20 mg/day among type IIb patients. The cost effectiveness of lipid therapy varies widely and can be maximized by selecting specific drugs for specific lipid abnormalities.

Bezafibrate↗

PubMed2003

Antioxidants, statins, and atherosclerosis.

Research into the oxidation of lipoproteins has yielded many new insights into the pathogenesis of atherosclerosis. However, despite lipoprotein oxidation's biologically plausible role in atherogenesis, several studies have reported inconsistent effects of antioxidants on clinical coronary end points, in sharp contrast with the studies of lipid modification with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, or statins. There appears to be little support for the use of antioxidants in coronary prevention. However, the picture remains incomplete. What are the limitations of available antioxidant studies and the agents used? Until the picture can be clarified, lipid modification with strategies proved to reduce the risk for coronary events, such as statins or dietary changes in the style of the Mediterranean diet, should be better implemented in clinical practice.

Animals↗

PubMed1997

Retargeting of cytosolic proteins to the plasma membrane by the Lck protein tyrosine kinase dual acylation motif.

Several members of the Src family of protein tyrosine kinases have a N-terminal dual acylation motif which specifies their myristoylation and S-acylation. These lipid modifications are necessary for correct intracellular localisation to the plasma membrane and to detergent-resistant glycolipid-enriched membrane domains (GEMs). Using chimaeras of the Lck dual acylation motif with two normally cytosolic proteins (chloramphenicol acetyl transferase and galectin-3), we show here that this motif is sufficient to encode correct lipid modification and to target these chimaeras to the plasma membrane, as demonstrated by subcellular fractionation and confocal immunofluorescence microscopy of transiently transfected COS cells. In addition, the chimaeras are resistant to extraction with cold non-ionic detergent, indicating targeting to GEM subdomains in the plasma membrane. The dual acylation motif has potential for targeting proteins to specific plasma membrane subdomains involved in signalling.

Acylation↗

PubMed1986

Modifications of lipid structure and their influence on mesomorphism in model membranes: the influence of hydrocarbon chains.

The influence of hydrocarbon chains on the temperature (TG-LC) of the gel to liquid-crystalline phase transition of model membranes has been investigated over an extensive variety of phosphatidylcholines (PC). The TG-LC is dependent upon the length of the hydrocarbon chains, on whether or not the chains are saturated or have been modified in some way, and on the position of any modification along the chain. For PC having two different acyl chains (heteroacid PC) in the sn-1 and sn-2 positions, the TG-LC is dependent on the chain position and on the inequivalence of chain penetration into the bilayer. Positional isomers of PC have different TG-LC. The first two double bonds introduced in each chain of a PC cause a much greater reduction in TG-LC and in the enthalpy change of the transition than does the subsequent introduction of additional double bonds. Dipolyunsaturated PC have uncooperative (broad) transitions that occur at low temperatures and have small enthalpy changes. While each PC has unique transitional characteristics, there are a number of patterns in the TG-LC which emerge on consideration of all the available data. One such pattern may be useful in predicting TG-LC from analytical data on the composition and positions of acyl chains of various lipids.

Chemical Phenomena↗

PubMed2004

Localization and activity of the SNARE Ykt6 determined by its regulatory domain and palmitoylation.

Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) catalyze compartment-specific membrane fusion. Whereas most SNAREs are bona fide type II membrane proteins, Ykt6 lacks a proteinaceous membrane anchor but contains a prenylation consensus motif (CAAX box) and exists in an inactive cytosolic and an active membrane-bound form. We demonstrate that both forms are farnesylated at the carboxyl-terminal cysteine of the CCAIM sequence. Farnesylation is the prerequisite for subsequent palmitoylation of the upstream cysteine, which permits stable membrane association of Ykt6. The double-lipid modification and membrane association is crucial for intra-Golgi transport in vitro and cell homeostasis/survival in vivo. The membrane recruitment and palmitoylation is controlled by the N-terminal domain of Ykt6, which interacts with the SNARE motif, keeping it in an inactive closed conformation. Together, these results suggest that conformational changes control the lipid modification and function of Ykt6. Considering the essential and central role of Ykt6 in the secretory pathway, this spatial and functional cycle might provide a mechanism to regulate the rate of intracellular membrane flow.

Cytosol↗

PubMed1995

Mutation of the htrB locus of Haemophilus influenzae nontypable strain 2019 is associated with modifications of lipid A and phosphorylation of the lipo-oligosaccharide.

The HtrB protein was first identified in Escherichia coli as a protein required for cell viability at high temperature, but its expression was not regulated by temperature. We isolated an htrB homologue from non-typable Haemophilus influenzae strain (NTHi) 2019, which was able to functionally complement the E. coli htrB mutation. The promoter for the NTHi 2019 htrB gene overlaps the promoter for the rfaE gene, and the two genes are divergently transcribed. The deduced amino acid sequence of NTHi 2019 HtrB had 56% homology to E. coli HtrB. In vitro transcription-translation analysis confirmed production of a protein with an apparent molecular mass of 32-33 kDa. Primer extension analysis revealed that htrB was transcribed from a sigma 70-dependent consensus promoter and its expression was not affected by temperature. The expression of htrB and rfaE was 2.5-4 times higher in the NTHi htrB mutant B29 than in the parental strain. In order to study the function of the HtrB protein in Haemophilus, we generated two isogenic htrB mutants by shuttle mutagenesis using a mini-Tn3. The htrB mutants initially showed temperature sensitivity, but they lost the sensitivity after a few passages at 30 degrees C and were able to grow at 37 degrees C. They also showed hypersensitivity to deoxycholate and kanamycin, which persisted on passage. SDS-polyacrylamide gel electrophoresis analysis revealed that the lipo-oligosaccharide (LOS) isolated from these mutants migrated faster than the wild type LOS and its color changed from black to brown as has been described for E. coli htrB mutants. Immunoblotting analysis also showed that the LOS from the htrB mutants lost reactivity to a monoclonal antibody, 6E4, which binds to the wild type NTHi 2019 LOS. Electrospray ionization-mass spectrometry analysis of the O-deacylated LOS oligosaccharide indicated a modification of the core structure characterized in part by a net loss in phosphoethanolamine. Mass spectrometric analysis of the lipid A of the htrB mutant indicated a loss of one or both myristic acid substitutions. These data suggest that HtrB is a multifunctional protein and may play a controlling role in regulating cell responses to various environmental changes.

Bacterial Proteins↗

PubMed1988

Expression of the gene encoding the 17-kilodalton antigen from Rickettsia rickettsii: transcription and posttranslational modification.

Recently, we reported the molecular cloning and nucleotide sequence analysis of a gene from Rickettsia rickettsii that codes for a 17-kilodalton antigen (17K antigen) and is preceded by sequences closely resembling the -10 and -35 consensus sequences for recognition by Escherichia coli RNA polymerase (Anderson et al., J. Bacteriol. 169:2385-2390, 1987). Experiments described in this report indicate that the start sites for initiating transcription of the 17K antigen gene are identical in the E. coli clone and in intact R. rickettsii. In each case, initiation was shown to begin 9 bases downstream of the presumed Pribnow box sequence (TATACT). A 169-base-pair fragment containing the promoter sequence initiated transcription in both directions when cloned into an E. coli promoter probe vector. The rickettsial fragment was found to contain sequences identical to the -10 region (but not the -35 region) of the E. coli promoter consensus sequence directed away from the 17K antigen gene. The amino-terminal portion (residues 17 to 20) of the deduced amino acid sequence for the 17K antigen contained the tetrapeptide Leu-Gln-Ala-Cys, a sequence that conforms favorably to those described for lipid modification and cleavage by lipoprotein signal peptidase II. The 17K antigen produced by the E. coli clone was shown to be labeled with [3H]palmitate and [3H]glycerol, indicative of lipid modification. In vitro mutagenesis designed to alter the cysteine at residue 20 to a glycine abolished incorporation of [3H]palmitate, suggesting that posttranslational modification occurs via a mechanism similar to that described for other gram-negative bacterial lipoproteins.

Amino Acid Sequence↗

PubMed2000

Localization of a peripheral membrane protein: Gbetagamma targets Galpha(Z).

To explore the relative roles of protein-binding partners vs. lipid modifications in controlling membrane targeting of a typical peripheral membrane protein, Galpha(z), we directed its binding partner, betagamma, to mislocalize on mitochondria. Mislocalized betagamma directed wild-type Galpha(z) and a palmitate-lacking Galpha(z) mutant to mitochondria but did not alter localization of a Galpha(z) mutant lacking both myristate and palmitate. Thus, in this paradigm, a protein-protein interaction controls targeting of a peripheral membrane protein to the proper compartment, whereas lipid modifications stabilize interactions of proteins with membranes and with other proteins.

Amino Acid Substitution↗

PubMed1995

Myristoylation cannot functionally replace the isoprenylation of Rab5.

C-terminal isoprenylation is necessary for the small GTPase Rab5 to associate with early endosomes and to exert its regulatory function in endocytosis. In this study, we tested whether Rab5 could retain its membrane association and biological function if the isoprenylation were replaced by another type of lipid modification (myristoylation). Rab5 mutants were constructed that contained both isoprenylation and myristoylation (Gag-Rab5), myristoylation only (Gag-Rab5 delta C4), and neither of the modifications (Rab5 delta C4), respectively. These mutants and wild-type Rab5 were expressed, via a Sindbis virus vector, in cultured BHK-21 cells and their membrane association and biological activity (stimulation of endocytosis) were examined. Wild-type Rab5 was isoprenylated, membrane associated, and biologically active. With additional myristoylation, Gag-Rab5 showed increased affinity for membranes but decreased biological activity. Rab5 delta C4 contained no lipid modifications, failed to associate with membranes, and had no biological activity. With myristoylation (Gag-Rab5 delta C4), there was a significant increase in membrane association (approximately 30%). However, this increased membrane association did not result in any recovery of Rab5 activity. In light of these data, we conclude that N-terminal myristoylation cannot functionally replace the C-terminal isoprenylation of Rab5. Furthermore, myristoylation of Rab5 (Gag-Rab5) interferes with its normal function.

Animals↗

PubMed2004

Palmitoylation is required for the production of a soluble multimeric Hedgehog protein complex and long-range signaling in vertebrates.

Hedgehog (Hh) signaling plays a major role in multiple aspects of embryonic development. A key issue in Hh signaling is to elucidate the molecular mechanism by which a Hh protein morphogen gradient is formed despite its membrane association. In this study, we used a combination of genetic, cellular, and biochemical approaches to address the role of lipid modifications in long-range vertebrate Hh signaling. Our molecular analysis of knockout mice deficient in Skn, the murine homolog of the Drosophila ski gene, which catalyzes Hh palmitoylation, and gene-targeted mice producing a nonpalmitoylated form of Shh indicates that Hh palmitoylation is essential for its activity as well as the generation of a protein gradient in the developing embryos. Furthermore, our biochemical data show that Hh lipid modifications are required for producing a soluble multimeric protein complex, which constitutes the major active component for Hh signaling. These results suggest that soluble Hh multimeric complex travels in the morphogenetic field to activate Hh signaling in distant Hh-responsive cells.

Animals↗

PubMed1999

Ceramide enhances susceptibility of membrane phospholipids to phospholipase A2 through modification of lipid organization in platelet membranes.

The effects of ceramide on agonist-stimulated phospholipase A2 (PLA2) activity were studied in platelets. Cell-permeable C6-ceramide (N-hexanoylsphingosine) exogenously added to platelet suspension enhanced U46619-stimulated arachidonic acid release and lysophosphatidylcholine production. Treatment of platelets with sphingomyelinase also led to an enhancement of the release. The enhanced arachidonic acid release by exogenous ceramide was completely inhibited by methyl arachidonyl fluorophosphonate, a cytosolic PLA2 inhibitor. However, U46619-stimulated PLA2 activity was not significantly potentiated by ceramide. These results suggest that enrichment of ceramide in membranes causes modification of intermolecular organization, leading to increased susceptibility of substrate phospholipids to PLA2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2006

Lipid-protein modifications during ascorbate-Fe2+ peroxidation of photoreceptor membranes: protective effect of melatonin.

The rod outer segment (ROSg) membranes are essentially lipoprotein complexes. Rhodopsin, the major integral protein of ROSg, is surrounded by phospholipids highly enriched in docosahexaenoic acid (22:6 n3). This fluid environment plays an important role for conformational changes after photo-activation. Thus, ROSg membranes are highly susceptible to oxidative damage. Melatonin synthesized in the pineal gland, retina and other tissues is a free radical scavenger. The principal aim of this work was to study the changes in the ROSg membranes isolated from bovine retina submitted to nonenzymatic lipid peroxidation (ascorbate-Fe2+ induced), during different time intervals (0-180 min). Oxidative stress was monitored by increase in the chemiluminescence and fatty acid alterations. In addition we studied the in vitro protective effect of 5 mm melatonin. The total cpm originated from light emission (chemiluminescence) was found to be lower in those membranes incubated in the presence of melatonin. The docosahexaenoic acid content decreased considerably when the membranes were exposed to oxidative damage. This reduction was from 35.5 +/- 2.9% in the native membranes to 12.65 +/- 1.86% in those peroxidized during 180 min. In the presence of 5 mm melatonin we observed a content preservation of 22:6 n3 (23.85 +/- 2.77%) at the same time of peroxidation. Simultaneously the alterations of membrane proteins under oxidative stress were studied using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Loss of protein sulfhydryl groups and increased incorporation of carbonyl groups were utilized as biomarkers of protein oxidation. In membranes exposed to Fe2+ -ascorbate, we observed a decrease of protein thiols from 50.9 +/- 3.38 in native membranes to 1.72 +/- 2.81 nmol/mg of protein after 180 min of lipid peroxidation associated with increased incorporation of carbonyl groups into proteins from 7.20 +/- 2.50 to 12.50 +/- 1.12 nmol/mg of protein. In the SDS-PAGE we observed a decrease in the content of all the proteins, mainly rhodopsin, as a consequence of peroxidation. Melatonin, prevent both lipid peroxidation and protein oxidation.

Animals↗

PubMed2005

Significant modification of lipid metabolism in aged persons following the treatment with a nutritive supplement containing embryonary peptides--preliminary results.

HUMANOFORT is a nutritive supplement extracted and purified from embryonated chicken eggs according to an original procedure under licence. Humanofort received the suitable consent from the Romanian Ministry of Health. The main components of Humanofort are two oligopeptides of 5,000 and 10,000 D molecular weight. 40 subjects aged 50-75 years (18 men and 22 women) consumed, daily, 4 caps of Humanofort for 60 days. The samples of blood from each subject were obtained before and after treatment. Therefore, each subject was his own control. In all subjects, after treatment, total cholesterol and LDL-cholesterol decreased approximately 30% as compared with the initial values. In 80% of patients, an increase of HDL cholesterol and a decrease of the insulin level in blood were also observed. After treatment, the cardiac risk factors (Aethna 2000 Program), such as total cholesterol/HDL and Apolipoproteins B/A were shifted towards lower range. These long-lasting modifications have an adaptative-regulatory character and seem to be produced by the growth factors contained in Humanofort.

Aged↗

PubMed1999

Oxidative modification of lipids and proteins in aniline-induced splenic toxicity.

Our earlier studies with aniline suggested the involvement of oxidative stress as an early toxic event in the spleen. In order to understand the status and consequences of the damaging oxidative reactions, especially during the progression of characteristic splenic lesions, time-dependent subchronic studies were conducted in rats. Male Sprague-Dawley rats were treated with 65 mg/kg/day aniline in the drinking water, while control rats received drinking water only. The animals were euthanized after 1, 2, or 3 months of aniline exposure. Total iron content was remarkably greater in the aniline-treated rats than in age-matched controls. There were time-dependent increases in splenic lipid peroxidation of aniline-treated rats. Malondialdehyde-protein adducts were quantitated by a competitive ELISA and showed greater concentrations in the spleens of aniline-treated rats, further substantiating our lipid peroxidation results. Protein oxidation in the spleens of aniline-treated rats was also greater, with a maximum increase of approximately 76% at 3 months. Western blot analysis for oxidized proteins showed two distinct protein bands at approximately 114 kD and approximately 69 kD in both post-nuclear and mitochondrial fractions of the spleens. Furthermore, densitometric analysis of the blot showed increased band intensities of the oxidized proteins in both these spleen fractions from aniline-treated rats, suggesting the susceptibility of these proteins to aniline-induced oxidative stress. The most prominent morphological changes in the spleens of aniline-treated rats included thickening of the capsule, and capsular cells with nuclear prominence and hyperchromia indicative of capsular hyperplasia. These capsular changes and fibrosis of capsule, splenic trabeculae, and red pulp were noted at all three time points after aniline exposure. Our studies thus suggest that aniline-induced oxidative stress in the spleen is an ongoing event that leads to oxidative modifications of biomolecules. Such oxidative modifications, directly or indirectly, could contribute to the splenic toxicity leading to deleterious consequences, including capsular hyperplasia and fibrosis, as observed in this study, and possibly tumorigenesis in chronic aniline exposure conditions.

Aniline Compounds↗

PubMed2005

The lipopolysaccharide of Brucella abortus BvrS/BvrR mutants contains lipid A modifications and has higher affinity for bactericidal cationic peptides.

The two-component BvrS/BvrR system is essential for Brucella abortus virulence. It was shown previously that its dysfunction abrogates expression of some major outer membrane proteins and increases bactericidal peptide sensitivity. Here, we report that BvrS/BvrR mutants have increased surface hydrophobicity and susceptibility to killing by nonimmune serum. The bvrS and bvrR mutant lipopolysaccharides (LPSs) bound more polymyxin B, chimeras constructed with bvrS mutant cells and parental LPS showed augmented polymyxin B resistance, and, conversely, parental cells and bvrS mutant LPS chimeras were more sensitive and displayed polymyxin B-characteristic outer membrane lesions, implicating LPS as being responsible for the phenotype of the BvrS/BvrR mutants. No qualitative or quantitative changes were detected in other envelope and outer membrane components examined: periplasmic beta(1-2) glucans, native hapten polysaccharide, and phospholipids. The LPS of the mutants was similar to parental LPS in O-polysaccharide polymerization and fine structure but showed both increased underacylated lipid A species and higher acyl-chain fluidity that correlated with polymyxin B binding. These lipid A changes did not alter LPS cytokine induction, showing that in contrast to other gram-negative pathogens, recognition by innate immune receptors is not decreased by these changes in LPS structure. Transcription of Brucella genes required for incorporating long acyl chains into lipid A (acpXL and lpxXL) or implicated in lipid A acylation control (bacA) was not affected. We propose that in Brucella the outer membrane homeostasis depends on the functioning of BvrS/BvrR. Accordingly, disruption of BvrS/BvrR damages the outer membrane, thus contributing to the severe attenuation manifested by bvrS and bvrR mutants.

Acylation↗

PubMed1999

Reduced dietary fat intake increases parasympathetic activity in healthy premenopausal women.

1. Hypercholesterolaemia has been associated with decreased heart rate variability, a measure of cardiac parasympathetic activity. However, the effect of perturbation of the lipid profile on autonomic function has not been examined systematically. 2. The effects of short-term dietary lipid modification on autonomic function are studied in 25 normotensive, non-smoking, premenopausal women with normal bodyweight. Subjects consumed either a low (L, 25%) or high fat (H, 40%) diet for 2 weeks in an open, randomized, cross-over manner with a 2 week washout. 3. Baroreflex sensitivity was determined by gating beat-to-beat heart period (RR) interval and continuous non-invasive blood pressure recordings. Heart rate variability measures of cardiac parasympathetic nervous system activity were obtained in the time (standard deviation of RR intervals, root mean square of successive differences (rMSSD)) and frequency (high frequency power) domains. All assessments were made at the same timepoint in the menstrual cycle. 4. Both low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol decreased significantly (P < 0.05) with increased dietary fat intake (H, 2.7 +/- 0.1 vs L, 2.2 +/- 0.1; H, 1.3 +/- 0.1 vs L, 1.1 +/- 0.1 mmol/L, respectively) as did mean arterial pressure (H, 78.1 +/- 1.5 vs L, 74.3 +/- 1.5 mmHg). Weight was unchanged by dietary lipid intake (H, 62.6 +/- 8.5 vs L, 62.3 +/- 8.3 kg, P = NS). 5. There was a significant increase in rMSSD (H, 29.6 +/- 3.4 vs L, 38.8 +/- 6.4 msec, P < 0.05) and natural logarithm of high frequency power following low fat diet (H, 4.4 +/- 0.2 vs L, 4.8 +/- 0.3 msec2, P = 0.01). Baroreflex sensitivity also increased following the low fat diet (H, 13.91 +/- 2.2 vs L, 16.9 +/- 3.2 msec/mmHg, P = 0.23). 6. Short-term dietary lipid modification can significantly increase cardiac parasympathetic nervous system activity in healthy premenopausal women. These changes in autonomic status appear to be independent of changes in bodyweight and may be of clinical relevance considering the prognostic implications of heart rate variability in cardiovascular disease.

Adolescent↗