Plasma Lipoprotein Abnormalities Research Articles

Energy metabolism: a new target for gastric cancer treatment.

Gastric cancer is the fifth most common malignancy worldwide having the fourth highest mortality rate. Energy metabolism is key and closely linked to tumour development. Most important in the reprogramming of cancer metabolism is the Warburg effect, which suggests that tumour cells will utilise glycolysis even with normal oxygen levels. Various molecules exert their effects by acting on enzymes in the glycolytic pathway, integral to glycolysis. Second, mitochondrial abnormalities in the reprogramming of energy metabolism, with consequences for glutamine metabolism, the tricarboxylic acid cycle and oxidative phosphorylation, abnormal fatty acid oxidation and plasma lipoprotein metabolism are important components of tumour metabolism. Third, inflammation-induced oxidative stress is a danger signal for cancer. Fourth, patterns of signalling pathways involve all aspects of metabolic transduction, and many clinical drugs exert their anticancer effects through energy metabolic signalling. This review summarises research on energy metabolism genes, enzymes and proteins and transduction pathways associated with gastric cancer, and discusses the mechanisms affecting their effects on postoperative treatment resistance and prognoses of gastric cancer. We believe that an in-depth understanding of energy metabolism reprogramming will aid the diagnosis and subsequent treatment of gastric cancer.

High prevalence of plasma lipid abnormalities in human and canine Duchenne and Becker muscular dystrophies depicts a new type of primary genetic dyslipidemia

Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are allelic X-linked recessive muscle diseases caused by mutations in the DMD gene, with DMD being the more severe form. We have recently shown that increased plasma low-density lipoprotein-associated cholesterol causes severe muscle wasting in the mdx mouse, a mild DMD model, which suggested that plasma lipids may play a critical role in DMD. We have also observed that loss of dystrophin in mice causes unexpected elevations in plasma lipoprotein levels. The objectives of the study were to determine whether patients with DMD and BMD also present with clinically relevant plasma lipoprotein abnormalities and to mitigate the presence of confounders (medications and lifestyle) by analyzing the plasma from patients with DMD/BMD and unmedicated dogs with DMD, the most relevant model of DMD. Levels of low-density lipoprotein-associated cholesterol, high-density lipoprotein cholesterol, and triglycerides were analyzed in patients with DMD and BMD and female carriers. Samples from unmedicated, ambulatory dogs with DMD, unaffected carriers, and normal controls were also analyzed. We report that 97% and 64% of all pediatric patients with DMD (33 of 36) and BMD (6 of 11) are dyslipidemic, along with an unusually high incidence in adult patients with BMD. All dogs with DMD showed plasma lipid abnormalities that progressively worsened with age. Most strikingly, unaffected carrier dogs also showed plasma lipid abnormalities similar to affected dogs with DMD. Dyslipidemia is likely not secondary to liver damage as unaffected carriers showed no plasma aminotransferase elevation. The high incidence of plasma lipid abnormalities in dystrophin-deficient plasma may depict a new type of genetic dyslipidemia. Abnormal lipid levels in dystrophinopathic samples in the absence of muscle damage suggest a primary state of dyslipidemia. Whether dyslipidemia plays a causal role in patients with DMD warrants further investigation, which could lead to new diagnostic and therapeutic options.

Correlations of serum magnesium with dyslipidemia in patients on maintenance hemodialysis

Correlations of serum magnesium with dyslipidemia in patients on maintenance hemodialysis

Selective PPAR modulators (SPPARs) may fill the need for treatment of the atherogenic dyslipidemia of insulin resistance and type 2 diabetes: Can they reduce the associated cardiac risk?

Selective PPAR modulators (SPPARs) may fill the need for treatment of the atherogenic dyslipidemia of insulin resistance and type 2 diabetes: Can they reduce the associated cardiac risk?

Trends of lipid abnormalities among newly detected type-2 diabetes mellitus in a tertiary care hospital in Karnataka, India

Background: Diabetes mellitus is a common and a chronic disease with chronic complications and constitutes a substantial burden for both patient and health care system. Insulin resistance and type 2 diabetes are associated with a clustering of interrelated plasma lipid and lipoprotein abnormalities, which include reduced HDL cholesterol, a predominance of small dense LDL particles, and elevated triglyceride levels. Aims and objectives were to study the pattern of lipid abnormalities in newly detected type-2 diabetic patients. Methods: A cross sectional study was conducted at Vijayanagara Institute of Medical Sciences Hospital and College, Bellary from May 2014 to November 2014. A total of 300 newly detected diabetic patients were included in the study. Blood Examination was done to estimate low density lipoprotein (LDL), high density lipoprotein (HDL) and triglycerides (TG). Results: Out of 300 patients, lipid abnormality was seen in 200/300 (66.67%) of the patients. Increased LDL noted in 152 (50.67%), triglycerides in 112 (40.67%), decreased HDL in 130 (43.34%) of patients. Conclusions: It is clearly evident that dyslipidaemia is very common association of type 2 diabetes mellitus, and culprit of majority diabetic related cardiovascular mortality.

Prevalence of High Lipid Profile in Diabetes Meellitus Patients: A Study in a Tertiary Care Centre

Introduction: Diabetes mellitus is a group of metabolic diseases characterized by increased blood glucose levels resulting from defects in insulin secretion, insulin action, or both. It is also associated with interrelated plasma lipid and lipoprotein abnormalities, including reduced HDL cholesterol, elevated triglyceride and LDL levels. Each of these dyslipidemic features is associated with increased cardiovascular risk and as a result, mortality. Materials and Methods: 476 patients between 18 – 80 years were selected randomly and included into the study. The patients were divided into 2 groups, one with blood sugar levels below 110mg/dl and the other within normal limits. Biochemical tests such as fasting blood sugar, post parandial blood sugar, lipid profile including triglyceride levels, HDL cholesterol, LDL cholesterol and total cholesterol were done for all the patients. Results: Out of 476 patients, 249 were diabetic with fasting blood sugar above 110mg/dl and 227 patients had FBS levels within the normal limits. Out of the diabetic patients, 51% were males and 49% were females. In the controls group, there were 52.4% males and 47.6% females. Conclusion: There is a high prevalence of high degree of elevated lipid and lipoprotein levels among the diabetic patients showing that they are more prone to these abnormalities. Keywords: Diabetes mellitus, lipid levels, lipoproteins, cholesterol, triglycerides

Comparison of lipid profile and new atherogenic indices among the coronary artery disease (CAD)-negative and -positive diabetic dyslipidemia subjects

Background: Type 2 diabetes mellitus (T2DM) is associated with a cluster of interrelated plasma lipid and lipoprotein abnormalities including reduced HDL cholesterol. Objective: To compare the lipid profile and new atherogenic indices among the coronary artery disease (CAD)-negative and -positive diabetic dyslipidemia subjects and determine the use of atherogenic indices in the early prediction of CAD in diabetic subjects. Materials and Methods: A total number of 194 subjects participated in our study, of which 65 people with diabetic dyslipidemia were considered cases and 129 nondiabetic people with normal lipid profile were considered control subjects based upon their fasting blood glucose (FBG) and lipid profiles. Furthermore, among the 65 cases, 38 subjects were identified as CAD negative and rest of the 27 subjects were CAD-positive subjects. Result: Lipid profiles of both CAD-negative and -positive diabetic subjects showed significantly different values than the control subjects except for high-density lipoprotein cholesterol (HDL-c) value (41.89 ± 1.49; p > 0.05) of CAD-negative subjects. The comparison between the CAD-negative and -positive diabetic dyslipidemia subjects observed significantly higher values of triglycerides (339.59 ± 52.24; p < 0.001) and very low-density lipoprotein cholesterol (VLDL-c) (67.91 ± 10.44; p < 0.001) and lower values of HDL-c (35.59 ± 1.40; p < 0.001) in CAD-positive subjects. When compared with control subjects, both CAD-negative and -positive subjects showed higher values of atherogenic indices that were significantly (p < 0.01 and p < 0.001, respectively) different. Conclusion: Our results indicate that atherogenic indices may be useful for identifying individuals at higher risk of cardiovascular disease in the clinical practices, especially, not markedly deranged or in centers with insufficient resources.

Association of plasma lipid levels with atherosclerosis prevalence in psittaciformes.

The prevalence of atherosclerosis is high in the captive psittacine population and increases with age and female sex. The genera Psittacus, Amazona, and Nymphicus are predisposed to atherosclerosis, whereas the genera Cacatua and Ara are less susceptible. Plasma cholesterol and lipoprotein abnormalities have been suggested as risk factors in the development of atherosclerosis as observed in mammals. To investigate whether the psittacine genera susceptibility to atherosclerosis and the known risk factors of age and sex could be associated with differences in the lipid profile, a retrospective analysis was conducted on blood lipid values from 5625 birds. Prevalence values were obtained from a previously published, large, case-control study and were compared with identified trends in plasma lipid profiles. Genus-specific differences were identified in plasma total cholesterol values that corresponded to observed trends in the prevalence of clinically important atherosclerotic lesions, which were also highly correlated. The effect of age was significant but was mild and may not account for the dramatic increase in atherosclerosis prevalence observed with age. In addition, Quaker parrots ( Myiopsitta monachus ), which were used as experimental models for psittacine atherosclerosis and dyslipidemia, were found to have the highest values in all lipid profile parameters. The results of this study suggest that the differences observed in prevalence among species of the psittacine genera may partly be explained by differences in plasma total cholesterol levels. Results also support the use of Quaker parrots as models for studying atherosclerosis and dyslipidemia.

Lipoprotein glomerulopathy: a case report of a rare disease in a brazilian child

Lipoprotein glomerulopathy (LPG) is a rare autosomal recessive glomerulopathy associated with the deposition of lipoprotein thrombi in the capillary lumina due to apoE gene mutations. Abnormal plasma lipoprotein profile and marked increase in serum apoliprotein E (apoE) are characteristic clinical data. The compromised patients can present nephrotic syndrome, hematuria, and progressive renal failure. Herein, the authors present the first described case of LPG in a Brazilian male patient, 11 years, who presented with a steroid-resistant nephrotic syndrome. Renal function was normal. Kidney biopsy showed markedly enlarged glomerulus, with dilated capillary loops and weak eosinophilic lipoprotein thrombi in the capillary lumina. Interstitium, tubules, arteries, and veins showed normal histologic aspect. Genotypic study for the apoE gene showed the presence of the alleles E3 and E4. The diagnosis of LPG was then performed. The patient received lipid-lowering treatment. After 2 years of follow-up, renal function is gradually decreasing, with persisting heavy proteinuria, despite a marked decrease in serum cholesterol and triglycerides levels.

Lipoprotein metabolism and CKD: overview

Patients with chronic kidney disease (CKD) frequently display abnormalities of plasma lipids and lipoproteins. These abnormalities include hypertriglyceridemia associated with elevated levels of very low-density lipoproteins (VLDLs) and chylomicrons. There is often also an increase in the concentration of the atherogenic, cholesterol-enriched remnants of VLDLs and chylomicrons. The concentration of low-density lipoprotein cholesterol is usually normal, but there is frequently a decrease in concentration of the cardio-protective high-density lipoproteins. There is also often an increase in the concentration of the atherogenic lipoprotein (a) particles. This article provides an overview of plasma lipoprotein transport and identifies mechanisms responsible for the abnormalities observed in patients with CKD.

A Study of Serum Apolipoprotein A1, Apolipoprotein B and Lipid Profile in Stroke

Role of Serum Lipids, Lipoproteins and Lipoprotein related variables in the prediction of Stroke is less clear. Abnormalities in plasma Lipoproteins are the most firmly established and best understood risk factors for Atherosclerosis and they are probable risk factors for Ischaemic stroke, largely by their link to Atherosclerosis. Apo B reflects the concentration of potentially atherogenic particles (LDL), and Apo A1 reflects the corresponding concentration of anti- atherogenic particles (HDL), represent additional lipoprotein related variables that may indicate the vascular risk. To study serum concentration of Apolipoprotein A1, Apolipoprotein B, Apo B/Apo A1 ratio and Lipid profile in Stroke Cases and to compare with healthy controls. A total number of 100 subjects within 30 - 70 years were considered for the study. 50 subjects with Stroke (both clinically as well as Computed tomographically proven cases) and 50 age and sex matched healthy individuals were taken for the study. Total cholesterol, HDL cholesterol and Triglycerides are estimated by Enzymatic method using Semiautoanalyser. LDL cholesterol is estimated by Friedewald formula. Apo B and Apo A1 are estimated by Immunoturbidimetric method using Semiautoanalyser. Student 't' test was used to compare the data between cases and controls. Diagnostic validity tests were conducted to assess the Diagnostic efficiency of Apo A1, Apo B and Apo B/Apo A1 ratio. Total cholesterol, LDL cholesterol and Triglycerides are significantly increased in Cases compared to Controls. HDL - cholesterol is significantly decreased in Cases compared to Controls. Apo B and Apo B/Apo A1 ratio are significantly increased and Apo A1 is significantly decreased in Cases compared to Controls. Diagnostic validity tests showed that, Apo B , Apo A1 and Apo B /Apo A1 ratio have highest Sensitivity, Specificity and Diagnostic efficiency. Apo B , Apo A1 and Apo B / Apo A1 ratio can be used as predictors of stroke along with traditional lipid profile components.

Lipoprotein metabolism in nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD), an escalating health problem worldwide, covers a spectrum of pathologies characterized by fatty accumulation in hepatocytes in early stages, with potential progression to liver inflammation, fibrosis, and failure. A close, yet poorly understood link exists between NAFLD and dyslipidemia, a constellation of abnormalities in plasma lipoproteins including triglyceride-rich very low density lipoproteins. Apolipoproteins are a group of primarily liver-derived proteins found in serum lipoproteins; they not only play an extracellular role in lipid transport between vital organs through circulation, but also play an important intracellular role in hepatic lipoprotein assembly and secretion. The liver functions as the central hub for lipoprotein metabolism, as it dictates lipoprotein production and to a significant extent modulates lipoprotein clearance. Lipoprotein metabolism is an integral component of hepatocellular lipid homeostasis and is implicated in the pathogenesis, potential diagnosis, and treatment of NAFLD.

Extracellular Nucleotides Inhibit Insulin Receptor Signaling, Stimulate Autophagy and Control Lipoprotein Secretion

Hyperglycemia is associated with abnormal plasma lipoprotein metabolism and with an elevation in circulating nucleotide levels. We evaluated how extracellular nucleotides may act to perturb hepatic lipoprotein secretion. Adenosine diphosphate (ADP) (>10 µM) acts like a proteasomal inhibitor to stimulate apoB100 secretion and inhibit apoA-I secretion from human liver cells at 4 h and 24 h. ADP blocks apoA-I secretion by stimulating autophagy. The nucleotide increases cellular levels of the autophagosome marker, LC3-II, and increases co-localization of LC3 with apoA-I in punctate autophagosomes. ADP affects autophagy and apoA-I secretion through P2Y13. Overexpression of P2Y13 increases cellular LC3-II levels by ∼50% and blocks induction of apoA-I secretion. Conversely, a siRNA-induced reduction in P2Y13 protein expression of 50% causes a similar reduction in cellular LC3-II levels and a 3-fold stimulation in apoA-I secretion. P2Y13 gene silencing blocks the effects of ADP on autophagy and apoA-I secretion. A reduction in P2Y13 expression suppresses ERK1/2 phosphorylation, increases the phosphorylation of IR-β and protein kinase B (Akt) >3-fold, and blocks the inhibition of Akt phosphorylation by TNFα and ADP. Conversely, increasing P2Y13 expression significantly inhibits insulin-induced phosphorylation of insulin receptor (IR-β) and Akt, similar to that observed after treatment with ADP. Nucleotides therefore act through P2Y13, ERK1/2 and insulin receptor signaling to stimulate autophagy and affect hepatic lipoprotein secretion.

Is combination therapy an effective way of reaching lipid goals in Type 2 diabetes mellitus?

Type 2 diabetes mellitus is associated with a specific pattern of plasma lipid and lipoprotein abnormalities. Lipid goals are often not attained with statins alone, and combination lipid-lowering strategies may need to be considered in an attempt to further reduce the residual cardiovascular risk. Combination therapy utilizes various classes of lipid-lowering medications with different mechanisms of action and different effects on lipid levels. Clinical trial data support the efficacy of combining statins with fibrates, niacin, ezetimibe (cholesterol absorption inhibitor) and colesevelam (bile acid sequestrant) with the caveat that there are insufficient clinical trial data to show a further robust benefit on cardiovascular outcomes. Of the different combination therapy options to potentiate low-density lipoprotein cholesterol lowering in combination with a statin, colesevelam provides additional beneficial effects by further reducing hemoglobin A1c levels in Type 2 diabetes mellitus.

Evolution of Lipid Profiles after Bariatric Surgery

The most commonly encountered dyslipidemia in obese individuals is characterized by a cluster of interrelated plasma lipid and lipoprotein abnormalities including hypertriglyceridemia, low HDL cholesterol values, and increased small, dense LDL cholesterol particles. The aim of this study was to assess the changes in lipid profiles at baseline (pre-operatively) and at follow-up (6, 12, and 18months) after a laparoscopic Roux-en-Y gastric bypass (LRYGBP). A retrospective observational study was performed involving all patients who consecutively underwent a LRYGBP between January 1, 2007 and December 31, 2009. Fasting lipids sub-fractions (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides) were measured and HOMA-IR calculated pre-operatively and at follow-up post-LRYGBP. Pearson's correlation coefficients were used to assess the relationship between excess weight loss (EWL) and lipid sub-fractions. ANOVA was used to assess the differences between each lipid sub-fraction at various time-points. One hundred twenty eight (N = 128) medical charts were reviewed, and those containing data on lipid fractions at the three follow-up time-points were analyzed. One hundred fourteen patients (N = 114), 84 of whom were women (73.7%), were finally included in the study. Total cholesterol, LDL cholesterol, triglycerides, and HOMA-IR were significantly reduced after LRYGBP (P < 0.0005 for all). Inversely, HDL cholesterol disclosed a significant rise (P < 0.0005). Noteworthy significant associations between lipid subfractions and EWL were detected overall (P < 0.0005 for all). A gender effect was found since female patients displayed a milder association than male patients (P < 0.0005). LRYGBP-induced weight loss improves the lipid profile while reducing insulin resistance, with male patients showing a better profile than female patients.

Effects of hypolipidemic and hypoglycemic agents on atherogenic small, dense LDL in Type 2 diabetes

Type 2 diabetes is associated with a cluster of inter-related plasma lipid and lipoprotein abnormalities, including reduced HDL-C, a predominance of small, dense LDL and elevated triglycerides. These abnormalities occur even in prediabetes, before blood sugars rise sufficiently in order to confirm a diagnosis of diabetes, and this transition phase incurs important cardiovascular risk. This is the rationale for paying attention to dyslipidemia through the use of the hypolipidemic, rather than hypoglycemic drugs only. A literature search (by Medline and Scopus) was performed. The authors also manually reviewed the references of selected articles for any pertinent material. Beyond the ‘quantity’ of LDL, several lipid-lowering agents and particularly statins, are only in part beneficial on the ‘quality’ of LDL, so that their net effect on small, dense LDL is moderate. Among hypoglycemic agents, insulin and metformin have shown a limited role on small, dense LDL, while pioglitazone is more beneficial. The effi...

慢性腎不全患者― 特にCAPD患者におけるLp(a)リポ蛋白の検討

Cerebrovascular and cardiovascular diseases are important predictors for survival in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), and account for about half the deaths in these patients. Lipoprotein(a) [Lp(a)] is known to show high values in diabetics with proteinuria, and albuminuric renal disease. The purpose of this study was to determine Lp(a) levels and to investigate the association of Lp(a) and atherosclerotic risk factors in patients treated by CAPD. Lp(a) concentration were measured in 20 CAPD patients in the age range 31 to 83 years. Mean (+/- SD) levels of serum Lp(a) were elevated in the CAPD patients compared to age, sex matched 17 controls (49.5 +/- 27.7 vs. 15.5 +/- 12.4 mg/dl, p < 0.001). The levels of Lp(a) were significantly higher in the diabetic CAPD patients than in non-diabetics. There were significant positive correlations between serum Lp(a) concentrations and fasting blood sugar. However, when the above two groups were matched for age, sex, body mass index and FBS, Lp(a) concentrations were also significantly higher in CAPD patients than those in normal controls. We found no statistically significant correlations of Lp(a) with either age, body mass index, blood pressure, serum lipoprotein, apoprotein, glycated hemoglobin, BUN, creatinine or serum protein levels. There were no correlations between serum Lp(a) levels and albumin and LP(a) concentrations in the dialysate in all CAPD patients. Along with assessment of other known established cardiovascular risk factors such as elevated blood pressure, atherogenic abnormalities of plasma lipids and lipoproteins, and impaired glucose tolerance, we suggest that elevated levels of Lp(a) may lead to the accelerated atherosclerosis in these patients.

In Vitro and in Vivo Analysis of the Binding of the C Terminus of the HDL Receptor Scavenger Receptor Class B, Type I (SR-BI), to the PDZ1 Domain of Its Adaptor Protein PDZK1

The PDZ1 domain of the four PDZ domain-containing protein PDZK1 has been reported to bind the C terminus of the HDL receptor scavenger receptor class B, type I (SR-BI), and to control hepatic SR-BI expression and function. We generated wild-type (WT) and mutant murine PDZ1 domains, the mutants bearing single amino acid substitutions in their carboxylate binding loop (Lys(14)-Xaa(4)-Asn(19)-Tyr-Gly-Phe-Phe-Leu(24)), and measured their binding affinity for a 7-residue peptide corresponding to the C terminus of SR-BI ((503)VLQEAKL(509)). The Y20A and G21Y substitutions abrogated all binding activity. Surprisingly, binding affinities (K(d)) of the K14A and F22A mutants were 3.2 and 4.0 μM, respectively, similar to 2.6 μM measured for the WT PDZ1. To understand these findings, we determined the high resolution structure of WT PDZ1 bound to a 5-residue sequence from the C-terminal SR-BI ((505)QEAKL(509)) using x-ray crystallography. In addition, we incorporated the K14A and Y20A substitutions into full-length PDZK1 liver-specific transgenes and expressed them in WT and PDZK1 knock-out mice. In WT mice, the transgenes did not alter endogenous hepatic SR-BI protein expression (intracellular distribution or amount) or lipoprotein metabolism (total plasma cholesterol, lipoprotein size distribution). In PDZK1 knock-out mice, as expected, the K14A mutant behaved like wild-type PDZK1 and completely corrected their hepatic SR-BI and plasma lipoprotein abnormalities. Unexpectedly, the 10-20-fold overexpressed Y20A mutant also substantially, but not completely, corrected these abnormalities. The results suggest that there may be an additional site(s) within PDZK1 that bind(s) SR-BI and mediate(s) productive SR-BI-PDZK1 interaction previously attributed exclusively to the canonical binding of the C-terminal SR-BI to PDZ1.

Management of dyslipidemia in people with type 2 diabetes mellitus

Cardiovascular disease is a major complication of type 2 diabetes mellitus, and this is partly due to associated abnormalities of plasma lipid and lipoprotein metabolism. Although glycemic control improves plasma lipoprotein abnormalities and may have an independent benefit on cardiovascular risk reduction, the magnitude of this benefit is less than cholesterol lowering therapy. Current treatment guidelines for the management of dyslipidemia in people with type 2 diabetes are based on the results of cardiovascular outcome clinical trials. Primary emphasis of treatment should be on lowering LDL-C to < 100 mg/dl with statins. If cardiovascular disease is present, then high dose statins should be used, and an optional LDL-C goal < 70 is recommended. If triglycerides are > 200 mg/dl, then a secondary goal is to lower non-HDL-C < 130 mg/dl (< 100 mg/dl if cardiovascular disease is present) is recommended. Low HDL-C levels are common in type 2 diabetes but are not currently recommended as a target for treatment because of the lack of definitive cardiovascular outcome studies supporting this goal, and because of the difficulty in raising HDL-C. The additional benefit of combination therapy with fibrates, ezetimibe or niacin added to a statin on cardiovascular risk is uncertain pending the results of on-going cardiovascular outcome studies.

Smoking Gain?: Secondhand Smoke Exposure Influences Body Weight, Lipid Profiles in Offspring

Vol. 117, No. 7 NewsOpen AccessSmoking Gain?: Secondhand Smoke Exposure Influences Body Weight, Lipid Profiles in Offspring Victoria McGovern Victoria McGovern Search for more papers by this author Published:1 July 2009https://doi.org/10.1289/ehp.117-a310aCited by:1AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit An estimated 780,000 U.S. women continue smoking throughout pregnancy each year despite warnings about the elevated risk of birth defects in the children of female smokers. A new mouse study provides experimental evidence that exposure to secondhand cigarette smoke during pregnancy may lead to weight gain in offspring as well as changes in lipid profiles that may increase the chances of cardiovascular disease later in life [EHP117:1042–1049; Ng et al.].Oxidants in cigarette smoke have previously been shown to promote local and systemic inflammation and increase the risk of cardiovascular disease in both smokers and those exposed to secondhand smoke. Lipid oxidation in particular has been associated with cardiovascular diseases. Women have a higher risk of dying from cardiovascular disease than men and are more likely to die following a heart attack.The current study may shed light on this observed sex-specific difference. Female pups of mice that were exposed to cigarette smoke for 4 hours a day, 5 days a week, throughout pregnancy grew up to have a higher body weight than their unexposed peers and had significant increases in plasma high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total protein. However, these differences were not observed when the adult female offspring were fed a high-fat diet instead of a regular diet. On the other hand, smoke-exposed male pups gained more weight and displayed altered lipid profiles compared with their sex-matched, unexposed counterparts when they were fed a high-fat diet but showed little evidence of an effect of smoke exposure when fed a normal diet.Although maternal exposure to cigarette smoke appeared to influence weight gain and lipid profiles in their offspring, lipid parameters in the dams themselves showed little change in response to smoke exposure. Additional work is necessary to understand why lipoprotein levels—which reflect cholesterol metabolism—are altered in the offspring in response to cigarette smoke exposure during pregnancy.Abnormal body weight and dyslipidemia (abnormal plasma lipoprotein levels) are among the best-established risk factors for cardiovascular diseases. Although the new study does not investigate the mechanisms of the observed changes, it does suggest that prevention programs that emphasize avoidance of cigarette smoke during pregnancy could reap long-range health benefits for the newborn.FiguresReferencesRelatedDetailsCited by Hang B, Snijders A, Huang Y, Schick S, Wang P, Xia Y, Havel C, Jacob P, Benowitz N, Destaillats H, Gundel L and Mao J (2017) Early exposure to thirdhand cigarette smoke affects body mass and the development of immunity in mice, Scientific Reports, 10.1038/srep41915, 7:1, Online publication date: 1-Dec-2017. Vol. 117, No. 7 July 2009Metrics About Article Metrics Publication History Originally published1 July 2009Published in print1 July 2009 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.