Journal of Lipids

Lipid oxidation has been identified as a major deterioration process of vegetable oils, which leads to the production of primary and secondary oxidative compounds that are harmful to human health. Oleoresins of ginger, garlic, nutmeg, pepper, cloves, and cinnamon were extracted and incorporated into coconut oil, and change occurrence on physicochemical properties, thermal stability, shelf life, and antioxidant activity was monitored against the same properties of pure coconut oil. Lipid oxidation was assessed in terms of the free fatty acid level and peroxide value. For the comparison purpose, another oil sample was prepared by incorporating vitamin E too. Results revealed that both peroxide value and FFA of pure and flavored coconut oil samples after a one-week storage period were and  mEq/kg and and (%), respectively. Saponification value, iodine value, smoke point, and the flashpoint of flavored oil were decreased while increasing the viscosity during storage. The highest phenolic content and DPPH free radical scavenging activity were found in flavored coconut oil. Since spices containing antioxidants, the thermal stability of flavored oil was better than that of pure coconut oil. Both oleoresins and vitamin E-incorporated samples showed the same pattern of increment of FFA and peroxide value during storage; however, those increments were slower than those of pure coconut oil.

Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

We examined the effects of unsaturated fatty acid (UFA) species and their concentration on the expression of OLE1, which encodes the stearoyl CoA desaturase, in Saccharomyces cerevisiae. We controlled the amount of UFA taken up by the cell by varying the concentration of tergitol in the medium. When cultured with 1 mM fatty acid in 0.1% tergitol, cells took up much more fatty acid than when cultured with the same concentration of fatty acid at 1% tergitol, although the amount incorporated was dependent on UFA species. For each fatty acid tested, we found that the higher uptake (0.1% tergitol condition) had a stronger impact on OLE1 regulation. A principal product of the desaturase 16:1∆9, and the nonnative UFA 18:2∆9,12, most strongly repressed the reporter construct OLE1-lacZ transcription, while the other major product of the desaturase, 18:1∆9, and the nonnative UFA 17:1∆10 caused a more diminished response. Based on these results, our initial hypothesis was that OLE1 was regulated in response to membrane fluidity; however, subsequent work does not support that idea; we have found that conditions that affect membrane fluidity such as growth temperature and growth with saturated or trans fatty acid supplementation, do not regulate OLE1 in the direction predicted by fluidity changes. We conclude that at least one signal that regulates OLE1 transcriptional expression is most likely based on the fatty acids themselves.

Dyslipidemia is an important cause of cardiovascular diseases (CVDs), which are the most prevalent causes of morbidity and mortality. The purpose of this study was to assess the effects of cinnamon on body weight gain, food intake, and serum lipid profiles of albino rats. This study was conducted on 30 healthy male albino rats weighing approximately 130 ± 5 g. The study was divided into the following two experiments: experiment (1), wherein rats were fed a laboratory diet; and experiment (2), wherein rats were fed a high-fat diet. In experiment 1, a total of 15 rats were divided into three groups. Group A (, untreated control) was fed laboratory diet, Group B was fed laboratory diet and cinnamon powder (2 g/kg body weight), and Group C was fed laboratory diet and cinnamon powder (4 g/kg body weight) for 30 days. In experiment (2), a total of 15 rats were similarly divided into three groups. Group D (, treated control) was fed laboratory diet plus high-fat diet, Group E was fed cinnamon powder (2 g/kg body weight) mixed with laboratory diet plus high-fat diet, and Group F was fed cinnamon powder (4 g/kg body weight) mixed with laboratory diet plus high-fat diet daily for 30 days. An administration of 4 g/kg body weight of cinnamon extract powder decreased the final weight by 4.4%, body weight gains by 31.41%, food intake by 1.7%, and food efficiency ratio by 22.38% in hypercholesterolemic adult male rats as well as serum total cholesterol by 31.22%, triglyceride by 24.05%, and LDL-C by 43.49%, with an increase in the levels of HDL-C by 30.16%, furthermore, a significant decrease in serum total cholesterol, triglycerides, and LDL-C levels and increasing serum HDL-C on day 30 were observed . This finding provides scientific evidence to substantiate the traditional use of cinnamon to treat hyperlipidemia.

Introduction. Dyslipidemia is the most important modifiable risk factor that leads to cardiovascular diseases. The screening for dyslipidemia in Palestine is not established in primary health care centers for healthy people. Our study aims to determine the prevalence of dyslipidemia among healthy undiagnosed adult men in Palestine in order to assess the need for screening and preventive programs for dyslipidemia. Materials and Methods. A cross-sectional observational study was carried out in 10 secondary schools at Nablus municipality (Palestine) from August 2017 to February 2018. The study included 140 teachers based on sample calculations. The age of participants ranged between 24 and 60 years. A questionnaire was used to collect demographic data about the lifestyle, past medical, and family histories. Serum lipid profile, and fasting blood glucose levels for each participant were measured. Lipoprotein levels were categorized based on the adult treatment panel III criteria. Results. The overall prevalence of dyslipidemia among Palestinian men was 66.4%. The most prevalent type of dyslipidemia was hypo HDL ( < 40 mg/dl, 59.3%), followed by hypertriglyceridemia ( ≥ 200 mg/dl, 20%). The prevalence of hyper LDL ( ≥ 160 mg/dl), hypercholesterolemia ( ≥ 240 mg/dl) was 8.5%, and 3.6%, respectively. About 15% of participants had glucose intolerance, and 4.3% had hyperglycemia (undiagnosed). Those with glucose intolerance, 13 (9.2%) have hypo HDL, while 9 (6.42%) have hypertriglyceridemia. On the other hand, out of hyperglycemic patients: 5 (3.5%) had hypo HDL, and 1 (0.7%) had hypertriglyceridemia. Conclusion. Around two-thirds of undiagnosed participants had at least one lipid abnormality. None of them were aware of having dyslipidemia. The prevalence of undiagnosed dyslipidemia was higher than the prevalence of undiagnosed glucose intolerance, and diabetes. This suggests that dyslipidemia plays a major role in developing diabetes. Hence, profound efforts should be done to manage and treat those with dyslipidemia, in order to prevent progression to type II diabetes mellitus.

Background. The apolipoprotein E (APOE) polymorphisms are associated with cardiovascular (CV) disease, but its interaction with type 2 diabetes mellitus (T2DM) long-term incidence is unknown. We investigated the association between APOE genotype and long-term (i) CV events and (ii) T2DM incidence in a Southern European primary prevention cohort. Methods. We assessed individual APOE genotypes in a total of 436 patients followed at a lipid clinic, with a 15-year median follow-up time. We collected data on major CV events (CV death, myocardial infarction, and stroke) and T2DM development. Results. No differences were found regarding major CV event incidence among the different APOE genotypes. However, after excluding 39 patients with a prior history of T2DM, APOE2 carriers displayed a higher incidence of T2DM during follow-up (42.2%) than APOE3 (27.1%) and APOE4 (28.7%) carriers. The age-, sex-, triglycerides-, and statin usage-adjusted OR for T2DM incidence in APOE2 carriers was 1.8 (95%CI 1.1-2.9, p=0.03), compared with wild-type APOE3. To address the role of statins as a confounder, we analyzed T2DM incidence in statin-treated patients. Statin-treated APOE2 carriers also had a higher T2DM incidence (57.9%), in comparison with APOE3 homozygotes (31.6%) and APOE4 carriers (32.5%). After adjustment for confounding, APOE2 carriers on statins displayed a similar twofold increase in T2DM risk compared to APOE3 homozygotes (OR 2.1, 95%CI 1.1-4.0, p=0.03). Conclusion. Our findings suggest a twofold increase in T2DM incidence in APOE2 carriers. This may prompt for a specific glucose dysmetabolism follow-up that might be tailored on the APOE genotype.