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Cannabis effects on lipoproteins.
Lazarte, J, Hegele, RA
Current opinion in lipidology. 2019;(2):140-146
Abstract
PURPOSE OF REVIEW The endocannabinoid system affects several physiological functions. A family of endocannabinoid receptors is susceptible to cannabis constituents. Cannabis is widely used in our society and following its recent legalization in Canada, we focus on how exposure to cannabis and pharmacologic cannabinoid receptor type 1 (CB1) inhibition affect lipoprotein levels. RECENT FINDINGS Several groups have reported that exposure to cannabis does not increase weight despite the marked increase in caloric intake. In observational studies, the effect of smoked cannabis exposure on plasma lipids is variable. Some studies in specific patient populations with longer exposure to cannabis seemed to identify slightly more favorable lipoprotein profiles in the exposed group. Several larger controlled clinical trials using orally administered rimonabant, a CB1 receptor antagonist, have consistently shown relative improvements in weight and plasma levels of triglyceride and high-density lipoprotein cholesterol among patients receiving the treatment. SUMMARY The widely variable findings on the relationship of cannabis in various forms with plasma lipids preclude any definitive conclusions. Cannabis has complex effects on the cardiovascular system and its effects on lipid profile must be considered in this overall context. Further properly controlled research is required to better understand this topic.
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Ratio of triglyceride to high-density lipoprotein cholesterol and risk of major cardiovascular events in kidney transplant recipients.
Kim, JE, Yu, MY, Kim, YC, Min, SI, Ha, J, Lee, JP, Kim, DK, Oh, KH, Joo, KW, Ahn, C, et al
Clinical and experimental nephrology. 2019;(12):1407-1417
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Abstract
BACKGROUND Dyslipidemia is common in kidney transplant (KT) recipients. We analyzed the ratio of triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) in KT recipients to identify risk factors for major cardiovascular events (MACE). METHODS We retrospectively included KT recipients with a lipid profile performed 1 year after transplantation. We classified patients according to the TG/HDL-C divided into quintiles. Subsequently, we analyzed the association between TG/HDL-C and MACE, defined as heart failure, coronary artery disease, and cerebrovascular disease confirmed by imaging studies. RESULTS A total of 1301 KT recipients were enrolled. The median follow-up duration was 7.4 years (interquartile range 4.4-11.1 years). During the follow-up period, 80 (6.2%) patients developed MACE, which included 38 of unstable anginas, 9 of MIs, 19 of heart failures, 18 of cerebral infarcts, and 4 of cerebral hemorrhages. The fourth and fifth quintiles of TG/HDL-C showed a significantly increased risk of MACE [fourth quintile: adjusted hazard ratio (aHR), 3.38; 95% confidence interval (CI) 1.44-7.95; p = 0.005, fifth quintile: aHR, 2.67; 95% CI 1.13-6.30; p = 0.02]) compared to the second quintile of TG/HDL-C. This association is particularly evident in subgroups of non-DM, HTN, no history of CVD, and statin users. CONCLUSIONS Higher TG/HDL-C levels may be associated with MACE risk in KT recipients.
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2018 Guidelines for the management of dyslipidemia.
Rhee, EJ, Kim, HC, Kim, JH, Lee, EY, Kim, BJ, Kim, EM, Song, Y, Lim, JH, Kim, HJ, Choi, S, et al
The Korean journal of internal medicine. 2019;(4):723-771
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The role of the triglyceride (triacylglycerol) glucose index in the development of cardiovascular events: a retrospective cohort analysis.
Li, S, Guo, B, Chen, H, Shi, Z, Li, Y, Tian, Q, Shi, S
Scientific reports. 2019;(1):7320
Abstract
This study aimed to evaluate the role of the triglyceride (triacylglycerol) glucose (TyG) index in predicting and mediating the development of cardiovascular disease (CVD). This cohort study included 6078 participants aged over 60 years who participated in a routine health check-up programme from 2011 to 2017. The competing risk model, cox regression model and multimediator analyses were performed. TyG was calculated as ln [fasting triglyceride (mg/dl) × fasting plasma glucose (mg/dl)/2]. During a median 6 years of follow-up, 705 (21.01/1000 person-years) CVD events occurred. In fully adjusted analyses, quartiles 3 and 4 versus quartile 1 of TyG index (adjusted subhazard ratios [SHRs] 1.33 [95% CI: 1.05-1.68] and 1.72 [1.37-2.16]) were associated with an increased risk of CVD events. The continuous time-dependent TyG remained significant in predicting CVD events (adjusted hazard ratios [HR] 1.43 [1.24-1.63]). The adverse estimated effects of body mass index (BMI) or resting heart rate (RHR) on CVD mediated through the joint effect of the baseline and follow-up TyG index. In addition, an effect mediated only through the follow-up TyG existed (P < 0.05). Thus, it is necessary to routinely measure the TyG. The TyG index might be useful for predicting CVD events in clinical practice.
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Gastrointestinal motility, gut hormone secretion, and energy intake after oral loads of free fatty acid or triglyceride in older and middle-aged men.
Madsen, JL, Damgaard, M, Fuglsang, S, Dirksen, C, Holst, JJ, Graff, J
Appetite. 2019;:18-24
Abstract
In young individuals, oral free fatty acid delays gastric emptying, promotes gut hormone release, and reduces energy intake more than an isocaloric load of triglyceride does. The objective of this study was to compare the effects of the free fatty acid oleic acid (OA) and the triglyceride olive oil (OO) on gastrointestinal motility, gut hormone secretion, and energy intake in older and middle-aged healthy volunteers. In a double-blind, randomized, cross-over, study 10 older (age 83.0 ± 3.4 (mean ± SD) years) and 10 middle-aged (age 43.1 ± 8.9 years) men were examined on two occasions to evaluate the effect of isocaloric and isovolaemic loads of radiolabelled OA or OO on gastric emptying, oro-caecal transit, glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) secretions, and energy intake. Gastric emptying was slower in older than in middle-aged men (lipid p < 0.001, water p = 0.010), while no difference between these groups was found for oro-caecal transit. In comparison with OO, OA caused slower gastric emptying (lipid p < 0.001, water p = 0.020) and faster oro-caecal transit (p = 0.025). Postprandial secretion of GLP-1 and PYY was comparable for older and middle-aged men, as well as for OA and OO. Older men ingested less energy than middle-aged men did (p < 0.001) and their energy intake was lower after OA than OO (p = 0.002). Thus, gastric emptying of an oral lipid load is slower in older than in middle-aged men; gastric emptying is slower and oro-caecal transit faster after OA than OO in both age groups; and older men ingest less energy than middle-aged men and less energy after OA than OO.
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TIMD4 rs6882076 SNP Is Associated with Decreased Levels of Triglycerides and the Risk of Coronary Heart Disease and Ischemic Stroke.
Khounphinith, E, Yin, RX, Cao, XL, Huang, F, Wu, JZ, Li, H
International journal of medical sciences. 2019;(6):864-871
Abstract
Background: The T-cell immunoglobulin and mucin domain 4 gene (TIMD4) rs6882076 single nucleotide polymorphism (SNP) has been associated with serum total cholesterol, low-density lipoprotein cholesterol and triglycerides (TG) levels, but the results are inconsistent. Moreover, little is known about such association in Chinese populations. The aim of this study was to detect the association of the TIMD4 rs6882076 SNP and serum lipid levels and the risk of coronary heart disease (CHD) and ischemic stroke (IS) in a Southern Chinese Han population. Methods: Genotypes of the TIMD4 rs6882076 SNP in 1765 unrelated subjects (CHD, 581; IS, 559 and healthy controls, 625) were determined by the Snapshot Technology. Results: The genotypic and allelic frequencies of the TIMD4 rs6882076 SNP were different between the CHD/IS patients and controls (P < 0.05 for all). The subjects with CT/TT genotypes were associated with decreased risk of CHD (P = 0.014 for CT/TT vs. CC genotypes, P = 0.010 for T vs. C alleles) and IS (P = 0.003 for CT/TT vs. CC genotypes; P = 0.016 for T vs. C alleles). The T allele carriers in healthy controls were also associated with decreased levels of serum TG. Conclusions: The results of the present study suggest that the TIMD4 rs6882076 SNP is associated with decreased risk of CHD and IS in our study population. It is likely to decrease the CHD and IS risk by reducing serum TG levels.
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Postprandial lipaemia 10 and 34 hours after playing football: Does playing frequency affect the response?
Paul, DJ, Nassis, GP, Kerouani, AC, Bangsbo, J
PloS one. 2019;(7):e0218043
Abstract
Elevated postprandial triglyceride (TG) is associated with increased risk of cardiovascular disease. The time window for the last bout beneficial effect on postprandial lipaemia after football play is unknown. The aim of the present study was to examine whether playing affects postprandial TG during 1.5 day of reduced activity. Eighteen males were randomly allocated to perform either 1 (1FOOT; n = 9; age = 33.0 ± 5.0 yrs; body mass index = 24.2 ± 3.6 kg/m2) or 3 (3FOOT) consecutive days of 60-min 5 vs 5 football (n = 9; age = 32.8 ± 5.2 yrs; body mass index = 26.2 ± 4.1 kg/m2) matches across a 5-day study period. They arrived to the laboratory 10 hrs and 34 hrs after the final football session and blood samples were collected at fasted (0 min) and 45, 90, 240 and 360 min post a high fat load meal. There were non significant increase for postprandial TG AUC (9.1%; p = 0.17; 95%CI = -0.43 to 2.0; ES = -0.23) and iAUC (14.2%; p = 0.43; 95%CI = -0.92 to 1.9; ES = -0.24) between 10 and 34 hrs after the 1FOOT. For the 3FOOT, there was a non significant decrease in postprandial TG AUC (-2.7%; p = 0.73; 95%CI = -2.0 to 1.5; ES = 0.05) and iAUC (-17.5%; p = 0.41; 95%ci = -2.5 to 1.1; ES = 0.31) from 10 to 34 hrs, respectively. Performing three consecutive days of football exercise may offer no greater protective effect for postprandial TG before a period of reduced activity, compared to a single session.
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Contribution of Liver Fat to Weight Loss-Induced Changes in Serum Hepatokines: A Randomized Controlled Trial.
Telgenkamp, I, Kusters, YHAM, Schalkwijk, CG, Houben, AJHM, Kooi, ME, Lindeboom, L, Bons, JAP, Schaper, NC, Joris, PJ, Plat, J, et al
The Journal of clinical endocrinology and metabolism. 2019;(7):2719-2727
Abstract
CONTEXT Hepatokines have emerged as potential mediators of obesity-associated comorbidities, such as type 2 diabetes, cardiovascular disease, fractures, and central hypogonadism. OBJECTIVE To assess whether weight loss-induced changes in hepatokines are mediated by intrahepatic triglyceride (IHTG) content. DESIGN Cross-sectional study and randomized controlled trial. SETTING General community. PARTICIPANTS Metabolically healthy, lean men (waist <94 cm; n = 25) and men with abdominal obesity (waist 102 to 110 cm; n = 52). INTERVENTION Men with abdominal obesity were randomized to 8-week dietary weight loss or no weight loss. MAIN OUTCOME MEASURES IHTG and serum hepatokines, that is, serum IGF1, IGF binding protein 1 (IGFBP1), SHBG, fibroblast growth factor 21 (FGF21), fetuin A, and plasma fetuin B. RESULTS All hepatokines, except for fetuin B, were significantly different between lean men and men with obesity. After the weight-loss intervention (-10.3 kg; 95% CI, -11.4 to-9.2), serum IGF1, IGFBP1, SHBG, and fetuin A approached the values observed in lean men. Cross-sectional associations were observed between IHTG and IGF1 (β = -0.51; 95% CI, -0.82 to -0.20), IGFBP1 (β = -4.2; 95% CI, -7.7 to -0.7), and FGF21 (β = 2.1; 95% CI, 1.3 to 2.9) in lean men and men with abdominal obesity combined. Weight loss resulted in a reduction of IHTG (treatment effect, -2.2%; 95% CI, -3.4% to -1.2%) that was associated with a change in IGF1 (β = -0.9; 95% CI, -1.3 to -0.4), IGFBP1 (β = -0.17; 95% CI, -0.31 to -0.03), and SHBG levels (β = -0.18; 95% CI, -0.29 to -0.07). Mediation analyses showed that only the weight loss-induced change in serum IGF1 was mediated by IHTG (mediated effect, 32.7%; 95% CI, 4.6% to 79.2%). CONCLUSIONS Dietary weight loss has differential effects on hepatokines. This study shows that the change in serum IGF1 levels after dietary weight loss is mediated by the change in IHTG content.
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Effects of Ramadan intermittent fasting on lipid and lipoprotein parameters: An updated meta-analysis.
Mirmiran, P, Bahadoran, Z, Gaeini, Z, Moslehi, N, Azizi, F
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2019;(9):906-915
Abstract
AIMS: This systematic review and meta-analysis aimed to clarify several aspects of intermittent fasting during the month of Ramadan on lipid and lipoprotein levels in apparently healthy subjects. DATA SYNTHESIS We searched PubMed, Scopus, and Embase databases and the reference lists of previous reviews, up to Feb 2019 for studies that investigated the effects of Ramadan fasting on fasting levels of triglycerides (TG), total cholesterol (TC), HDL-C, LDL-C, and VLDL-C among healthy subjects including pregnant women and athletic subjects. Studies were selected for quality assessment, meta-analyses, subgroup analyses, and meta-regressions; data of 33 eligible studies, conducted between 1978 and 2019, were included in the analysis. RESULTS Intermittent fasting showed no significant effect on circulating TG (WMD = -0.38 mg/dl, 95% CI = -5.33, 4.57), TC (WMD = -1.58 mg/dl, 95% CI = -6.04, 2.88), and LDL-C levels (WMD = 1.85 mg/dl, 95% CI = 0.77, 2.92). Overall, HDL-C (WMD = -2.97 mg/dl; 95% CI = -6.43, 0.48 mg/dl) and VLDL-C (WMD = -1.41 mg/dl; 95% CI = -2.73, -0.10 mg/dl) significantly decreased after Ramadan fasting. A significant increase in LDL-C levels was observed in athletic subjects (WMD = 2.97 mg/dl; 95% CI = 0.80, 5.13) and apparently healthy subjects (WMD = 1.81 mg/dl; 95% CI = 0.55, 3.07). Change in TG levels was associated with age (β = -0.94, P = 0.043), its baseline values (β = -0.44, P = 0.001), and weight change during the fasting period (β = -0.57, P = 0.032). CONCLUSION Ramadan fasting may be accompanied by a moderate improvement of lipid and lipoprotein parameters, especially HDL-C levels; fasting appears to be more beneficial for men and athletic subjects.
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Elevated Serum Non-HDL (High-Density Lipoprotein) Cholesterol and Triglyceride Levels as Residual Risks for Myocardial Infarction Recurrence Under Statin Treatment.
Suzuki, K, Oikawa, T, Nochioka, K, Miura, M, Kasahara, S, Sato, M, Aoyanagi, H, Shiroto, T, Takahashi, J, Miyata, S, et al
Arteriosclerosis, thrombosis, and vascular biology. 2019;(5):934-944
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Abstract
Objective- Secondary prevention for recurrent myocardial infarction (MI) is one of the most important therapeutic goals in patients with old MI (OMI). Although statins are widely used for this purpose, there remains considerable residual risk even after LDL (low-density lipoprotein cholesterol) is well controlled by statins. Approach and Results- We examined clinical impacts of nHDL (nonhigh-density lipoprotein cholesterol) and its major components triglyceride and LDL as residual risks for acute MI recurrence, using the database of our CHART (Chronic Heart Failure Analysis and Registry in the Tohoku District)-2 Study, the largest-scale cohort study of cardiovascular patients in Japan. We enrolled 1843 consecutive old MI patients treated with statins (mean age 67.3 years, male 19.2%) in the CHART-2 Study. The incidence of recurrent acute MI during the median 8.6-year follow-up was compared among the groups divided by the levels of nHDL (<100, 100-129, and ≥130 mg/dL), LDL (<70, 70-99, and ≥100 mg/dL), triglyceride (<84, 84-149, and ≥150 mg/dL), and combination of LDL and triglyceride. Kaplan-Meier curves and multiple Cox proportional hazards models showed that higher levels of nHDL, but not LDL or triglyceride alone, were associated with higher incidence of recurrent acute MI. Furthermore, higher triglyceride levels were associated with higher incidence of recurrent MI in patients with LDL <100 mg/dL but not in those with LDL ≥100 mg/dL. Conclusions- These results indicate that management of residual risks for acute MI recurrence should include nHDL management considering both LDL and triglyceride in old MI patients under statin treatment. Clinical Trial Registration- URL: http://www.clinicaltrials.gov . Unique identifier: NCT00418041.