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Disparities in cardio metabolic risk between Black and White women with polycystic ovary syndrome: a systematic review and meta-analysis.
Kazemi, M, Kim, JY, Parry, SA, Azziz, R, Lujan, ME
American journal of obstetrics and gynecology. 2021;(5):428-444.e8
Abstract
OBJECTIVE We conducted a systematic review and meta-analysis to summarize and quantitatively pool evidence on cardiometabolic health disparities between Black and White women with polycystic ovary syndrome in the United States in response to the call for further delineation of these disparities in the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. DATA SOURCES Databases of MEDLINE, Web of Science, and Scopus were searched initially through March 05, 2020, and confirmed on September 11, 2020. STUDY ELIGIBILITY CRITERIA Observational studies documenting cardiometabolic risk profile (glucoregulatory, lipid profile, anthropometric, and blood pressure status) in Black and White women with polycystic ovary syndrome were included. Studies on children (<17 years old) and pregnant or menopausal-aged women (>50 years) were excluded. The primary outcome was fasting glucose. Furthermore, data on major cardiovascular events (stroke, coronary heart disease, heart failure) and mortality rate (cardiovascular death, total mortality) were evaluated. METHODS Data were pooled by random-effects models and expressed as mean differences and 95% confidence intervals. Studies were weighted based on the inverse of the variance. Heterogeneity was evaluated by Cochran Q and I2 statistics. Study methodologic quality was assessed by the Newcastle-Ottawa scale. RESULTS A total of 11 studies (N=2851 [652 Black and 2199 White]) evaluated cardiometabolic risk profile and all had high quality (Newcastle-Ottawa scale score of ≥8). No studies reported on cardiovascular events and mortality rate. Black women had comparable fasting glucose (-0.61 [-1.69 to 2.92] mg/dL; I2=62.5%), yet exhibited increased fasting insulin (6.76 [4.97-8.56] μIU/mL; I2=59.0%); homeostatic model assessment of insulin resistance (1.47 [0.86-2.08]; I2=83.2%); systolic blood pressure (3.32 [0.34-6.30] mm Hg; I2=52.0%); and decreased triglyceride (-32.56 [-54.69 to -10.42] mg/dL; I2=68.0%) compared with White women (all, P≤.03). Groups exhibited comparable total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and diastolic blood pressure (all, P≥.06). CONCLUSIONS Black women with polycystic ovary syndrome have a greater tendency for an adverse cardiometabolic risk profile (increased insulin, homeostatic model assessment of insulin resistance, and systolic blood pressure) despite lower triglycerides than White women. Our observations support the consideration of these disparities for diagnostic, monitoring, and management practices in Black women and for future guideline recommendations. Given the heterogeneity among studies, future research should address the relative contributions of biologic, environmental, socioeconomic, and healthcare factors to the observed disparities. Furthermore, longitudinal research is required to address patient-pressing complications, including cardiovascular events and mortality rate in Black women with polycystic ovary syndrome as a high-risk yet understudied population.
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2.
THADA_rs13429458 Minor Allele Increases the Risk of Polycystic Ovary Syndrome in Asian, but Not in Caucasian Women: A Systematic Review and Meta-Analysis.
Park, S, Liu, M, Zhang, T
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2019;(10):661-670
Abstract
Polycystic ovary syndrome (PCOS) is a highly prevalent disease in young women that also features increased insulin resistance. Genetic factors have a strong relationship with the etiology of PCOS. We assessed whether carrying THADA rs13429458 is associated with the development of PCOS by meta-analysis and whether the association is influenced by ethnicity. Articles were searched using PubMed, EMBASE, Cochrane Library, Korean scientific database, and Chinese and Indian medical databases to identify all eligible studies for evaluating the association of THADA rs13429458 and PCOS risk. The association was assessed in five genetic random effects models including the allelic (AG), recessive (RG), dominant (DG), homozygous (HMG), and heterozygous (HTG) genetic models. Subgroup analyses stratified by ethnicity (Asians and non-Asians) were assessed. Nine articles were selected and 1 association analysis of Korea PCOS study met Hardy-Weinberg equilibrium criteria. A set of 38 224 PCOS women and 120 173 healthy women were included. The AG and RG showed heterogeneity in the overall and Asian subjects, but the other genetic model did not exhibit heterogeneity in all subjects. AG, RG, DG, and HMG, but not HTG, exhibited publication bias in total subjects but there was no publication bias in all genetic models among Asians and non-Asians. The overall effect of THADA_rs13429458 on PCOS risk showed significant positive associations in pooling 10 studies. In sub-group analysis only Asians, but not non-Asians, had a positive association (AG: OR=1.24, p=0.001; RG: OR=1.32, p=0.002; DG: OR, 1.70, p<0.00001; HMG: OR, 1.71, p=0.002; HTG: OR=1.34, p=0,006). In conclusions, young Asian women with the minor allele (C) for THADA rs13429458 were at increased risk of PCOS.
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Discovery and fine-mapping of loci associated with MUFAs through trans-ethnic meta-analysis in Chinese and European populations.
Hu, Y, Tanaka, T, Zhu, J, Guan, W, Wu, JHY, Psaty, BM, McKnight, B, King, IB, Sun, Q, Richard, M, et al
Journal of lipid research. 2017;(5):974-981
Abstract
MUFAs are unsaturated FAs with one double bond and are derived from endogenous synthesis and dietary intake. Accumulating evidence has suggested that plasma and erythrocyte MUFA levels are associated with cardiometabolic disorders, including CVD, T2D, and metabolic syndrome (MS). Previous genome-wide association studies (GWASs) have identified seven loci for plasma and erythrocyte palmitoleic and oleic acid levels in populations of European origin. To identify additional MUFA-associated loci and the potential functional variant at each locus, we performed ethnic-specific GWAS meta-analyses and trans-ethnic meta-analyses in more than 15,000 participants of Chinese and European ancestry. We identified novel genome-wide significant associations for vaccenic acid at FADS1/2 and PKD2L1 [log10(Bayes factor) ≥ 8.07] and for gondoic acid at FADS1/2 and GCKR [log10(Bayes factor) ≥ 6.22], and also observed improved fine-mapping resolutions at FADS1/2 and GCKR loci. The greatest improvement was observed at GCKR, where the number of variants in the 99% credible set was reduced from 16 (covering 94.8 kb) to 5 (covering 19.6 kb, including a missense variant rs1260326) after trans-ethnic meta-analysis. We also confirmed the previously reported associations of PKD2L1, FADS1/2, GCKR, and HIF1AN with palmitoleic acid and of FADS1/2 and LPCAT3 with oleic acid in the Chinese-specific GWAS and the trans-ethnic meta-analyses. Pathway-based analyses suggested that the identified loci were in unsaturated FA metabolism and signaling pathways. Our findings provide novel insight into the genetic basis relevant to MUFA metabolism and biology.
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4.
Urate transporter gene SLC22A12 polymorphisms associated with obesity and metabolic syndrome in Caucasians with hypertension.
Shafiu, M, Johnson, RJ, Turner, ST, Langaee, T, Gong, Y, Chapman, AB, Gums, JG, Johnson, JA
Kidney & blood pressure research. 2012;(6):477-82
Abstract
BACKGROUND/AIMS: Hyperuricemia is associated with obesity and the metabolic syndrome. URAT1 is a urate transporter, and we tested the association of URAT1 transporter gene (SLC22A12) polymorphisms with obesity and the metabolic syndrome in hypertensive subjects. METHODS Patients with essential hypertension (n = 414) from a randomized controlled study were genotyped for SLC22A12 SNPs rs11602903, rs505802 and rs11231825. RESULTS In Caucasians, SLC22A12 SNPs were associated with the body mass index (BMI). rs11602903 was associated with BMI (p < 0.0001), waist circumference (p = 0.003), HDL cholesterol (p = 0.018) and the metabolic syndrome (p = 0.033), and accounted for 7% of the variation of BMI in Caucasians. In African Americans, SLC22A12 SNP rs11602903 was not associated with BMI, waist circumference, HDL cholesterol or triglycerides. CONCLUSION The URAT1 gene SLC22A12 polymorphism may play a role in obesity and the metabolic syndrome in Caucasian hypertensive subjects.
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The moderating impact of ethnicity on metabolic outcomes during treatment with olanzapine and aripiprazole in patients with schizophrenia.
Meyer, JM, Rosenblatt, LC, Kim, E, Baker, RA, Whitehead, R
The Journal of clinical psychiatry. 2009;(3):318-25
Abstract
OBJECTIVE Race is strongly associated with risk for metabolic dysfunction, but there is limited prospective data concerning the impact of race on antipsychotic metabolic outcomes among patients with schizophrenia. METHOD This study is a post hoc analysis of data from a 26-week, double-blind, randomized trial of aripiprazole (N = 155) and olanzapine (N = 159) conducted from April 2000 through June 2001 in patients aged >or= 18 years with acute schizophrenia according to DSM-IV criteria. The data were analyzed on the basis of racial breakdown: white and black/Hispanic. Between-drug and within-drug outcomes were analyzed separately for each racial cohort across weight, lipid, and glucose parameters. RESULTS For white subjects (N = 167), olanzapine significantly worsened all metabolic parameters except high-density lipoprotein (HDL) cholesterol and fasting glucose, and this was significantly different than aripiprazole for every outcome except fasting glucose. In the black/Hispanic cohort (N = 137), olanzapine treatment resulted in adverse metabolic outcomes, and these changes were significantly different from aripiprazole for adiposity, total cholesterol, and non-HDL cholesterol. Aripiprazole decreased the odds of endpoint metabolic syndrome compared with olanzapine for all subjects (OR = 0.33, 95% CI = 0.19 to 0.55), the white cohort (OR = 0.20, 95% CI = 0.10 to 0.41), and black/Hispanic subjects (OR = 0.53, 95% CI = 0.25 to 1.12), but the black/Hispanic result was not statistically significant (p = .096). Within the aripiprazole group, white subjects had significantly lower risk for metabolic syndrome, but there was no significant difference in metabolic syndrome between white and black/Hispanic subjects exposed to olanzapine. CONCLUSIONS Race may be an important moderator of metabolic risk during atypical antipsychotic therapy. Olanzapine treatment is associated with greater effects on adiposity and lipids than aripiprazole in both white and black/Hispanic subjects, suggesting that antipsychotic choice and intensive monitoring are important in minimizing metabolic risk, especially in nonwhite patients.
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Pro12Ala mutation in the peroxisome proliferator-activated receptor gamma2 (PPARgamma2) and severe obesity: a case-control study.
Vaccaro, O, Mancini, FP, Ruffa, G, Sabatino, L, Colantuoni, V, Riccardi, G
International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. 2000;(9):1195-9
Abstract
OBJECTIVE To explore the association of the Pro12Ala mutation in the peroxisome proliferator-activated receptor gamma2 with severe obesity and the features of the metabolic syndrome in a population-based sample of Caucasians. PARTICIPANTS AND METHODS The study is based on a case-control design: 95 non-diabetic severely obese (body mass index, BMI > 35 kg/m2) cases and 280 normal weight (BMI < 25 kg/m2), age- and sex-matched controls selected from the same population were studied. Height, weight, waist circumference, as well as blood pressure were measured according to a standard protocol. BMI at age 25 y was calculated on the basis of current height and reported weight at age 25 y Biochemical measurements included fasting glucose, triglycerides, high-density lipoprotein cholesterol and insulin. DNA analysis was conducted by PCR and gel electrophoresis. RESULTS Age and gender distribution were similar in obese and normal weight participants. The percentage of people with the Pro12Ala mutation was not significantly different in obese or normal weight participants (20% and 15%, respectively; P = 0.32). Conversely, in obese participants with obesity starting in early adulthood (ie with BMI at age 25 above 26.9kg/m2 which represents the median of the whole obese group), the Pro12Ala mutation was observed significantly more frequently than in the normal weight controls (29% vs 15%; chi square = 4.5, P < 0.05; odds ratio 2.4; 95% CI 1.03-5.36). No association of the Pro12Ala variant with any of the component of the metabolic syndrome measured in the study was observed in either obese, juvenile obese or normal weight participants. CONCLUSIONS Results of this study indicate that the Pro12Ala mutation does not play a major role as a determinant of severe obesity and/or features of the metabolic syndrome in the general population. However, this mutation may be of greater importance as a contributor to early onset obesity.