Risk of arterial stiffness according to metabolically healthy obese phenotype: a combined cross-sectional and longitudinal study in kailuan cohort.
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SUBMITTER: Wang A
PROVIDER: S-EPMC8221340 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background: In pediatric age the prevalence of obesity is high. Obese children who do not have other risk factors than excess weight have been defined as "metabolically healthy obese" (MHO). Aim: The aim of this study is to evaluate, in a population of obese children, the prevalence of the MHO and "metabolically unhealthy obese" (MUO) phenotype. Furthermore, we evaluated the distribution of Uric Acid, HOMA index and Waist-Height ratio (W-Hr) in the MHO and MUO sub-groups and the impact of these non-traditional risk factors on the probability to be MUO. Methods: In 1201 obese children and adolescents [54% males, age (±SD) 11.9 (±3.0) years] weight, height, waist circumference, systolic (SBP) and diastolic (DBP) blood pressure, pubertal status, glucose, insulin, HDL cholesterol, triglycerides and Uric Acid serum values were assessed. MUO phenotype was defined as the presence of at least one of the following risk factors: SBP or DBP ? 90th percentile, glycaemia ? 100 mg/dl, HDL cholesterol <40 mg/dl, triglycerides ?100 mg/dl (children <10 years) or ?130 mg/dl (children ?10 years). A multivariate logistic regression analysis was used to estimate the association between MUO phenotype and non-traditional cardiovascular risk factors. Results: The prevalence of the MUO status was high (61%). MUO subjects were more often male, older and pubertal (p < 0.001). The levels of the three non-traditional risk factors were significantly higher in MUO children compared to MHO children (p < 0.001) and all of them were independent predictors of the fact of being MUO [OR 1.41 (95% CI 1.24-1.69); 1.15 (95% CI 1.06-1.23) and 1.03 (95% CI1.01-1.05) for Uric Acid, HOMA index and W-Hr, respectively]. About 15% of MHO subjects had serum Uric Acid, HOMA index and W-Hr values within the highest quartile of the study population. Conclusion: The prevalence of MUO subjects in a large pediatric population is high and serum Uric Acid, HOMA index and W-Hr values are independent predictors of the probability of being MUO. A non-negligible percentage of subjects MHO has high values of all three non-traditional risk factors.
| S-EPMC7025459 | biostudies-literature
Project description:BACKGROUND/OBJECTIVES:The clinical relevance of the metabolically healthy overweight/obese (MHO) phenotype is controversial and the relationships between weight change and the development of cardiometabolic risk factors is unknown. Therefore, we aim to: (1) Assess the long-term risk of developing one or more components of the metabolic syndrome in MHO adults compared with metabolically healthy normal weight (MHNW); (2) Evaluate risk of a composite of death, cardiovascular disease (CVD), and risk of developing type 2 diabetes between adults defined according to baseline body mass index and metabolic health. SUBJECTS/METHODS:Retrospective cohort study of adults 18-65 years of age seen at our institution between 1998 and 2000 who lived in Olmsted County. Metabolically healthy was defined as the absence of all components of the metabolic syndrome (except for waist circumference). Main outcome was the development of metabolic risk factors. The secondary outcome was a composite of mortality, CVD and heart failure. RESULTS:Of the 18?070 individuals with complete data at baseline, 1805 (10%) were MHO (mean age 38±11 years) and 3047 were MHNW (mean age 35±11 years). After a median follow-up of 15 years, interquartile range 10-17, 80% of MHO vs 68% of MHNW developed at least one cardiometabolic risk factor (P<0.001). In multivariate analysis, MHO individuals who gained ?10% of their body weight were more likely to have developed metabolic complications compared to MHO individuals that did not gain weight (P=0.001 for 10-15%, P<0.001 for >15% weight gain). The risk for the secondary composite end point was similar between MHO and MHNW, number of events 218/1805 vs 217/3048 for MHO and MHNW, respectively, (hazard ratio: 1.16, 95% confidence interval: 0.96-1.40). CONCLUSIONS:MHO are more likely to develop metabolic complications than MHNW, especially if they gain weight.
| S-EPMC5867190 | biostudies-literature
Project description:Background:Metabolically healthy obesity (MHO) has been reported to be associated with the development of vascular damage by the carotid intima-media thickness, but the relationship between metabolic health and obesity phenotypes and arterial stiffness is still unknown. Our hypothesized that different metabolic health and obesity phenotypes might be associated with the development of arterial stiffness, and that subjects in MHO phenotype might not have increased risks of arterial stiffness compared with those in metabolically healthy nonobesity phenotype (MHNO), while metabolic unhealthy individuals might have increased risks of arterial stiffness. Methods:A prospective cohort of 2076 participants (aged 36-48?years) who were enrolled in the Hanzhong Adolescent Hypertension Cohort Study in 2017 was analyzed in a cross-sectional analysis. A subgroup of 202 participants from 2005 to 2017 was selected by an isometric sampling method and was included in the final longitudinal analysis. Results:We identified four metabolic health and obesity phenotypes for both the cross-sectional and longitudinal analyses as follows: MHNO, metabolically unhealthy nonobesity (MUNO), MHO, and metabolically unhealthy obesity (MUO). In the cross-sectional analysis, individuals with the MHO phenotype had the lowest brachial-ankle pulse wave velocity (baPWV) levels of the four phenotypes (P?<?0.001), and participants with the MHO phenotype had a similar risk of arterial stiffness after fully adjustment [odds ratio (OR)?=?0.99 (0.61-1.60)] as the MUNO subjects. Subjects with metabolically unhealthy status had a significantly higher risk of arterial stiffness than the MHNO individuals, particularly females (P?<?0.005). In the longitudinal analysis, subjects with the MUNO and MUO phenotypes had a significantly higher risk of arterial stiffness than the MHNO individuals after adjustment for age and sex [OR?=?5.21 (2.26-12.02), OR?=?3.32 (1.18-9.32), respectively]. Conclusions:The MHO phenotype did not significantly increase the progression of arterial stiffness. Metabolically unhealthy individuals (MUNO, MUO), regardless of obesity status, showed a worse effect for the development of arterial stiffness, particularly females. Trial registration:NCT02734472. Registered 12 April 2016 - Retrospectively registered, http:www.clinicaltrials.gov.
| S-EPMC7330959 | biostudies-literature
Project description:BackgroundThis study aimed to investigate whether increased arterial stiffness, measured by brachial-ankle pulse wave velocity (baPWV) is associated with cancer.Materials and methodsA total of 45,627 Chinese adults underwent a baPWV examination. The participants were followed up from 1st January 2012 to 31st December 2018. Cox proportional hazards model was used to assess the association between the baPWV values and cancer.ResultsDuring a total follow-up duration of 172,775.69 person-years, there were 553 new cases of cancer. The subjects in the highest baPWV group showed an increased risk of cancer when compared with the lowest baPWV group as confirmed by multivariate-adjusted hazard ratios (HR = 1.51, 95% CI = 1.14∼2.00) in the entire cohort. Compared with participants in the lowest baPWV group, the HRs (95% CI) for digestive cancer in the second and third groups were 1.55 (1.00∼2.40) and 1.99 (1.19∼3.33), respectively. The Kaplan-Meier analysis demonstrated a significant increase in cancer in participants with a baPWV ≥ 18 m/s (P < 0.001). Compared with the lowest baPWV group, the highest baPWV group showed an increased risk of cancer in men (HR = 1.72, 95% CI = 1.22∼2.43) and those < 60 years (HR = 1.75, 95% CI = 1.20∼2.55), respectively.ConclusionIncreased arterial stiffness measured by baPWV is associated with cancer occurrence, especially digestive cancer occurrence.Clinical trial registrationClinicalTrials.gov, identifier ChiCTR-TNRC-11001489.
| S-EPMC10014543 | biostudies-literature
Project description:BackgroundMetabolic dysfunction is known to be associated with arterial stiffness. However, the risks of metabolic syndrome and diabetes due to arterial stiffness and the potential mechanism remain unclear. We aimed to investigate the association of arterial stiffness with the risk of metabolic syndrome and diabetes, and determine whether this association is mediated by liver fat.MethodsA prospective study was conducted with 4,139 Chinese adults who were metabolically healthy at baseline. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV). Obesity was defined as body mass index ≥25 kg/m2. The primary outcomes were incident metabolic syndrome and diabetes.ResultsDuring a median follow-up of 4.4 years, 1,022 (24.7%) and 354 (9.5%) participants developed metabolic syndrome and diabetes, respectively. Compared with those in the lowest quartile of baPWV, participants in the highest quartile had 85 and 91% higher risks of metabolic syndrome and diabetes [risk ratio (RR) 1.85, 95% confidence interval (CI) 1.41, 2.42 for metabolic syndrome; RR 1.91, 95% CI 1.16, 3.15 for diabetes]. Mediation analyses indicated that fatty liver significantly mediated the association of arterial stiffness with metabolic syndrome and diabetes risk. Specifically, 18.4% of metabolic syndrome and 12.6% of diabetes risk due to arterial stiffness were mediated through fatty liver.ConclusionsArterial stiffness was associated with higher risks of metabolic syndrome and diabetes in individuals with obesity. This association may be partially mediated by fatty liver.
| S-EPMC9261979 | biostudies-literature
Project description:Obesity has evolved into a global pandemic that constitutes a major threat to public health. The majority of obesity-related health care costs are due to cardiometabolic complications, such as insulin resistance, dyslipidemia, and hypertension, which are risk factors for Type 2 diabetes and cardiovascular disease. However, many obese individuals, often called metabolically healthy obese (MHO), seem to be protected from these cardiometabolic complications. Conversely, there is a group of individuals who suffer from cardiometabolic complications despite being of normal weight; a condition termed metabolically obese normal weight (MONW). Recent large-scale genomic studies have provided evidence that a number of genetic variants show an association with increased adiposity but a favorable cardiometabolic profile, an indicator for the genetic basis of the MHO and MONW phenotypes. Many of these loci are located in or near genes that implicate pathways involved in adipogenesis, fat distribution, insulin signaling, and insulin resistance. It has been suggested that a threshold for subcutaneous adipose tissue expandability may be at play in the manifestation of MHO and MONW, where expiry of adipose tissue storage capacity could lead to ectopic lipid accumulation in non-adipose tissues such as liver, muscle, heart, and pancreatic beta cells. Understanding the genetic aspects of the mechanisms that underpin MHO and MONW is crucial to define appropriate public health action points and to develop effective intervention measures.
| S-EPMC6048453 | biostudies-literature
Project description:There is some evidence to suggest that obesity is a risk factor for the development of depression, although this is not a universal finding. This discordance might be ascribed to the existence of a 'healthy obese phenotype'--that is, obesity in the absence of the associated burden of cardiometabolic risk factors. We examined whether the association of obesity with depressive symptoms is dependent on the individual's metabolic health. Participants were 3851 men and women (aged 63.0±8.9 years, 45.1% men) from the English Longitudinal Study of Ageing, a prospective study of community dwelling older adults. Obesity was defined as body mass index ?30 kg?m(-2). Based on blood pressure, high-density lipoprotein cholesterol, triglycerides, glycated haemoglobin and C-reactive protein, participants were classified as 'metabolically healthy' (0 or 1 metabolic abnormality) or 'unhealthy' (?2 metabolic abnormalities). Depressive symptoms were assessed at baseline and at 2 years follow-up using the 8-item Centre of Epidemiological Studies Depression (CES-D) scale. Obesity prevalence was 27.5%, but 34.3% of this group was categorized as metabolically healthy at baseline. Relative to non-obese healthy participants, after adjustment for baseline CES-D score and other covariates, the metabolically unhealthy obese participants had elevated risk of depressive symptoms at follow-up (odds ratio (OR)=1.50; 95% confidence interval (CI), 1.05-2.15), although the metabolically healthy obese did not (OR=1.38; 95% CI, 0.88-2.17). The association between obesity and risk of depressive symptoms appears to be partly dependent on metabolic health, although further work is required to confirm these findings.
| S-EPMC3428506 | biostudies-literature
Project description:Obesity is closely associated with cardiovascular diseases and type 2 diabetes, but some obese individuals, despite having excessive body fat, exhibit metabolic health that is comparable with that of lean individuals. The 'healthy obese' phenotype was described in the 1980s, but major advancements in its characterization were only made in the past five years. During this time, several new mechanisms that may be involved in health preservation in obesity were proposed through the use of transgenic animal models, use of sophisticated imaging techniques and in vivo measurements of insulin sensitivity. However, the main obstacle in advancing our understanding of the metabolically healthy obese phenotype and its related long-term health risks is the lack of a standardized definition. Here, we summarize the proceedings of the 13th Stock Conference of the International Association of the Study of Obesity. We describe the current research and highlight the unanswered questions and gaps in the field. Better understanding of metabolic health in obesity will assist in therapeutic decision-making and help identify therapeutic targets to improve metabolic health in obesity.
| S-EPMC4519075 | biostudies-literature
Project description:ObjectiveMetabolically healthy obesity (MHO) is often defined as the absence of metabolic syndrome in the presence of obesity. However, phenotypic features of MHO are unclear. Insulin sensitivity in MHO was cross-sectionally compared with metabolically unhealthy obesity (MUO) and a reference group of young healthy participants without obesity.MethodsSedentary adults (n = 96) undergoing anthropometric, blood chemistries, maximal aerobic capacity, and euglycemic-hyperinsulinemic clamp measurements were classified by BMI (<25 and ≥30 kg/m2 ). MUO was defined as having obesity with metabolic syndrome (≥2 additional risk factors). Data were analyzed using a linear mixed models approach.ResultsBody weight was similar between MHO and MUO. Body fat (percentage) and high-density lipoprotein cholesterol were higher (p < 0.001), and systolic blood pressure, triglycerides, glucose, and insulin were lower in MHO versus MUO (p < 0.03, all). The MHO group also had lower high-density lipoprotein cholesterol and higher low-density lipoprotein cholesterol, diastolic blood pressure, and insulin compared with the reference. Both the MHO and MUO groups displayed impaired insulin sensitivity compared with the reference control (p < 0.001).ConclusionsParticipants with MHO had distinct clinical measures related to hypertension, lipid metabolism, and glycemic control compared with a healthy reference group. Peripheral insulin resistance in obesity independent of metabolic status portends increased risk for type 2 diabetes in the MHO patient population.
| S-EPMC9136885 | biostudies-literature
Project description:Arterial stiffness is an emerging risk factor for cardiovascular disease and dietary anthocyanins may be important in mediating vascular tone. The present study investigated the effect of consumption of an anthocyanin-rich potato, Purple Majesty on arterial stiffness measured as pulse wave velocity in 14 healthy male and female adults. Participants consumed 200 g/day of cooked purple potato containing 288 mg anthocyanins, or a white potato containing negligible anthocyanins for 14 days, separated by a 7-day washout period. Non-invasive assessment of vascular tone by pulse wave velocity was determined in addition to systolic and diastolic blood pressure, high-density lipoproteins, low-density lipoproteins, triglycerides, glucose, insulin and C-reactive protein. Pulse wave velocity was significantly reduced (p?=?0.001) following Purple Majesty consumption for 14-days. There were no significant changes with any other clinical parameter measured, and no changes following white potato consumption. The findings from this short-term study indicate a potential effect of Purple Majesty consumption on arterial stiffness.
| S-EPMC6096904 | biostudies-other