Cardiometabolic Alterations Research Articles

Comorbidities in childhood associated with extrauterine growth restriction in preterm infants: a scoping review.

Extrauterine growth restriction (EUGR) is a frequent morbidity of preterm infants that can affect short- and long-term prognosis as it involves different EUGR-related alterations in growth and neurological development, as well as cardiometabolic risk. However, knowledge about the prognosis of EUGR is scarce. Thus, the objective of this study is to review the evidence regarding EUGR-related comorbidities in childhood by a systematic approach. This review was carried out using the Joanna Briggs Institute Reviewers' Manual Methodology and the PRISMA (Preferred Reporting Items for Systematic Review and Meta-Analyses)-Search Extension for scoping review. The MEDLINE and EMBASE databases were used to identify papers published until September 2017. Twenty-four publications were included and 19 examined cohort studies. EUGR is mainly associated with (1) lower weight, length, and head circumference measures in childhood; (2) poor neurodevelopment; and (3) alterations in cardiometabolic risk markers. The definition for EUGR and the populations studied differ among authors.Conclusion: EUGR is mainly associated with poor growth and neurodevelopment, as well as with cardiometabolic alterations in childhood. Evidence is based on observational studies with variability in the included populations due to the lack of consensus regarding the definition for EUGR. Finding a gold standard definition becomes paramount in order to select phenotypes at risk later in life. What is known? • EUGR is a frequent condition of preterm infants. Up to date little is known about the effect of the metabolic programming on prognosis. What is new? • The available evidence, which is based on observational studies with variability in the population and the existing different definitions for EUGR, do not enable appropriate data collection. EUGR is mainly associated with poor growth and neurodevelopment, as well as with cardiometabolic alterations in childhood.

Relevance of control diet choice in metabolic studies: impact in glucose homeostasis and vascular function

The experimental approach for the study of cardiometabolic disorders requires the use of animal models fed with commercial diets whose composition differs notably, even between diets used for control groups. While chow diets are usually made of agricultural by-products, purified low-fat diets (LF) contain a higher percentage of easy metabolizable carbohydrates, together with a reduced amount of polyunsaturated fatty acids, micronutrients and fiber, all associated with metabolic and vascular dysfunction. We hypothesize that the LF diet, commonly used in control animals, could promote adverse vascular and metabolic outcomes. To address this issue, 5-week-old male C57BL6J mice were fed with a standard (Chow) or a LF diet for 6 weeks. Changes in body weight, adiposity, biochemical parameters, systemic and aortic insulin sensitivity and endothelial function were recorded. LF diet did not modify body weight but significantly impaired systemic glucose tolerance and increased triglycerides and cholesterol levels. Endothelial function and aortic insulin sensitivity were significantly impaired in the LF group, due to a reduction of NO availability. These findings highlight the importance of selecting the proper control diet in metabolic studies. It may also suggest that some cardiometabolic alterations obtained in experimental studies using LF as a control diet may be underestimated.

Plasma tocopherols and carotenes are decreased in Spanish metabolically unhealthy children and adolescents independently of obesity

AbstractIntroductionChildhood obesity is associated with multiple cardio-metabolic abnormalities. A sensitive hypothesis underlying these alterations is oxidative stress, shown to be present in obesity, often accompanied by a diminished antioxidant defense. Specifically, plasma vitamin concentrations have been observed to be associated with obesity in adults and children. However, their association with cardio-metabolic alterations in children is less clear.Materials and Methods985 children (49.2% males, 71.7% prepubertal, 71.9% excess weight) were recruited in a case-control study of obesity in three Spanish hospitals. Pubertal status was assessed and anthropometry (weight, height), systolic and diastolic blood pressure (SBP, DBP) and serum glucose, insulin, triacylglycerols (TAG) and high-density lipoprotein cholesterol (HDL-C) were measured. Plasma concentrations of tocopherols and carotenes were determined with HPLC-MS and referred to TAG. Children were classified as MU if showing one or more of these criteria: SBP or DBP ≥ 90th percentile (age, sex, height), serum TAG > 90th percentile (age, sex), HDL-C < 10th percentile (age, sex), glucose ≥ 100 mg/dL or elevated HOMA-IR (≥ 2.5 prepubertal, ≥ 3.38 pubertal males, ≥ 3.905 pubertal females). Non-fulfillment was indicative of MH status. General linear models adjusted for sex, age, recruitment center and BMI were used to evaluate differences in vitamins between MH and MU children.ResultsPrepubertal and pubertal children with excess weight showed lower tocopherols (Pre: 0.133 ± 0.061 vs 0.165 ± 0.065, P < 0.001; Pub: 0.120 ± 0.057 vs 0.163 ± 0.066, P < 0.001) and carotenes (Pre: 15.63 ± 13.72 vs 30.31 ± 26.04, P < 0.001; Pub: 12.34 ± 9.86 vs 22.98 ± 19.25, P < 0.001) plasma concentrations than normal-weight children. MU prepubertal and pubertal children showed lower tocopherols (Pre: 0.120 ± 0.056 vs 0.165 ± 0.064, P < 0.001; Pub: 0.111 ± 0.051 vs 0.154 ± 0.066, P < 0.001) and carotenes (Pre: 14.07 ± 12.61 vs 25.97 ± 21.94, P < 0.001; Pub: 10.90 ± 8.54 vs 19.03 ± 14.58, P < 0.001) plasma concentrations than MH children, independently of BMI. Individual MU components analyses showed similar associations between tocopherols and carotenes and insulin resistance, low HDL-C values and hypertriglyceridemia in prepubertal children; and between tocopherols and carotenes and elevated SBP, hyperglycemia and hypertriglyceridemia in pubertal children.DiscussionOur findings agree with previous studies that showed decreased plasma concentrations of tocopherols and carotenes in children with obesity. However, we observe further implications of low circulating concentrations of non-enzymatic antioxidants in terms of their negative association with cardio-metabolic alterations such as insulin resistance and dyslipidemia in prepubertal and pubertal children, independently of BMI. These results must be considered when designing prevention and treatment strategies of obesity and its complications.

Sleep-disordered breathing in adolescents with obesity: When does it start to affect cardiometabolic health?

Background and aimsPediatric obesity and sleep-disordered breathing (SDB) are associated with cardiometabolic risk (CMR), but the degree of severity at which SDB affects cardiometabolic health is unknown. We assessed the relationship between the CMR and the apnea-hypopnea index (AHI), to identify a threshold of AHI from which an increase in the CMR is observed, in adolescents with obesity. We also compared the clinical, cardiometabolic and sleep characteristics between adolescents presenting a high (CMR+) and low CMR (CMR-), according to the threshold of AHI. Methods and results114 adolescents with obesity were recruited from three institutions specialized in obesity management. Sleep and SDB as assessed by polysomnography, anthropometric parameters, fat mass (FM), glucose and lipid profiles, and blood pressure (BP) were measured at admission. Continuous (MetScoreFM) and dichotomous (metabolic syndrome, MetS) CMR were determined. Associations between MetScoreFM and AHI adjusted for BMI, sex and age were assessed by multivariable analyses.Data of 82 adolescents were analyzed. Multivariable analyses enabled us to identify a threshold of AHI = 2 above which we observed a strong and significant association between CMR and AHI (Cohen's d effect-size = 0.57 [0.11; 1.02] p = 0.02). Adolescents with CMR+ exhibited higher MetScoreFM (p < 0.05), insulin resistance (p < 0.05), systolic BP (p < 0.001), sleep fragmentation (p < 0.01) and intermittent hypoxia than CMR- group (p < 0.0001). MetS was found in 90.9% of adolescents with CMR+, versus 69.4% in the CMR- group (p < 0.05). ConclusionsThe identification of a threshold of AHI ≥ 2 corresponding to the cardiometabolic alterations highlights the need for the early management of SDB and obesity in adolescents, to prevent cardiometabolic diseases. Clinical trialsNCT03466359, NCT02588469 and NCT01358773

Dietary habits and physical activity in first-episode psychosis patients treated in community services. Effect on early anthropometric and cardio-metabolic alterations

People with psychosis often develop metabolic and cardiovascular disorders, due to several factors including unhealthy lifestyle and antipsychotic treatment. This study aims to evaluate in a sample of first episode psychosis (FEP) patients lifestyle factors, with a specific emphasis on dietary habits and physical activity, and cardio-metabolic and anthropometric profile at illness onset and at 9 months. Moreover, this study aims to evaluate the impact of lifestyle factors on short term changes in cardio-metabolic and anthropometric profile. A 9-month follow-up study was conducted on a sample of 96 FEP patients recruited within the context of the GET UP program. Standardised assessments of dietary habits (EPIC) and physical activity (IPAQ) were retrospectively performed at 9 months; cardiovascular measures (blood pressure, heart rate), metabolic parameters (glucose, cholesterol, triglycerides), BMI and antipsychotic treatment were assessed at illness onset and at 9 months. We found that most FEP patients (60%) displayed poor dietary habits, as defined in terms of adherence to the Mediterranean diet. A significant increase for both BMI and cholesterol levels was found in the overall sample over 9 months. However, when considering the effect of lifestyle factors, BMI and total cholesterol were specifically raised in patients with low adherence to Mediterranean diet. The association with antipsychotic medication was found for SGA only, with a significant increase in both BMI and total cholesterol overtime. Our findings confirm the need to implement specific and early strategies to promote healthy lifestyle in people with FEP, since metabolic alterations occur within the first months of treatment.

Towards Prepared mums (TOP-mums) for a healthy start, a lifestyle intervention for women with overweight and a child wish: study protocol for a randomised controlled trial in the Netherlands

IntroductionPericonception obesity is associated with a higher risk for adverse perinatal outcomes such as gestational diabetes mellitus, preeclampsia, large for gestational age, operative delivery and preterm birth. Lifestyle interventions during...

Altilix® Supplement Containing Chlorogenic Acid and Luteolin Improved Hepatic and Cardiometabolic Parameters in Subjects with Metabolic Syndrome: A 6 Month Randomized, Double-Blind, Placebo-Controlled Study.

The objective was to evaluate the effects of 6 months of supplementation with Altilix®, containing chlorogenic acid and its derivatives, and luteolin and its derivatives, on cardiovascular risk and hepatic markers in subjects with metabolic syndrome (MetS). A randomized, double-blind, placebo-controlled study was performed in 100 subjects with MetS with a follow-up period of 6 months; 50 subjects were randomized to Altilix® (26 men and 24 women, mean age 63 ± 8 years) and the other 50 to placebo (28 men and 22 women, mean age 63 ± 11 years). Anthropometric, cardiometabolic, and hepatic parameters were assessed at baseline and at the end of follow-up. Carotid intima-media thickness and endothelial function were assessed by doppler ultrasound and by flow-mediated dilation of the brachial artery, respectively. The presence and degree of non-alcoholic fatty liver disease (NAFLD) was assessed by the fatty liver index (FLI), and subjects were divided into three subgroups: (1) without NAFLD; (2) with borderline NAFLD; and (3) with NAFLD. After 6 months of Altilix® supplementation, we found a significant improvement vs. placebo in most of the evaluated parameters, including body weight (−2.40% (95% CI −3.79, −1.01); p < 0.001), waist circumference (−2.76% (95% CI −4.55, −0.96); p = 0.003), HbA1c (−0.95% (95% CI −1.22, −0.67); p < 0.001), plasma lipids, FLI (−21.83% (95% CI −27.39, −16.27); p < 0.001), hepatic transaminases, flow-mediated dilation (10.56% (95% CI 5.00, 16.12); p < 0.001), and carotid intima-media thickness (−39.48% (95% CI −47.98, −30.97); p < 0.001). Further, the improvement in cardiometabolic variables was independent of the degree of hepatic steatosis. Altilix® supplementation improved hepatic and cardio-metabolic parameters in MetS subjects. Altilix® supplementation was a beneficial approach in the management of hepatic and cardiometabolic alterations in MetS subjects.

Forced internal desynchrony induces cardiometabolic alterations in adult rats.

Disruptions in circadian rhythms have been associated with several diseases, including cardiovascular and metabolic disorders. Forced internal desynchronization induced by a period of T-cycles of 22 h (T22 protocol) reaches the lower limit of entrainment and dissociates the circadian rhythmicity of the locomotor activity into two components, driven by different outputs from the suprachiasmatic nucleus (SCN). The main goal of this study was to evaluate the cardiovascular and metabolic response in rats submitted to internal desynchronization by T22 protocol. Male Wistar rats were assigned to either a control group subjected to a usual T-cycles of 24 h (12 h-12 h) or an experimental group subjected to the T22 protocol involving a 22-h symmetric light-dark cycle (11 h-11 h). After 8 weeks, rats subjected to the T22 exhibited desynchrony in their locomotor activity. Although plasma glucose and insulin levels were similar in both groups, desynchronized rats demonstrated dyslipidemia, significant hypertrophy of the fasciculate zone of the adrenal gland, low IRB, IRS2, PI3K, AKT, SOD and CAT protein expression and an increased expression of phosphoenolpyruvate carboxykinase in the liver. Furthermore, though they maintained normal baseline heart rates and mean arterial pressure levels, they also presented reduced baroreflex sensitivity. The findings indicate that circadian timing desynchrony following the T22 protocol can induce cardiometabolic disruptions. Early hepatic metabolism dysfunction can trigger other disorders, though additional studies are needed to clarify the causes.

A Pilot Study About the Dysfunction of Adipose Tissue in Male, Sleep Apneic Patients in Relation to Psychological Symptoms.

Introduction: Obstructive sleep apnea (OSA) and its cardiometabolic alterations are closely associated with visceral obesity. Patients with OSA frequently present with symptoms of depression and anxiety. Although these subjective symptoms of OSA are the result of complex biological dysregulation, it remains unclear if they have a direct effect on the dysfunction of adipose tissue. Methods: In a pilot, prospective, randomized study, we evaluated 10 recently diagnosed male patients with severe OSA by full polysomnography (PSG) and 4 male non-apneic subjects matched for age and body mass index (BMI) with abdomen adipose tissue biopsies. Subjects with diabetes/prediabetes and cardiovascular and psychiatric diseases and who are current smokers were excluded. All patients underwent anthropometric measurements and completed the following questionnaires: Epworth Sleepiness Scale (ESS), Fatigue Severity Scale (FSS), and Hospital Anxiety and Depression Scale (HADS-A and HADS-D). Fasting venous blood samples were collected on the day after PSG, between 8:00 and 9:00 a.m., after an overnight fast. Fat biopsies were performed at the same time periods and adipose tissue samples of 300 mg were obtained from abdominal fat. Fat cell size, extent of fibrosis, vascularity, leukocyte common antigen inflammatory infiltration, and tissue macrophage accumulation were microscopically evaluated. Results: The mean age of the group was 47.4 ± 13.8 years, with mean BMI of 35.8 ± 4.8 kg/m2 and mean apnea-hypopnea index of 79.4 ± 46.1 events per hour of sleep (severe OSA). HADS-A and HADS-D scores were 5.8 ± 2.3 (3.0–8.0) and 4.7 ± 2.3 (2.0–8.0), respectively. HADS-A score correlated positively with macrophage accumulation in fat biopsy (r = 0.82, p = 0.047), whereas ESS, FSS, and HADS-D did not. Severity of fibrosis correlated largely with waist circumference (r = -0.66, p = 0.038) and neck circumference (r = -0.790, p = 0.006). Respiratory events correlated negatively with the extent of vascularization of adipose tissue (r = -0.614, p = 0.05). Conclusions: In the preliminary results of our pilot study, we assessed that the symptoms of anxiety mainly contribute to macrophage accumulation, whereas the increased number of respiratory events reduces the extent of vascularization in visceral fat in OSA. Based on this observation, further larger studies are required to verify if anxious OSA patients are more vulnerable to the metabolic manifestations of the syndrome.

Diagnostic accuracy of triglyceride/glucose and triglyceride/HDL index as predictors for insulin resistance in children with and without obesity

ObjectiveTo investigate which of two indexes (TyG or TG/HDL) are the best predictors for insulin resistance (IR) and to evaluate the magnitude of each cardiometabolic risk factor in Mexican schoolchildren of 5–9 years with overweight-obesity and normal weight. Material and methodsWe realized a comparative cross-sectional prospective study in accordance of STARD guidelines. Setting was Family Medicine Unit (FMU) No. 80 of Mexican Institute of Social Security(IMSS) of Morelia, Michoacán, Mexico. Children between 5 and 9 years, both genders, 104 with normal weight(NW), 97 with Overweight-Obesity(OO Group) were included. Once the informed consent was signed we obtained the BMI, waist circumference, blood pressure(BP) and 5 mL of blood collected for glucose, cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, uric acid and insulin. As main outcome measures TyG or TG/HDL, HOMA-IR, and Receiving Operating Curves(ROC), sensitivity, specificity by ROC were obtained. ResultsCutoff point TyG: 8.5 by ROC had an area under curve (AUC):0.802 IC95% 0.77to0.893, P = 0.0001; diagnostic accuracy of 73%. TG/HDL: 2.22; AUC:0.729 IC95% 0.622to0.837, P = 0.014; diagnostic accuracy of 52%. TyG can identify cardiometabolic alterations more than HOMA and TG/HDL. Cardiometabolic alterations in the OO group were hypertriglyceridemia:49.5%, low HDL:63.9%, IR:39.2% and in NW group were hypertriglyceridemia:30.8%, low HDL:60.6%, IR:9.6%. ConclusionsWe reported high frequency of hypertriglyceridemia and low HDL in Mexican children. TyG and TG/HDL are good predictors for IR. TyG has a better diagnostic accuracy. We need implementing TyG for identifying alterations and intervening in a timely manner to delay the onset of chronic diseases in children.

Dietary sugars, metabolic effects and child health.

To describe current findings on sugar intake in children worldwide, including sugar sources and their impact on child health focusing on cardiometabolic alterations usually associated to obesity. In children less than 4 years, intakes of added sugars across countries ranged from 9.8 to 11.2% of total energy; in children 4-10 years, it ranged from less than 3-18%; and in adolescents, it ranged from 13.6 to 16.6%. For most countries, intakes of added sugars were greater than the recommended upper limit of 10% of total energy for children and adolescents and less or around 10% in infants. In most studies, soft drinks and fruit-based drinks accounted for the greatest proportion of the added sugars intake, followed by milk products and sweet bakery products. High added sugar intake has been associated with increased obesity risk and fat deposition in the liver, contributing to dyslipidemia, high blood pressure, insulin resistance and cardio-metabolic risk. As a high added sugar intake is associated with cardio-metabolic conditions in children and adolescents, the current scenario supports the need for stronger targeted long-term policies that prevent the excessive sugar intake in young populations.

Respective roles of genetic background and high fat diet in a rodent model of metabolic syndrome

The metabolic syndrome is a worldwide public health problem. Major cause is the junk food associated with a genetic predisposition. To better understand the mechanisms it is imperative to develop animal models closest to human problem. Cardiometabolic alterations were studied in a polygenic rat model of metabolic syndrome. We therefore evaluated the respective roles of the substrain and the diet. Ten obese prone (OP), obese resistant (OR) and control (CTRL) Sprague–Dawley rats were fed with high fat (HF) or standard diet (SD) for 16 weeks. Feeding behaviour and criteria of the metabolic syndrome were determined. Arterial pressure was weekly recorded. Leptin and adiponectin were measured. CTRL and OR rats regulated their appetite to maintain a reasonable global calorie intake irrespective of the diet. OP rats showed higher food consumption and their calorie intake increased on HF. The mean abdominal fat % increase when on HF was higher in OP compared to CTRL and OR (236.1% vs. 89.97% and 65.99%). Total cholesterol and triglycerides were increased in OP-HF rats compared to the 5 other groups while OP showed a high nonHDL/HDL ratio already on SD. OP-HF rats had glucose intolerance. OP-HF rats showed an over time increase of systolic and diastolic arterial pressures and increased diastolic pressure at week 16 (117 ± 6 vs. 89 ± 6 and 93 ± 3 mmHg in OR-HF and CTRL-HF). Plasma leptin was increased in OP rats irrespective of the diet, suggesting a leptin resistance (4.8 ± 0.8 and 5.8 ± 0.5 ng/ml in OP-SD and OP-HF). In accordance with their satiety, leptin increased in CTRL and OR fed with HF (2.95 ± 0.6 and 2.98 ± 0.7 ng/ml vs. 0.65 ± 0.1 and 1 ± 0.1 ng/ml in CTRL-SD and OR-SD). The leptin/adiponectin ratio was elevated in OP regardless of the diet. The OP substrain is characterized by high plasma leptin and a loss of satiety leading to obesity and increased nonHDL/HDL ratio. When associated with HF, OP rats develop a metabolic syndrome.

Moderate Physical Training Ameliorates Cardiovascular Dysfunction Induced by High Fat Diet After Cessation of Training in Adult Rats

We aimed to test whether moderate physical training can induce long-lasting protection against cardiovascular risk factors induced by high fat diet (HFD) intake, even after cessation of training. 90-days-old Wistar rats were submitted to a sedentary lifestyle or moderate physical training, three times a week, for 30 days. Following this, at 120 days-of age, sedentary and trained rats received a hypercaloric diet (HFD) or a commercial diet normal fat diet (NFD) for 30 days. Body weight (BW) and food intake were evaluated weekly. At 150 days-of age, hemodynamic measures (systolic, diastolic, mean blood pressure, pulse pressure, pulse interval and heart rate) were made via an indwelling femoral artery catheter. Beat-to-beat data were analyzed to calculate power spectra of systolic blood pressure (SBP) and pulse interval. After euthanasia, mesenteric fat pads were removed and weighted and total blood was stored for later analysis of lipid profile. Consumption of a HFD increased blood pressure (BP), pulse pressure, low frequency BP variability, BW gain, fat pad stores and induced dyslipidemia. Interestingly, prior physical training was able to partially protect against this rise in BP and body fat stores. Prior physical training did not totally protect against the effects of HFD consumption but previously trained animals did demonstrate resistance to the development of cardiometabolic alterations, which illustrate that the benefits of physical training may be partially maintained even after 30 days of detraining period.

Adiponectin-leptin Ratio is a Functional Biomarker of Adipose Tissue Inflammation

Obesity favors the development of cardiometabolic alterations such as type 2 diabetes (T2D) and the metabolic syndrome (MS). Obesity and the MS are distinguished by an increase in circulating leptin concentrations, in parallel to a drop in the levels of adiponectin. Consequently, the Adpn/Lep ratio has been suggested as a maker of dysfunctional adipose tissue. We aimed to investigate in humans (n = 292) the reliability of the Adpn/Lep ratio as a biomarker of adipose tissue dysfunction. We considered that an Adpn/Lep ratio of ≥1.0 can be considered normal, a ratio of ≥0.5 <1.0 suggests moderate-medium increased risk, and a ratio of <0.5 indicates a severe increase in cardiometabolic risk. Using these cut-offs, 5%, 54% and 48% of the lean, normoglycemic and without-MS subjects, respectively, fall within the group with an Adpn/Lep ratio below 0.5; while 89%, 86% and 90% of the obese, with T2D and with MS patients fall within the same group (p < 0.001). A significant negative correlation (r = −0.21, p = 0.005) between the Adpn/Lep ratio and serum amyloid A (SAA) concentrations, a marker of adipose tissue dysfunction, was found. We concluded that the Adpn/Lep ratio is a good indicator of a dysfunctional adipose tissue that may be a useful estimator of obesity- and MS-associated cardiometabolic risk, allowing the identification of a higher number of subjects at risk.

Neural Responsivity to Food Cues in Patients With Unmedicated First-Episode Psychosis

ImportanceSchizophrenia is associated with a reduced life expectancy of 15 to 20 years owing to a high prevalence of cardiometabolic disorders. Obesity, a key risk factor for the development of cardiometabolic alterations, is more prevalent in individuals with schizophrenia. Although obesity is linked to the altered reward processing of food cues, no studies have investigated this link in schizophrenia without the confounds of antipsychotics and illness chronicity.ObjectiveTo investigate neural responsivity to food cues in first-episode psychosis without the confounds of antipsychotic medication or illness chronicity.Design, Setting, and ParticipantsA case-control study was conducted from January 31, 2015, to September 30, 2018, in London, United Kingdom, of 29 patients with first-episode psychosis who were not taking antipsychotic medication and 28 matched controls.Main Outcomes and MeasuresParticipants completed a food cue paradigm while undergoing a functional magnetic resonance imaging scan. Neural activation was indexed using the blood oxygen level–dependent hemodynamic response. The Dietary Instrument for Nutrition Education was used to measure diet, and the International Physical Activity Questionnaire was used to measure exercise.ResultsThere were no significant differences in age, sex, or body mass index between the 29 patients (25 men and 4 women; mean [SD] age, 26.1 [4.8] years) and 28 controls (22 men and 6 women; mean [SD] age, 26.4 [5.5] years). Relative to controls, patients consumed more saturated fat (t46 = –3.046; P = .004) and undertook less high-intensity (U = 304.0; P = .01) and low-intensity (U = 299.5; P = .005) weekly exercise. There were no group differences in neural responses to food vs nonfood cues in whole-brain or region-of-interest analyses of the nucleus accumbens, insula, or hypothalamus. Body mass index was inversely correlated with the mean blood oxygen level–dependent signal in the nucleus accumbens in response to food vs nonfood cues in controls (R = –0.499; P = .01) but not patients (R = 0.082; P = .70).Conclusions and RelevanceRelative to controls, patients with first-episode psychosis who were not taking antipsychotic medication consumed more saturated fat and showed an altered association between body mass index and neural response to food cues in the absence of differences in neural responses to food cues. These findings highlight how maladaptive eating patterns and alterations in the association between body mass index and neural responses to food cues are established early in the course of schizophrenia.

Reduction of relative handgrip strength and cardiometabolic risk in individuals with HIV/AIDS.

Low handgrip strength (HS) is associated with cardiometabolic alterations that have affected people with HIV/AIDS. This was a cross-sectional study performed in adults receiving antiretroviral treatment. HS was evaluated using a dynamometer and divided by body weight to obtain the relative strength. The association between relative HS and overweight, increased waist circumference (WC), high body fat percentage, glycemia, and lipid ratios were assessed using logistic regression. Low relative HS was identified in 35% of participants and associated with increased WC (odds ratio = 9.7; 95% confidence interval = 2.8-33.0). The prevalence of low HS was high and associated with increased WC.

The role of one-hour post-load hyperglycemia in prediction and prevention of type 2 diabetes

One-hour post-load glucose concentration (1hPG) ≥155 mg/dl (8.6 mmol/L) in individuals with normal glucose tolerance (NGT) was correlated with increased risk for type 2 mellitus. This paper is the Chinese translation One-hour post-load hyperglycemia: implications for prediction and prevention of type 2 diabetes , published on The Journal of Clinical Endocrinology & Metabolism [Fiorentino TV, Marini MA, Succurro E, et al. J Clin Endocrinol Metab, 2018, 103(9): 3131-3143] after obtaining the copyright of the original journal. In this review, the authors analyzed the role of 1hPG measurement in prediction of type 2 and cardiovascular disease. They used MEDLINE and included all English studies published up to February 2018 in peer-reviewed journals that examined the relationship between 1hPG and diabetes, cardio-metabolic alterations, organ damage, and cardiovascular disease. The results showed that although 1hPG was not adopted by American Diabetes Association for identifying high-risk individuals, the available evidence indicated that, among subjects with NGT, a value of 1hPG≥155 mg/dl is helpful to identify those at increased risk of type 2 and cardiovascular disease. (Chin J Endocrinol Metab, 2018, 34: 1060-1066) Key words: 1-h post-load glucose concentration; Diabetes mellitus, type 2; Blood-derived biomarkers

Luteolin Prevents Cardiometabolic Alterations and Vascular Dysfunction in Mice With HFD-Induced Obesity.

Purpose: Luteolin exerts beneficial effects against obesity-associated comorbidities, although its influence on vascular dysfunction remains undetermined. We examined the effects of luteolin on endothelial dysfunction in a mouse model of diet-induced obesity.Methods: Standard diet (SD) or high-fat diet (HFD)-fed mice were treated daily with luteolin intragastrically. After 8 weeks, body and epididymal fat weight, as well as blood cholesterol, glucose, and triglycerides were evaluated. Endothelium-dependent relaxations of resistance mesenteric vessels was assessed by a concentration-response curve to acetylcholine, repeated upon Nw-nitro-L-arginine methylester (L-NAME) or ascorbic acid infusion to investigate the influence of nitric oxide (NO) availability and reactive oxygen species (ROS) on endothelial function, respectively. Intravascular ROS production and TNF levels were measured by dihydroethidium dye and ELISA, respectively. Endothelial NO synthase (eNOS) and superoxide dismutase 1 (SOD1), as well as microRNA-214-3p expression were examined by Western blot and RT-PCR assays, respectively.Results: HFD animals displayed elevated body weight, epididymal fat weight and metabolic indexes. Endothelium-dependent relaxation was resistant to L-NAME and enhanced by ascorbic acid, which restored also the inhibitory effect of L-NAME, suggesting a ROS-dependent reduction of NO availability in HFD vessels. Moreover, media-lumen ratio, intravascular superoxide anion and TNF levels were increased, while vascular eNOS, SOD1, and microRNA-214-3p expression were decreased. In HFD mice, luteolin counteracted the increase in body and epididymal fat weight, and metabolic alterations. Luteolin restored vascular endothelial NO availability, normalized the media-lumen ratio, decreased ROS and TNF levels, and normalized eNOS, SOD1 and microRNA-214-3p expression.Conclusion: Luteolin prevents systemic metabolic alterations and vascular dysfunction associated with obesity, likely through antioxidant and anti-inflammatory mechanisms.

Androgens and the Regulation of Adiposity and Body Fat Distribution in Humans.

The sexual dimorphism in human body fat distribution suggests a causal role for sex hormones. This is of particular importance when considering the role of excess visceral adipose tissue accumulation as a critical determinant of obesity-related cardiometabolic alterations. Scientific literature on the modulation of body fat distribution by androgens in humans is abundant, remarkably inconsistent and difficult to summarize. We reviewed relevant literature on this topic, with a particular emphasis on androgen replacement, androgen effects on selected parameters of adipose tissue function and adipose tissue steroid-converting enzymes. In men, low androgenic status mostly reflected by reduced total testosterone is a frequent feature of visceral obesity and the metabolic syndrome. Regarding testosterone therapy, however, studies must be appreciated in the context of current controversies on their cardiovascular effects. Analyses of available studies suggest that decreases in waist circumference in response to testosterone are more likely observed in men with low levels of testosterone and high BMI at study onset. In women with androgen excess, higher testosterone and free testosterone levels are fairly consistent predictors of increased abdominal and/or visceral adipose tissue accumulation, which is not the case in nonhyperandrogenic women. Regarding mechanisms, androgens decrease adipogenesis and markers of lipid storage in vitro in men and women. Evidence also suggest that local steroid transformations by adipose tissue steroid-converting enzymes expressed in a depot-specific fashion may play a role in androgen-mediated modulation of body fat distribution. Accumulating evidence shows that androgens are critical modulators of body fat distribution in both men and women. © 2018 American Physiological Society. Compr Physiol 8:1253-1290, 2018.

Interplay between epicardial adipose tissue, metabolic and cardiovascular diseases

Cardiovascular disease is the primary cause of death in obese and diabetic patients. In these groups of patients, the alterations of epicardial adipose tissue (EAT) contribute to both vascular and myocardial dysfunction. Therefore, it is of clinical interest to determine the mechanisms by which EAT influences cardiovascular disease. Two key factors contribute to the tight intercommunication among EAT, coronary arteries and myocardium. One is the close anatomical proximity between these tissues. The other is the capacity of EAT to secrete cytokines and other molecules with paracrine and vasocrine effects on the cardiovascular system. Epidemiological studies have demonstrated that EAT thickness is associated with not only metabolic syndrome but also atherosclerosis and heart failure. The evaluation of EAT using imaging modalities, although effective, presents several disadvantages including radiation exposure, limited availability and elevated costs. Therefore, there is a clinical interest in EAT as a source of new biomarkers of cardiovascular and endocrine alterations. In this review, we revise the mechanisms involved in the protective and pathological role of EAT and present the molecules released by EAT with greater potential to become biomarkers of cardiometabolic alterations.