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Resting‐state functional magnetic resonance imaging (rs‐fMRI) is frequently used to study brain function; but, it is unclear whether BOLD‐signal fluctuation amplitude and functional connectivity are associated with vascular factors, and how vascular‐health factors are reflected in rs‐fMRI metrics in the healthy population. As arterial stiffening is a known age‐related cardiovascular risk factor, we investigated the associations between aortic stiffening (as measured using pulse‐wave velocity [PWV]) and rs‐fMRI metrics. We used cardiac MRI to measure aortic PWV (an established indicator of whole‐body vascular stiffness), as well as dual‐echo pseudo‐continuous arterial‐spin labeling to measure BOLD and CBF dynamics simultaneously in a group of generally healthy adults. We found that: (1) higher aortic PWV is associated with lower variance in the resting‐state BOLD signal; (2) higher PWV is also associated with lower BOLD‐based resting‐state functional connectivity; (3) regions showing lower connectivity do not fully overlap with those showing lower BOLD variance with higher PWV; (4) CBF signal variance is a significant mediator of the above findings, only when averaged across regions‐of‐interest. Furthermore, we found no significant association between BOLD signal variance and systolic blood pressure, which is also a known predictor of vascular stiffness. Age‐related vascular stiffness, as measured by PWV, provides a unique scenario to demonstrate the extent of vascular bias in rs‐fMRI signal fluctuations and functional connectivity. These findings suggest that a substantial portion of age‐related rs‐fMRI differences may be driven by vascular effects rather than directly by brain function. [ABSTRACT FROM AUTHOR]

Background: Obesity is associated with cardiometabolic disturbances, which may have significant implications for musculoskeletal health and exercise tolerance. Objective: We sought to determine the association between muscle structure, function, and metabolism in adolescents across the weight spectrum. Methods: This cross‐sectional case–control study included overweight and obese participants (n = 24) 8–18 years of age with a body mass index (BMI) ≥ 85th percentile for age and gender, and non‐obese participants (n = 24) with a BMI < 85th percentile. Body composition, physical activity, peak aerobic capacity, cardiometabolic blood markers and insulin resistance (measured by the homeostatic model assessment of insulin resistance, HOMA‐IR), skeletal muscle mitochondrial oxidative capacity (via 31Phosphorous‐Magnetic Resonance Spectroscopy, 31P‐MRS, to assess phosphocreatine (PCr) recovery after exercise), and extramyocellular and intramyocellular lipid (IMCL) levels (via 1Hydrogen‐MRS) were assessed. Stepwise regression was performed to examine the factors associated with oxidative capacity. Results: bese and overweight patients had similar age, height, and physical activity to non‐obese controls, but obese and overweight participants exhibited higher insulin resistance. Obese and overweight participants had longer PCr recovery than non‐obese controls following 5x30s of moderate‐intensity exercise (51.2 ± 20.1 s vs. 23.9 ± 7.5 s, p = 0.004). In univariate correlation analysis, impaired PCr recovery was associated with a higher BMI z‐score (rs = 0.51, p < 0.001), circulating triglycerides (rs = 0.41, p = 0.005), and HOMA‐IR (rs = 0.46, p = 0.001). In stepwise multivariate regression analysis, impaired PCr recovery was associated with a higher BMI z‐score (β = 0.47, p = 0.002), but not insulin resistance (β = 0.07, p = 0.07) or circulating triglycerides (β = 0.16 p = 0.33). Conclusion: A slower phosphocreatine recovery following aerobic exercise is strongly associated with increasing adiposity. A slower metabolic recovery following aerobic exercise stress suggests that endurance exercise training in obese adolescents may be an optimal strategy to target exercise intolerance in this cohort. [ABSTRACT FROM AUTHOR]

Objective To study the relationships between parameters of glucose and insulin metabolism and visceral and abdominal ectopic fat in youth. Methods A cross sectional study of 50 children (24 females), 8-18 years old. Anthropometrics, body composition, blood-work and visceral and ectopic fat by magnetic resonance imaging were assessed. Insulin secretion, insulin sensitivity and beta cell function were calculated from an oral glucose tolerance test. Results BMI z-scores ranged between −1.3 and 4.5. The hepatic fat fraction (HFF) ranged between 0 and 36% and pancreatic fat fraction (PFF) between 0 and 14%. Visceral fat, HFF and PFF were associated with clinical and biochemical metabolic abnormalities, and correlated with markers of insulin sensitivity ( r = −0.60, P < 0.01; r = −0.64, P < 0.01; r = −0.48, P < 0.01, respectively) insulin secretion ( r = 0.55, P < 0.01; r = 0.57, P < 0.01; r = 0.41, P < 0.01, respectively), and beta cell function ( r = −0.49, P < 0.01; r = −0.59, P < 0.01; r = −0.39, P < 0.01, respectively). Conclusions Accumulations of pancreatic and hepatic fat have complementary clinical consequences in youth. While visceral and hepatic fat demonstrated a dominant effect, even relatively small degrees of pancreatic fat deposition may contribute to metabolic alterations. [ABSTRACT FROM AUTHOR]

Background and Objectives Turner syndrome ( TS) confers increased lifetime risk of type 2 diabetes mellitus and cardiovascular disease. We compared cardiometabolic risk factors and measures of subcutaneous, visceral adipose tissue and intra-myocellular lipid between young TS girls and an age- and BMI-standard deviation scores ( SDS)-matched healthy female cohort. Patients and Methods A cross-sectional cohort study was conducted at the Hospital for Sick Children, Toronto. Nineteen TS and 17 control girls (13·7 ± 2·5 vs 12·7 ± 3·4 years of age, respectively, P = 0·30). Multiple-sample oral glucose tolerance test with measurement of fasting insulin, LDL, HDL, triglycerides, adiponectin and highly sensitive C-reactive protein (hs CRP) was performed. Subcutaneous adipose tissue, visceral adipose tissue intramyocellular lipid levels evaluated by magnetic resonance techniques. Insulin secretion ( IS), sensitivity (Si) and the insulin secretion-sensitivity index ( ISSI-2) were calculated from oral glucose tolerance test data. Results Five TS and no controls had impaired fasting glucose or impaired glucose tolerance; none had type 2 diabetes mellitus. Insulin sensitivity and insulin secretion were similar between groups; ISSI-2 was lower in TS (923·5 ± 307·3 vs 659·1 ± 387·3; P = 0·03). TS girls had higher blood pressure (82·5 ± 13·6 vs 73·5 ± 5·5 mmHg; P = 0·0146), waist circumference (76·0 ±11·8 vs 65·9 ± 9·7; P = 0·0087) and subcutaneous adipose tissue (135·6 ± 88·6 vs 69·3 ± 59·9; P = 0·01) than controls. Visceral adipose tissue, intramyocellular lipid levels and adiponectin were not different between groups. TS girls also had higher triglycerides (1·1 ± 0·6 vs 0·7 ± 0·3; P = 0·003), total cholesterol (4·4 ± 0·7 vs 3·9 ± 0·4; P = 0·02) and hs CRP (2·0 ± 1·9 vs 0·8 ± 0·3; P = 0·01). Conclusions TS girls exhibit more cardiometabolic risk factors and reduced beta cell function compared with age- and BMI- SDS-matched girls. Increased awareness of early risk of type 2 diabetes mellitus and hypertension in TS girls is needed. [ABSTRACT FROM AUTHOR]

In industrialized countries, prenatal exposure to maternal cigarette smoking (PEMCS) is the most common environmental insult to the fetus. Here, we tested the hypothesis that PEMCS amplifies accumulation of abdominal fat during the accelerated weight gain occurring in late puberty. This hypothesis was tested in 508 adolescents (12–18 years, 237 exposed prenatally to maternal cigarette smoking) in whom subcutaneous and intra-abdominal fat were quantified with magnetic resonance imaging (MRI). We found that, in early puberty, exposed and nonexposed adolescents did not differ in MRI-based measures of adiposity. In late puberty, on the other hand, exposed compared with nonexposed adolescents demonstrated markedly higher quantities of both subcutaneous fat (by 26%, P = 0.004) and intra-abdominal fat (by 33%, P = 0.001). These group differences remained virtually unchanged after adjusting for sex and potential confounders, including birth weight and breastfeeding. As such, our results suggest that PEMCS may represent a major risk factor for the development of abdominal obesity at the later stages of puberty. [ABSTRACT FROM AUTHOR]