135 research outputs found

    Age at Adiposity Rebound Is Associated with Fat Mass in Young Adult Males—The GOOD Study

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    <div><h3>Objective</h3><p>Age at adiposity rebound (AR) is associated with obesity and Type 2 Diabetes in adults. The aim of the present study was to investigate the role of age at AR in adult fat mass, fat distribution and pubertal timing for a Swedish cohort.</p> <h3>Patients and Methods</h3><p>This is a retrospective cohort study. Detailed growth charts were retrieved for the men participating in the population-based GOOD (Gothenburg Osteoporosis and Obesity Determinants) study (n = 573). Body composition was analysed using dual X-ray absorptiometry and computed tomography at 18–20 years of age. Age and BMI at AR were calculated using pediatric growth charts and AR was defined as the lowest BMI between 3 and 9 years of age.</p> <h3>Results</h3><p>Subjects were divided into early (age at AR below 5.4 years of age), middle (age at AR 5.4 to 6.8 years of age) and late (age at AR after 6.8 years of age) age at AR tertiles. Subjects in the early age at AR tertile had higher young adult BMI (+8%), whole body fat mass (+34%) and amount of subcutaneous adipose tissue (+61%) than the subjects in the middle and late tertiles (p<0.01). The early age at AR tertile had an increased risk of obesity (Odds Ratio 4.1 [95% CI 1.2–13.9]) compared with the middle and late tertiles. In addition, the early age at AR tertile had Peak Height Velocity (PHV) 7 months earlier than the late tertile.</p> <h3>Conclusions</h3><p>Early age at AR was associated with young adult obesity as a consequence of a high amount of subcutaneous adipose tissue in men. In addition we made the novel observation that early age at AR was associated with an early puberty in men.</p> </div

    Linear regression analyses.

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    <p>Linear regression including only age at AR (adiposity rebound; = Crude) and after adjustment for body mass index (BMI) at adiposity rebound ( = adjusted for BMI at AR). Values are given as unstandardized β-values expressed per year. BMI = body mass index, CI = confidence interval, DXA = Dual X-ray Absorptiometry, CT = Computed Tomography, Sc = subcutaneous, Ip = intraperitoneal. Rp = retroperitoneal, AT = adipose tissue, PHV = Peak Height Velocity.</p

    Standardized childhood BMI for early age at AR versus middle and late age at AR.

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    <p>Values are given as Z-score (SD) means ± SEM. BMI = Body Mass Index, AR = Adiposity rebound. *p<0.05, **p<0.01 and ***p<0.001 vs. middle and late tertiles.</p

    Anthropometrics and fat variables.

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    <p>Values are given as median and Inter Quartile Range (IQR). BMI = body mass index, AR = adiposity rebound, PHV = Peak Height Velocity, DXA = Dual X-Ray Absorptiometry, CT = computed tomography. Sc = subcutaneous, Ip = intraperitoneal, Rp = retroperitoneal, AT = adipose tissue.</p

    Correlation analyses for age at AR.

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    <p>Pearson’s correlation coefficients are shown for associations with age at AR. All variables except age at AR and age at PHV have been log-transformed. AR = Adiposity rebound, BMI = body mass index, PHV = Peak Height Velocity, Sc = subcutaneous, Ip = Intraperitoneal, Rp = Retroperitoneal, AT = adipose tissue.</p

    Flowchart of study.

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    <p>GOOD = Gothenburg Osteoporosis and Obesity Determinants Study, AR = Adiposity Rebound, CT = Computed Tomography.</p

    Fat parameters according to age at AR tertiles.

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    <p>Histograms representing early, middle and late age at adiposity rebound tertiles for BMI (a), percentage body fat (b), whole body fat mass (c), serum leptin levels (d), Subcutaneous adipose tissue (ScAT; n = 194; e) and Intraperitoneal adipose tissue (IpAT; n = 194; f). Values are given as means ± SEM. BMI = Body Mass Index, **p<0.01, ***p<0.001.</p

    Resveratrol Treatment Delays Growth Plate Fusion and Improves Bone Growth in Female Rabbits

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    <div><p><i>Trans</i>-resveratrol (RES), naturally produced by many plants, has a structure similar to synthetic estrogen diethylstilbestrol, but any effect on bone growth has not yet been clarified. Pre-pubertal ovary-intact New Zealand white rabbits received daily oral administration of either vehicle (control) or RES (200 mg/kg) until growth plate fusion occurred. Bone growth and growth plate size were longitudinally monitored by X-ray imaging, while at the endpoint, bone length was assessed by a digital caliper. In addition, pubertal ovariectomized (OVX) rabbits were treated with vehicle, RES or estradiol cypionate (positive control) for 7 or 10 weeks and fetal rat metatarsal bones were cultured <i>in vitro</i> with RES (0.03 µM–50 µM) and followed for up to 19 days. In ovary-intact rabbits, sixteen-week treatment with RES increased tibiae and vertebrae bone growth and subsequently improved final length. In OVX rabbits, RES delayed fusion of the distal tibia, distal femur and proximal tibia epiphyses and femur length and vertebral bone growth increased when compared with controls. Histomorphometrical analysis showed that RES-treated OVX rabbits had a wider distal femur growth plate, enlarged resting zone, increased number/size of hypertrophic chondrocytes, increased height of the hypertrophic zone, and suppressed chondrocyte expression of VEGF and laminin. In cultured fetal rat metatarsal bones, RES stimulated growth at 0.3 µM while at higher concentrations (10 μM and 50 μM) growth was inhibited. We conclude that RES has the potential to improve longitudinal bone growth. The effect was associated with a delay of growth plate fusion resulting in increased final length. These effects were accompanied by a profound suppression of VEGF and laminin expression suggesting that impairment of growth plate vascularization might be an underlying mechanism.</p></div

    Liver-derived IGF-I were inactivated at 12 months of age.

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    <p>At 13 months of age, before there was any difference in body weight, food intake, feces output, activity level, and oxygen consumption at rest were determined in female control (n = 8) and LI-IGF-I<sup>-/-</sup> (n = 8) mice. Values are given as means (SEM).</p

    Reduced body weight in LI-IGF-I<sup>-/-</sup> mice.

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    <p>Body weight in A) female and B) male mice. Body weight was determined every third month during 3-30 months of age. Between 3 and 27 months of age, body weight was significantly lower in LI-IGF-I<sup>-/-</sup> compared with control mice in the total number of mice and also in the male and female subgroups (all analyses p<0.001). The vertical bars indicate the SE for the mean values shown.</p
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